|
 
 |
| REVIEW ARTICLE |
|
| Year : 2022 | Volume
: 12
| Issue : 1 | Page : 1-9 |
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Metabolic syndrome: a review
Chidiebube Jeremiah Ugwu1, Maryann K Oham2, Chioma S Eyisi1, Beatrice Nelson-Ogbonna1, Chidimma Brenda Nwatu1, Christian I Okafor1
1 Diabetes and Metabolism Unit, Department of Internal Medicine, University of Nigeria Teaching Hospital, Ituku Ozalla, Enugu, Nigeria
2 Department of Medicine, Enugu State University Teaching Hospital, Parklane, Enugu, Nigeria
| Date of Submission | 29-Mar-2022 |
| Date of Decision | 26-Jun-2022 |
| Date of Acceptance | 29-Jun-2022 |
| Date of Web Publication | 02-Sep-2022 |
Correspondence Address:
Dr. Chidiebube Jeremiah Ugwu
Diabetes and Metabolism Unit, Department of Internal Medicine, University of Nigeria Teaching Hospital, Ituku Ozalla, Enugu
Nigeria
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ajem.ajem_4_22
Metabolic Syndrome (MetS) is a clinical construct that has continued to gain increasing global relevance due to the rising levels of obesity. It represents a cluster of metabolic abnormalities that include hypertension, central obesity, insulin resistance, and atherogenic dyslipidemia, and is strongly associated with an increased risk of developing diabetes and atherosclerotic and non-atherosclerotic cardiovascular disease.
Regrettably, little consensus has been reached on the application of MetS despite several discoveries. This has limited its usefulness as a clinical tool. MetS as a clinical entity can be faulted as it lacks a scale to measure exactly how much each of its components contributes. Therefore, whether the syndrome as a whole counts more than the sum of its components is still uncertain. Even now, a clear pathophysiologic link between the components of MetS has not been identified, although many theories have been propoundedHowever, some progress has also been made on the link between Metabolic Syndrome and autoimmunity, rheumatic diseases, hyperuricaemia, cancer, dementias, infertility, and most recently non-alcoholic fatty liver disease. In these conditions, the metabolic dysfunction in MetS is believed to cause dysfunction in the immune system and also an elevation in inflammatory markers. There is an increased incidence of MetS in patients with autoimmune and autoinflammatory conditions which may account for the increased incidence of cardiovascular disease in these patients.
In this review, the advances in the understanding and management of MetS are discussed including the conditions associated with MetS. Keywords: Autoimmunity, inflammation, metabolic syndrome
How to cite this article:
Ugwu CJ, Oham MK, Eyisi CS, Nelson-Ogbonna B, Nwatu CB, Okafor CI. Metabolic syndrome: a review. Afr J Endocrinol Metab 2022;12:1-9 |
| Introduction | |  |
Metabolic syndrome (MetS) “represents a cluster of metabolic abnormalities that include hypertension, central obesity, insulin resistance, and atherogenic dyslipidemia, and is strongly associated with an increased risk for developing diabetes and atherosclerotic and non-atherosclerotic cardiovascular disease (CVD)”.[1] Other components include glucose intolerance, and non-alcoholic fatty liver disease.[2] The pathogenesis of MetS involves both genetic (innate) and acquired factors that promote inflammation which leads to CVD and other complications of MetS. MetS has gained appreciable importance now due to the exponential increase in obesity worldwide and its relationship with Atherosclerotic Cardiovascular Diseases (ASCVDs) and their negative impact on Non Communicable Diseases (NCDs).[1]
Metabolic syndrome (MetS) was theorized based on a group of risk factors, such as elevated fasting plasma glucose (FPG), dyslipidemia, elevated blood pressure, and abdominal obesity, in people at risk of cardiovascular disease (CVD) and T2DM.[3]
| History and definitions | | |
MetS, is also known as ‘insulin resistance syndrome’, ‘syndrome X’, ‘hypertriglyceridemic waist’, ‘the triumvirate’, ‘the deadly quartet’, ‘ominous octet’, ‘metabesity’, and ‘diabesity’, is being increasingly recognized as an important metabolic and cardiovascular risk factor.[1],[4],[5]
Ever since 1988, Reaven posited that insulin resistance (IR) was the cause of glucose intolerance, elevated very-low-density lipoprotein (VLDL), hyperinsulinemia, decreased high-density lipoprotein (HDL), and hypertension.[2] Later, the insulin resistance syndrome evolved to be called metabolic syndrome (MetS). MetS is thought to represent a cluster of cardiovascular risk determinants, including glucose intolerance and IR, obesity (especially central adiposity), dyslipidemia (including hypertriglyceridemia, increased free fatty acids (FFAs) and decreased HDL-cholesterol), hypertension, and more recently has also been linked with clinical conditions such as polycystic ovarian syndrome (PCOS), atherosclerosis, oxidative stress, proinflammatory state, and non-alcoholic fatty liver disease (NAFLD).[2],[6]
As a condition with many components, MetS imparts an estimated doubling of risk for atherosclerotic cardiovascular disease and T2DM.[7] However, it is currently not clear how each component of the syndrome confers this risk. Even now, there is still heated debate surrounding the identity of MetS and its utility and capacity.[7] MetS as a clinical entity can be faulted as it lacks a scale to measure exactly how much each of its components contributes. Therefore, whether the syndrome as a whole counts more than the sum of its components is still uncertain.[2] Even now, a clear pathophysiologic link between the components of MetS has not been clearly identified, although many theories have been propounded.[2],[8]
