obesity and dyslipidemia; a review running title: obesity
TRANSCRIPT
Obesity and dyslipidemia; A review
Running title: Obesity and dyslipidemia
Type: Original article
Key words: Obesity, Dyslipidemia, Obesity and dyslipidemia correlation.
Disclosure Statement: The authors have nothing to disclose
Authors
ALANAZ, MONA SALAH F
+966 53 207 6242
First Author
5th year faculty of medicine.
Northern border university .
ALENEZI, MANAL MOHAMMED L
+966 55 365 6730
Co Author
6th year faculty of medicine.
Northern border university
ALRUWAILI , NADA KAREEM S
+966 55 814 9226
Co Author
6th year faculty of medicine.
Northern border university.
AlANAZI , WEJDAN SALAMAH B
6th year faculty of medicine.
Northern border university
Email: [email protected]
Mobile ; 0506178047
AlANAZI , ANWAR SALAMAH B
6th year faculty of medicine.
Northern border university
Email: [email protected]
Mobile ; 0535028679
ALJOHANI, HANAN AWETAQ A
+966 55 638 7201
6th year faculty of medicine.
Northern border university .
MUNIRA SALEH ALMURJAN
+966 50 194 6423
5th year faculty of medicine.
Northern border university .
Arwa Ahmed Ayed Alshammari
+966 53 090 4904
6th year faculty of medicine.
Northern border university
Abstract
Background:
Obesity is a chronic health problem which affects large number of individuals.
Obesity prevalence has been increased in many countries, it is one of the major causes
of co-morbidities. The obesity-related co-morbidities including dyslipidemia, which
involves reduced HDL cholesterol, increase in LDL and hypertriglyceridemia.
Aim:
To review the prevalence, risk factors of obesity and dyslipidemia as well as the
correlation between them and their management.
Method:
Online scientific websites were used to search for articles related to the current
subject using different keywords such as obesity, dyslipidemia, obesity and
dyslipidemia.
Result:
30 articles were obtained, 10 of them were included and they were original and
review articles.
Conclusion:
Obesity is increasing globally as a result of modrinization, dyslipidemia is associated
with obesity and both can be managed by change lifestyle and pharmacological
treatment.
Keywords: Obesity, Dyslipidemia, Obesity and dyslipidemia correlation.
Introduction:
Obesity affects a large number of individuals, this number is increasing, obesity is a
chronic health problem which is now recognized as a global epidemic [1]. Obesity
prevalence has been increased in many countries of the world during the 3 past
decades and it is defined at 30 or higher BMI [2]. The prevalence of obesity has been
increased in several developing and developed countries [3]. It was reported that
obesity is one of the major causes of co-morbidities including diabetes, and
cardiovascular diseases, also it is a leading cause for morbidity and mortality [4]. It
has become a pandemic problem and it is the fifth leading cause of mortality globally
[5]. The increase of both overweight and obesity is directly correlated with rising of
the obesity-related co-morbidities prevalence such as dyslipidemia, hypertention,
cardiovascular disease, metabolic syndrome and type 2 diabetes mellitus [1]. Obesity
is associated with rising in plasma triglycerides, dyslipidemia involves reduced HDL
cholesterol, increase in LDL and hypertriglyceridemia [6]. In this review we aimed to
highlight the prevalence, risk factors and management of obesity and dyslipidemia as
well as the correlation between them.
Materials and methods:
Online research via scientific research was used to search for articles related to the
current subjects. Several key words was used to obtain the required articles such as
obesity, dyslipidemia, obesity prevalence, dyslipidemia prevalence, obesity and
dyslipidemia, obesity relation to dyslipidemia. We obtained 30 articles, 20 of them
were excluded as they didn’t focus on the subject, whereas 10 articles were included.
The included articles published between 2011 to 2017.
Discussion:
1.Obesity definition and prevalence:
Obesity is excessive abnormal fat accumulation in the adipose tissue resulting in
severe adverse effects [7]. Obesity is a major factor for the development of
dyslipidemia, hypertension, type II diabetes, cardiovascular diseases, metabolic
syndrome and certain cancers [8-11]. Obesity is measured by BMI and waist-to-hip
circumference ratio (WHR), however BMI is the most commonly used method to
define thinness and fatness and it is the ratio of weight per height (Kg/m2) [12]. WHO
recommended cutoffs of BMI as follows; 18.5-24.9 for normal, 25-29.2 for
overweight, ˃30 for obesity [13]. Obesity is a significant public health problem, it
was claimed that since 1980, obesity has more than doubled globally [4]. The
prevalence increased in the last year in both developing and developed countries [5].
