Running head: THE EFFECTS OF DIET AND STATINS ON HYPERLIPIDEMIA

The Effect of Diet and Statins on Hyperlipidemia

Sara Belcastro
Jason Hockey
Madalyn Lyons
Austin Mclean
Alex Mickler
Youngstown State University
April 13th, 2015

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Abstract
The purpose of this literature review is to evaluate the effectiveness of the use of prescribed
lifestyle modifications (with particular focus on diet) and pharmacological agents (specifically
statins) on hyperlipidemia. Critical review of statin use and their efficacy in treating
hyperlipidemia is performed. Secondly, non-pharmacological lifestyle modifications are
examined and critiqued. Critique and evaluation of these treatment modalities is done by
examination and analysis of several peer reviewed studies. After this examination and analysis
was concluded, the findings suggest that a combination of lifestyle modifications and statin use
is the ideal treatment for decreasing low density lipoprotein cholesterol (LDL) and increasing
high density lipoprotein cholesterol. The implication of this study is a further understanding for
the nursing community of the treatment modalities prescribed to patients with hyperlipidemia.
This extends to improved patient care, as well as allowing nurses to more effectively carry out
the roles of patient advocate and educator through the use of evidence based practice.

Introduction

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In 2014, the Center for Disease Control published a report stating that heart disease was
the leading cause of death in America (CDC, 2015). Heart disease is a general term that refers to
changes in the heart resulting from blockages, narrowing of the arteries, angina, stroke,
alterations in the structures of the heart such as valve malfunctions and dysrhythmias. Managing
blood lipid levels is essential to the prevention of CVD and the morbidity and mortality related.
Recently, elevation of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) has
received the most attention in prevention of cardiovascular risk. The modifiable factors like TC
and LDL-C can be managed by lifestyle changes and pharmacological therapies. Nurses must
consider the effectiveness of statins in lowering LDL-C levels in order to improve patients
quality and longevity of life. To further the understanding of the relationship between these
treatment modalities and patient outcomes, the question to be considered is as follow: How does
diet modifications and statin therapy affect cholesterol? Evaluation of literature will assist in
determining the effectiveness of dietary modifications and/or the use of statin therapy in reducing
lipid levels.
Review of Literature
Increased awareness of nutrition has brought about a change in treatment of
hyperlipidemia. Strong evidence has revealed that dietary choices influence factors on blood
pressure, glucose, and lipid levels. Hyperlipidemia, elevated blood lipid levels, may lead to
atherosclerosis, a contributing factor to heart disease. Thus, by reducing total cholesterol levels
to below 200 (the recommended value given by the American Heart Association)(AHA 2004),
risk for heart disease decreases. Concerning lipid level management, low density lipoprotein
cholesterol (LDL-C) is of particular importance. According to Dujrudee Chinwong, Jayanton
Patumanond, Surarong Chinwong, Khanchai Siriwattana, John Joseph Hall, and Arintaya

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Phrommintikul, whose credentials range from members of Department of Pharmaceutical Care in

Thailand to the Center of Excellence in Applied Epidemiology, intensive LDL-C-lowering
therapy is needed soon after it is diagnosed in order to reduce the likelihood of complications
from coronary artery disease (2015).
Dietary saturated fatty acids (SFAs) are the dietary factor with the strongest impact
(elevation) on LDL-C. Trans-unsaturated fatty acids are less commonly found in foods but have
a similar effect on LDL-C (Catapano, Reiner 2011). Conversely, polyunsaturated fatty acids aid
in lowering LDL-C levels as well as lowering triglyceride (TC) levels. Omega-3 is a specific
type of polyunsaturated fatty acid found in oily fish. Wild salmon and mackerel are great sources
of Omega-3 fatty acids. As of now, there are currently no dietary guidelines for optimal omega-3
intake, however, the American Heart Association recommends eating fatty fish at least twice per
week. Limiting consumption of saturated fats and increasing consumption of fish and omega-3
fatty acids can reduce cholesterol levels. This is observed in a study titled The Nurses Health
Study which showed that women with higher consumption of fish and omega-3 polyunsaturated
fatty acids had a lower risk of cardiovascular disease (Barrett 2013).One study has shown that a
combination of foods could reduce cholesterol as well as c-reactive protein levels similar to that
of a statin. An elevated c-reactive protein level increases a person's risk of cardiovascular
disease. The study completed by Jenkins, D. A., Kendall, C. C., Marchie, A., Faulkner, D. A.,
Josse, A. R., Wong, J. W., and Connelly, P. W.(2005), used participants that had previously
elevated LDL levels. The participants were randomized into three groups. The statin group was
on a very low-saturated-fat dairy and whole wheat cereal diet with a statin. The control group
was on a very low-saturated-fat dairy and whole wheat cereal diet without a statin. Lastly the
portfolio group was on a low-saturated-fat diet containing fibers, sterols, soy foods, and almonds.