The first internationally recognized definition of MetS was created by the Diabetes Consultation Group of the World Health Organization in 1998.[3] They defined MetS as “the presence of insulin resistance (impaired fasting glucose, impaired glucose tolerance, or type 2 diabetes mellitus) in addition to two of the following risk factors:
obesity (increased waist-hip ratio or body mass index),
hyperlipidemia hypertriglyceridemia,
low high-density lipoprotein [HDL] cholesterol),
hypertension, or
microalbuminuria”.[3]
Since this initial description of MetS, several iterations and modifications of this definition have been proposed [Table 1].[3],[9]
BMI, body mass index; HDL-C, high-density lipoprotein cholesterol; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; IR, insulin resistance; T2DM, type 2 diabetes mellitus; TG, triglycerides; WC, waist circumference; PCOS, Polycystic Ovary Syndrome.[3],[9]
Of interest in the evolution of these definitions is the inclusion of patients already on treatment for one or more components of MetS. Another improvement is the acknowledgment of how WC differs from country to country, and population to population..[3],[9] However, populations whose normative values are yet to be determined are may be said to be at a disadvantage. Several local works have attempted to do so, however, studies to validate these may be necessary and a good starting point for bringing such populations to be on the same pedestal as others.[10],[11],[12],[13] For instance, a study in Nigeria by Okafor C et al. to assess the population-based waist circumference in Nigeria revealed higher values and a different distribution when compared with the global and sub-Saharan waist circumference cut-off recommendations.[10]
| Epidemiology | | |
The epidemiology of MetS varies globally with its prevalence depending on the prevalence of obesity, gender, age, race/ethnicity, and the criteria used for diagnosis.[3],[14] MetS affects about 20% or more of the population of the USA and about 25% of the population of Europe.[3],[15]
A study done in the USA revealed that the prevalence of MetS in African-American women is more than 50% higher than in African-American men and 26% higher in Latin women compared with Latin men. Among the components of MetS, insulin resistance is seen more in Hispanics, hypertension in African-Americans, and dyslipidemia in Whites.[3]
The incidence of MetS increases with the severity of obesity and has been observed in half of the obese adolescents.[2]
Type 2 diabetes is five to six times more common in obese people (body mass index (BMI) 30 kg/m2) than in those of normal weight.[16] Even within different populations exposed to varying environmental factors, increasing BMI is positively linked with impaired glucose tolerance and type 2 diabetes. In turn, this increasing BMI also correlates positively with other MetS components, including increasing total cholesterol, triacylglycerols (TAGS), and low-density lipoprotein (LDL)-cholesterol and reduction in levels of HDL-cholesterol and hypertension.[2],[17]
| Clinical significance of mets | | |
MetS as a clinical construct has been used as a diagnosis, a risk factor, and even an outcome. Conflicting results have been obtained when the added value of MetS is weighed against the information derived from each one of its components for the diagnosis, prevention, and management of its long-term complications.[9]
Also, it has been viewed as a valuable pedagogic tool to help health professionals further understand and appreciate the repercussions of longstanding positive caloric balance and the deleterious metabolic effects of excess body weight.[9]
In an attempt to evaluate the importance of MetS as a diagnostic predictor, different models have been designed, one of which is the MetS-Z score.[9],[18],[19],[20] The MetS-Z score was developed based on the weighted contribution of each component of MetS on a sex- and race-specific basis obtained from the US National Health and Nutrition Examination Survey and is capable of predicting the incidence of type 2 diabetes and cardiovascular events. In a study by DeBoer et al,[19] MetS-Z score was applied to assess the response to a healthy lifestyle program in the Diabetes Prevention Program.[19] The 1- to 5-year risk of developing diabetes was greatly linked with 1-year changes in MetS-Z score and waist circumference, whereas the risk of CVD was associated with a 1-year change in MetS-Z score, blood glucose, and systolic blood pressure. These suggest that the MetS definition is still a work in progress. The use of continuous scores may be an option to improve the identification of people at risk and to assess their response to treatment.[9],[18],[19],[20] These approaches have been widely studied, however, its implementation into clinical practice will require evidence of a clear superiority of its use over the current established practice. As a consequence, MetS cannot be considered a treatment goal or an outcome.[20]
However, a lot of work is needed in sub-Saharan Africa to develop a model to weigh the usefulness of MetS in our population.