It was reported that there were 1.5 billion adults overweight in 2008 with over 200
million men and 300 million women were obese. The prevalence of obesity differs
between different nations, ranging from below 5% to over 75% [14]. In 2014, there
were more than 1.9 million overweight adults, and over 600 million were obese [15].
Childhood obesity also is highly prevalent where, it was stated that there were 22
million children under 5 years were overweight [14]. In 2014, the number of obese
and overweight children increased to 41 million for those less than 5 years old [15]
and in 2016, there were 43 million children under5 years old were overweight [16]. It
was reported by WHO that the rates of obesity were higher among females [17].
Saudi Arabia is one of the highest prevalence rates of obesity and overweight [18] it is
of great concern as 7 out of 10 individuals are suffering this problem [19]. This
occurred as a result of the economic rise happened and westernization as well as
modernization of the dietary habits among Saudi population which led to the sudden
rise in overweight and obesity prevalence [20,21]. A study from Dammam which
conducted on female nursing students found that 3.8% only were obese and 23.1%
were overweight [3]. However in a survey on 10,735 individuals with 5 years old
showed that obesity was prevalent in 28.7% of respondents, with more prevalence in
females than in males;33.5% and 24.1% respectively [22]. Higher prevalence of
obesity was reported from Hail region, where obesity was prevalent in 63.6%, with
prevalence of 71% in females and 56.2% in males [23]. One study on females in
KSA, showed that 36.9% of households were overweight, whereas 35.5% were obese
[24]. One study was conducted on 5 KSA military regions and it was demonstrated
that 42% had central obesity, 29% were obese and 40.9% were overweight [2]. It can
be concluded that males tend to be overweight, whereas females tend to be obese [4].
Also, WHO found that the prevalence of obesity in KSA was higher in females (30%)
than in males (23%) for those in age range of 18-21 years old [17].
2.Obesity risk factors:
The elevation in obesity and overweight prevalence resulted from combination and
interaction of several factors including genetic, environmental, metabolic, and
behavioural influences [4]. It was reported that high fat diet is the main cause of both
obesity and insulin resistance [26]. It was stated by Horaib et al[2] that obesity is
caused by the modernization of society such as less physical activity, faulty dietary
habits, unhealthy food, and increased stress. The increase in obesity prevalence in
Saudi Arabia returns to increasing in obesity main sources such as many diseases
including diabetes, obstructive sleep apnea hypertension, hyperlipidemia, and
osteoarthritis [22]. In several developing countries, the risk factors for obesity
prevalence including adoption of western lifestyle, decreased physical activity and
high caloric intake [22]. In Saudi Arabia, it was found that diabetes, diet,
hypertension, hypercholesterolemia and physical activity were risk factors for obesity
among men and among women, hypertension, and chronic diseases’ history were the
risk factors [22]. A study from Saudi Arabia showed that BMI increased by presence
of age, diabetes and family history of hypertension [2].
3.Dislipidemia definition, prevalence and outcomes:
Dyslipidemia is lipoprotein metabolism disorders, including overproduction and
deficiency of lipoprotein, it involves increase in the level of LDL, total cholesterol
and triglyceride as well as reduction in level of HDL, in case of promotion of insulin
resistance this results in metabolic syndrome in obesity [27-30]. Most dyslipidemia is
hyperlipidemia which involves high level of triglycerides (TGs), cholesterol or both
or low levels of high density lipoprotein (HDL) in blood [31]. Changes in lifestyle
lead to dyslipidemia development [32]. There are three types of dyslipidemia,
hyperchlosterolemia which involves the elevation of cholesterol level than 100 mg/dl,
hypertriglyceridemia when triglyceride level exceeds 150 mg/dl and HDL level
became lower than 40 mg/dl in male and 50 mg/dl in female, whereas mixed
hyperdislipidemia involves the presence of more than one abnormal lipid content[33].
The prevalence of dyslipidemia varies among different nations based on geographic
region, studied population, gender, socioeconomic development, and the presence of
metabolic disorders and genetic disorders [34]. The American Heart Association
evaluated that more than 34 million adult Americans had cholesterol levels higher
than 240 mg/dL indicating that they required treatment, whereas one third of
population had moderately high cholesterol levels in excess of 200 mg/dL [35]. It was
demonstrated that one third of population of the developed countries have
dyslipidemia [36,37]. However, the prevalence of dyslipidemia varies depending on
ethnicity of the studied group, cultural and socioeconomic characteristics [32,38].