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All diets used were vegetarian. The statin used was 20mg lovastatin. Jenkins et al (2005) found
that the
c-reactive protein was reduced similarly on both statin, -16.3+/-6.7% (n=23, p=0.013) and
dietary portfolio, -23.8+/-6.9% (n=25, p=0.001) but not the control, 15.3+/-13.6% (n=28,
p=0.907). The application of this study is limited due to how many patients could and would be
compliant with a vegetarian diet (Jenkins, 2005).
Using dietary supplements may also be a strategy to improve plasma lipid levels. Dietary
supplements can be used either as an alternative to or in junction with lipid-lowering drugs.
Phytosterols are found naturally in vegetable oil and small amounts in almonds, chestnuts, grains
and legumes. The daily consumption of 2g of phytosterols can effectively lower TC and LDL-C
by 7-10% with little effect on HDL-C. Soy protein can be used instead of animal proteins that are
high in saturated fatty acids. Soy proteins are expected to lower LDL-C by 3-5% (Catapano &
Reiner, 2011). In addition to dietary modification, statin treatment must also be considered when
evaluating methods of cholesterol reduction.
Statin use for treatment of hyperlipidemia has become quite common around the world,
and seems to be a first line treatment for many patients with hyperlipidemia.Statins primarily act
on reducing the synthesis of cholesterol in the liver by competitively inhibiting HMG-CoA
reductase. This would then cause a cascade effect lowering serum LDL-C levels (Catapano &
Reiner, 2011).With this increased use and dependence on statin therapy studies have begun to
flood in questioning their potency. In a meta analysis of 26 randomized trials of statins, 10%
reduction in all-cause mortality and 20% reduction in CAD death was recorded (Catapano,
Reiner 2011).This study also suggested that the capacity of statins to lower LDL-C depends
highly on the dosage and type of statin prescribed. Therefore, the prescribed statin should be

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chosen based on the individual patients goal or desired TC or LDL-C levels.While this meta
analysis provides evidence that statins can be effective in mitigating potential complications of
hyperlipidemia, it does not specify that these reductions are because of an optimal TC or LDL-C
level.
In a particular study, conducted by Bojadzievski, Gabbay, Hollenbeak, and
Schaefer(2012), the use of statins and their effect on LDL-C control found that there is a
positive relationship between Statin and LDL-C control in the community setting. This
conclusion was reached by a retrospective observational study. In this study they used a total of
109 primary care providers and simply observed patients who had levels of LDLs less than 130
as well as less than 100 and the number of those patients on statins. The findings of this study
were that there was a linear association of patients with the intended levels of LDL and statin
use. What this means as the patients were prescribed statins the number of patients who were
within the goal parameters for LDL increased (Bojadzievski, Gabbay, Hollenbeak, & Schaefer,
2012).
Statins are not without flaw though. One study found that alone statin therapy did not
lower LDL-C to optimal levels.In this study conducted by Al-Khateeb, Al-Talib, Mohd, Yusof,
and Zilfalil (2013) there was a list of 980 dyslipidemic files collected for research data from, but
in the studies only patients who were on the standard statin dose and those receiving the statin or
other dosages after the index date of January 2007 were selected.The studys findings were as
stated by Al-Khateeb, 2013 There was a significant difference in the lipid profiles between the
dyslipidemic patients in this study and healthy populations from other studies for total
cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol and
triglyceride level, respectively. (Al-Khateeb, Al-Talib, Mohd, Yusof, Zilfalil, 272, 2013). This

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statement explains that with just statin use, lipid levels of the subjects in the study were not near
the parameters of normal lipid levels in the healthy population. Further, regarding the use of
statins, a study conducted in Thailand based on their potency and effects on LDL-C will be
reviewed.
Dujrudee Chinwong and her colleagues performed a retrospective cohort study by
retrieving acute coronary syndrome patients information from the electronic database at Maharaj
Nakorn Chiang Mai Hospital. Patients selected were diagnosed with either angina pectoris or
acute myocardial infarction. A total of 1,089 patients diagnosed with ACS were identified, but
only 396 remained in the final analysis due to missing data or baselines already below the target
range (<70mg/dL). With this exclusion, the group used for the study had an average younger age
(64.411.9 years versus 67.812.7 years, respectively, P<0.001). The remaining sample was then
categorized into two groups by statin potency (Chinwong et al., 2015).
In total, 396 patients were included in the study, with 229 (57.8%)
treated with high potency statins and 167 (42.2%) with low potency statins.
Patients using high potency statins had higher total cholesterol and LDL-C
levels at baseline, therefore they were believed to have an increased
severity of illness (Chinwong et al., 2015). Patients in the high potency statin
group were treated with simvastatin (40 mg), rosuvastatin (10 mg or 20 mg),
atorvastatin (20 mg or 40 mg), or pitavastatin (2 mg) daily, and were
expected to achieve an LDL-C reduction of 40% based on previous studies.
The low potency statin group included patients on simvastatin (10 mg or 20
mg) or pravastatin (40 mg) daily, and were expected LDL-C reduction of
<40%. According to Chinwong et al., the patient goal was to reach below 70

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mg/dL (<1.8 mmol/L) during the follow-up period of 2 weeks to 1 year

(2015).
24.9% of the patients using high potency statins reached their target LDL-C, and 23.4%
of patients using low potency statin group reached their target. According to the authors, high
potency statins were not associated with increased LDL-C goal attainment (adjusted hazards
ratio 1.22, 95% confidence interval 0.791.88; P=0.363). Chinwong et al. (2015) stated,
"Patients using high potency statins were no more likely to reach their LDL-C target than
patients on low potency statins (hazards ratio 1.15, 95% confidence interval 0.761.73,
P=0.516), and the results remained the same after adjusting for propensity score (adjusted
hazards ratio 1.22, 95% confidence interval 0.791.88, P=0.363, Table 5)." (p. 127). Elements
pertaining the studys framework will be evaluated to establish its claims legitimacy.
This study was approved by the research ethics committee, Faculty of Medicine, and
Chiang Mai University in Thailand before commencement. The tertiary hospital used in the
analysis serves patients in Chiang Mai province, which has a population of 1,600,000, and
receives patients from 17 other provinces in northern Thailand. The selection of the population
involved those with either angina pectoris or mycardial infarction. These diagnoses confer with
Chinwongs reviewed literature sources, as valid candidates because coronary artery disease
usually occurs due to unstable angina, non-ST segment elevation myocardial infarction, or ST
segment elevation myocardial infarction. The researchers used a Cox proportional hazard model
to determine the relationship between statin potency and LDL-C goal attainment and a
propensity score adjustment to control for confounding by indication (Chinwong, et al., 2015).
Although there is substantial support for the studys credibility, other factors may have
contributed to the low success rate of statin therapy within the analysis.

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One factor which may have attributed to the low target attainment rate was the LDL-C
goal (<70 mg/dL), based on the guidelines of the European Society of Cardiology and the
European Atherosclerosis Society (ESC/EAS). This is a more difficult level to achieve than the
updated standard set by the National Cholesterol Education Program/Adult Treatment Panel III
(NCEP/ATP III) guideline (<200 mg/dL). However, more aggressive LDL-C targets are
recommended for ACS patients compared to healthy patients. (Chinwong, 2015). Also, the high
potency statins of this study, as they are defined, fall into the category of low to moderate
potency category used in the study by Rallidis et al. (Chinwong, 2015). These factors affect the
analysis itself, but other contributing factors may be more diversely generalized.
Approximately 25% of patients in this study (with LDL-C higher than 140 mg/dL at
baseline) would require combination therapy, including a statin to achieve their target LDL-C.
However, only seven patients (1.8%) were prescribed combination therapy, consistent with other
studies reviewed by Chinwong et al., reporting that statin combination therapy was used less
frequently in routine practice (2015). Due to potential adverse effects, including an increase in
muscle toxicity, cardiologists were possibly reluctant to titrate statin doses upwards, especially
since doubling the dose of a statin results in lowering LDL-C by only an additional 6%
(Chinwong et al., 2015). Simvastatin (40 mg), the most commonly used high potency statin, can
only result in about 43% LDL-C reduction and cannot decrease the LDL-C level to <70 mg/dL in
patients with a baseline level at <140 mg/dL, according to L. Osc, D. Budinski, N. Hounslow,
and V. Arneson. In this situation, atorvastatin, rosuvastatin or statin combination therapy should
be used to lower LDL-C to the target level (Chinwong et al., 2015, p. 130).
A positive relationship between statin potency and LDL-C goal attainment is well
established in some randomized controlled trials, while Chinwong et al. and other studies have

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shown results which suggest that the potency of the statin used does not increase the likelihood
of reaching the recommended goal (2015). Combination therapy may be necessary to reach ideal
patient outcomes.
In conclusion, both statin use and diet modifications can be effective in lowering LDL-C.
This does not however mean that one is a replacement for the other. Patients may not be able to
rely on statin therapy alone because doctors are hesitant to increase dosages due to increased
risks with minute benefits, and also are not prescribed sufficiently with other pharmacologic
drugs. The research presented here shows that diet modifications alone may only offer a
moderate decrease in LDL-C and to bridge the gap between, statins provide an adequate
reduction in LDL-C. Recommended based on the reviewed literature, a combination of diet
modification and statin use is superior to either singular treatment modality.

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Lowering Therapy in the Achievement of Therapuetic Goal among Malaysian
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1, 2015, from CINAHL.
American Heart Association. 2004. Building Healthier Lives Free of Cardiovascular Disease and
Stroke. Accessed April 6th 2015. http://www.heart.org/HEARTORG/
Barrett, S. (2013). The role of omega-3 polyunsaturated fatty acids in cardiovascular health.
Alternative Therapies in Health & Medicine, 1926-30.
Bojadzievski, T., Schaefer, E., Hollenbeak, C. S., & Gabbay, R. A. (2012). Association between statin use
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Primary Care, 20(6), 401-407
Catapano, A. L. , Reiner, Z (2011). ESC/EAS Guidelines for the management of dyslipidaemias The Task
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Chinwong, D., Patumanond, J., Chinwong, S., Siriwattana, K., Gunaparn, S., Hall, J. J., &
Phrommintikul, A. (2015). Statin therapy in patients with acute coronary syndrome: low-density
lipoprotein cholesterol goal attainment and effect of statin potency. Therapeutics & Clinical Risk
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