Globally, dyslipidemia prevalence ranged from 2.7% to 51.9% [39-42]. Recently,
dyslipidemia in Saudi Arabia became obvious as a result of changes in
dociodemographic, lifestyle and dietary habits [43]. It was reported that dyslipidemia
ranges from 20%- 44% in Saudi study [44]. It was reported that hypercholesterolemia
and hypertyiglyceridemia are prevalent in 50% of adult Saudi population [45].
Dyslipidemia is one of the main risk factors for many chronic non-communicable
diseases resulting in morbidity and mortality [44]. It is responsible for the
development of atherosclerosis [46,47], type 2 diabetes [48,49], stroke [50,51], and
cardiovascular diseases [52,53]. Dyslipidemia is an important risk factor for Coronary
heart disease (CHD) and WHO reported that dyslipidemia is responsible for more
than 4 million deaths/ year and more than half of global cases of ischemic heart
disease [54]. Also, diabetes mellitus is associated with dyslipidemia, where diabetic
patients have an average LDL-C levels in excess of 140 mg/dL [55].
4.Correlation between obesity and dislipidemia:
It was stated that obesity is associated with several comorbidities including
dyslipidemia, non-alcoholic fatty liver disease (NAFLD), hypertension and
hyperglycemia [38]. One study reported that the prevalence of dyslipidemia was
increased with increasing BMI, also it was reported that both overweight and obesity
are important risk factors for this disease [56]. In fact obesity is an independent risk
factor for dyslipidemia development [57]. Dyslipidemia of obesity involves increased
free fatty acids and triglycerides, while HCL-C decreased and normal or slightly
increased LDL-C with increased small dense LDL, also there is increase in plasma
apolipoprotein (apo) B [58,59]. It is thought that the other lipid abnormalities return to
hypertriglyceridemia as it leads to formation of small dense LDL [60,61] and delayed
clearance of the TG-rich lipoproteins [62-64]. In obesity, the lipolysis process of TG-
rich lipoprotein is impaired as a result of reduction in mRNA expression levels
leading to increase in TG [65]. The levels of free fatty acids rise as postprandial
lipemia increase [66]. TG content of LDL increase by CETP activity, while the
cholesterol-ester content of LDL decreases in the presence of hypertriglyceridemia
[66]. Small, dense LDL particles are formed by the action of hydrolyzation of hepatic
lipase on the TG content of LDL, so the small dense LDL in obesity results from TG
concentration and it is independent of total body fat mass [67]. Metabolism of HDL is
influenced by obesity, CETP activity increases by increasing the number of TG-rich
lipoproteins, which exchanges cholesterolesters from HDL for TG from VLDL and
LDL [68]. Also, the reduction of HDL-C result from the lipolysis of TG-rich HDL by
hepatic lipase producing small HDL with a reduction in its affinity for apo A-I,
leading to dissociation of apo A-I from HDL and finally decrease in HDL-C levels
[69]. A study from Iran showed that there was significant relation between BMI with
TG and LDL , where TG and LDL-C were significantly higher in obese and
overweight students [70]. A study in India demonstrated that the mean level of
cholesterol, LDL-C and TG were significantly higher in obese individuals, and there
was an increased risk for dyslipidemia among obese individuals than in normal ones
[57]. Another study from India showed that in individuals with high BMI, total
cholesterol, LDL, very LDL and TG were higher compared to normal ones, however
HDL showed no significant difference [71]. In Saudi study [72] it was found that
dyslipidemia was high in obese patients with more prevalence of hypertriglyceridemia
type, where 72.2% of obese patients had cholesterol level more than 200 mg/dl,
75.6% of obese patients had LDL level higher than 100 mg/dl, 77.78 % had
triglyceride more than 150 mg/dl and 55.6% had lower HDL. A study by Jacob et al
[57] revealed that cholesterol level was higher in obese persons. Study in Saudi
Arabia [73] showed that all types of dyslipidemia were associated with obesity except
HDL.
5.The management of obesity and dislipidemia:
Obesity-associated dyslipidemia treatment should based on changes in lifestyle such
as healthy diet, weight loss and physical exercise. Both dyslipidemia and insulin
resistance in turn are improved by changing life style [74]. Increasing HDL levels and
decreasing LDL can manage both obesity and dislipidemia [1]. It was showed that in
patients with low LDL, treatment by statin reduced the cardiovascular events [75]. By
loss of weight it is expected to decrease LDL-C which may be attributed to increased
LDL receptor activity, it was demonstrated that losing of 4-10 Kg in obese individuals
leads to reduction in LDL-C by 12% and increase in LDL receptor mRNA levels by
27% [76,77]. Weight loss was found to reduce fasting and non-fasting TG
concentrations which lead to decrease in CETP activity [78,79], hence increased
catabolism of TG-rich lipoproteins [80]. Reduction in intra-hepatic TG content is
induced by exercise even in absence of weight loss [81]. 16 weeks of exercise training
in NAFLD obese persons result in a small reduction in intra-hepatic TG content, but
with no changes in VLDL-TG [82]. In overweight men, intra-hepatic TG content was
reduced by ingestion of low fat diet for three weeks [83]. It was confirmed in studies
that focused on blood lipids that plasma TG was lowered by exercise and weight loss
[84], while the effect of exercise on HDL-C levels is controversial [85]. Dyslipidemia
can be affected by other types of food such as ingestion of dietary fiber and resistant
starch which has been associated with insulin metabolism and improve nutrient
absorption [66]. It was reported in a randomized study that intake of resistant starch
supplementation (40 g/day) for 8 weeks improved insulin resistance and subsequently
FFA metabolism in insulin resistant individuals. Also the ingestion of resistant starch
promoted the lipolysis of TG with increased FFA uptake by skeletal muscle and
lowered fasting FFA concentrations [86]. However, TG and cholesterol
concentrations weren’t affected by resistant starch supplementation [86,87]. The
changes in lifestyle seem to be insufficient to improve dyslipidemia and achieve
weight loss [66]. Combination of pharmacological treatment with modification of
lifestyle in obese individuals with dyslipidemia is dependent on the calculated
cardiovascular risk, the potential underlying primary lipid disorders and co-morbidity
[88,89]. In case of high risk individuals who suffer diabetes mellitus, cardiovascular
disease, primary lipid disorders like familial hypercholesterolemia or familial
combined hyperlipidemia require suitable pharmacological treatment independent
from obesity [89,90]. The first choice of drug is statins among all pharmacological
agents to reduce non-HDL-C, LDL-C, and/or apo B, however statins reduce TG only
and don’t totally correct the dyslipidemia seen in obesity and this in turn may assist in
the risk after initiating statin therapy [91]. Statins perform their action by the
inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) enzyme, this is
the rate limiting step in the hepatic cholesterol synthesis. This results in increase in
the fractional catabolic rate of both LDL and VLDL with a slight reduction in hepatic
secretion of VLDL. Hence, statins reduce both LDL-C levels and remnant cholesterol
[92]. Combination therapies with statain was investigated, it was found that statains
can be combined with ezetimibe, which inhibits the intestinal absorption of
cholesterol by interaction with NPC1L1 and this results in reduction of LDL-C by
20%, however there was no impact on TG or HDL-C. Fibrates which are fibric acid
derivatives are another agent that primarily indicated in the case of
hypertriglyceridemia, they result in increase in HDL-C by 9% as an average and TG
reduction by 30% as well as LDL-C reduction by 8% [93]. Fibrates transcriptionally
regulate lipid metabolism related genes as they are peroxisome proliferator-activated
receptor-α agonists [66]. Nicotinic acid inhibits the lipolysis of adipocytes, which
results in reduction in VLDL synthesis, decreased FFA levels, decreased catabolism
of HDL and a slight rise in HDL production rate [92]. These events lead to reduction
in TG levels by 15%–35% and increase in HDL-C concentration by 10%–25%
[88,92]. There is no clinical benefit by adding niacin to patients with typical
dyslipidemia, known history of cardiovascular disease, and intensively controlled
LDL-C levels with statin therapy, only fasting TG is reduced and HDL-C is increased
[94]. Data about combination of statins with niacin in obesity is scarce [66]. Omega-3
fatty acids decrease the accumulation and hepatic synthesis of TG [95], and it was
found that reduce plasma TG by 25%–30% by lowering the hepatic secretion of
VLDL in insulin resistant persons [92,96]. Omega-3 fatty acids also were found to
increase the conversion of VLDL into IDL, and this enhance the benefit for
combining omega-3 fatty acids with statins by increasing the catabolism of VLDL,
IDL and LDL [159of05].
Conclusion:
The current review concluded that obesity was increasing globally including
developing countries as developing countries started in changing the lifestyle and
their dietary habits. Obesity results in dyslipidemia development, dyslipidemia of
obesity involves decreased in HDL-C level and increased triglycerides, with normal
or slightly increased LDL-C as well as increased small dense LDL. Obesity as well as
dyslipidemia are associated with several diseases and co-morbidities. The
management of obesity and dyslipidemia based on two main strategy; changing
lifestyle and pharmacological treatment, however pharmacological treatment is
dependent on the individual conditions he suffers.
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