| Pathophysiological mechanisms in metabolic syndrome | | |
The pathogenesis of MetS is not fully understood. However, more specifically, one of the most important causal factors of MetS is the accumulation of ‘‘ectopic’’ fat. This often results in a pathological condition that is called ‘‘adiposopathy’’, and is defined as pathogenic adipose tissue that is promoted by a positive energy balance and sedentary lifestyle in genetically and environmentally susceptible patients.[2]
Adiposopathy manifests through a combination of adipose tissue growth, adipocyte hypertrophy, ectopic fat distribution, and, especially, visceral adipose tissue accumulation, all of which leads to deleterious immune and metabolic effects and leads to the development of MetS.[2]
Visceral adiposity has been demonstrated as an important trigger for most of the pathways involved in MetS, thus underlining the role of high caloric intake as an important cause of MetS.[3] Studies have demonstrated a strong association between abdominal obesity and T2DM, even when correcting for general obesity.[1],[8]
The pathways include - insulin resistance, neurohormonal activation, and chronic inflammation [Figure 1]. | Figure 1: Pathophysiological mechanisms in metabolic syndrome (AT2, angiotensin II type 2 receptor; CRP, C-reactive protein; IL-6, interleukin 6; LOX, lectin-like oxidized low-density lipoprotein; RAAS, renin-angiotensin-aldosterone system; ROS, reactive oxygen species; TNF, tumor necrosis factor).[3])
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A) Insulin resistance
Insulin resistance-mediated elevation in circulating free fatty acids (FFAs) is believed to play an important role in the development of MetS. Insulin increases the uptake of glucose in muscle and liver and inhibits hepatic gluconeogenesis and lipolysis.[3]
Insulin resistance in adipose tissue impairs insulin-facilitated inhibition of lipolysis, leading to an elevation in circulating FFAs that further hinders the antilipolytic effect of insulin.[21]
FFAs inhibit the activation of protein kinase in the muscle leading to a reduction in glucose uptake. They (FFA) increase the activation of protein kinase in the liver that promotes lipogenesis and gluconeogenesis. The net effect is the formation of a hyperinsulinemic state to sustain euglycemia.[22]
Eventually, the compensatory hyperinsulinemia fails and insulin secretion decreases. FFAs are also toxic to beta cells of the pancreas causing a reduction in insulin production.[23] Insulin resistance in addition promotes the development of hypertension due to vasoconstriction caused by FFAs, endothelin, and loss of the vasodilator effect of insulin.[23]
Additionally, there is increased sympathetic nervous system activation and reabsorption of sodium in the kidneys. Insulin resistance also causes an increase in viscosity of the serum, induction of a procoagulable state, and pro-inflammatory state due to the release of cytokines from the adipose tissue that contribute to increased risk of CVD and T2DM.[3]
The contribution of visceral fat deposits to insulin resistance is more than that of subcutaneous fat, as visceral lipolysis leads to an increased supply of FFAs to the liver through the splanchnic circulation.[24] Increased supply of FFAs to the liver leads to increased triglyceride synthesis and the production of very-low-density lipoprotein (LDL) in the liver. Elevation of small dense LDL cholesterol and reduction in HDL cholesterol are secondary effects of insulin resistance caused by changed lipid metabolism in the liver.[3],[23]
Visceral adipose tissue is also more metabolically active and produces higher amounts of secretory proteins such as plasminogen activator inhibitor, which promotes a prothrombotic state, and heparin-binding epidermal growth factor, which stimulates smooth muscle cell proliferation and vascular remodeling.[3]
B) Neurohormonal activation
The discovery of endocrine and immune properties of adipocytes has provided further insights into the development of MetS.[24]
Adipokines released from visceral adipose tissue are linked with MetS and CVD. Leptin is a type of adipokine that controls energy homeostasis mediated by the hypothalamus and stimulates the immune cells that activate the Th1 pathway. Obesity causes a rise in leptin levels and higher leptin levels are directly correlated to increased cardiovascular risk.[24],[25] Other pro-inflammatory adipokines include Resistin and Visfatin which cause upregulation of IL-6, IL-8, TNF alpha, and Matrix Metallo-Proteinases (MMPs).[26]
Adiponectin is an anti-atherogenic and anti-inflammatory adipokine and its effects counteract those of leptin. Adiponectin has anti-atherogenic properties and it decreases both vascular reactivity and smooth muscle proliferation and promotes plaque stability.[27] Adiponectin also increases insulin sensitivity, as well as pancreatic beta-cell life span and insulin secretion. Increased expression of adiponectin had positive effects on adipose tissue, e.g., reduction in the size of adipocytes, increase in mitochondrial density, and transcriptional promotion of factors related to efficient esterification of free fatty acids. Adiponectin is a protective factor against the development of diabetes, hypertension, and other cardiovascular complications.[27] Recently, adiponectin was found to be protective against metabolic syndrome in a polycystic ovary syndrome mouse model.[27],[28]
An increase in adipose tissue mass correlates with a reduction in adiponectin levels and higher levels of leptin, both of which enhance CVD risk.[14]
Activation of the renin-angiotensin-aldosterone system (RAAS) also serves as an important neurohumoral pathway leading to the formation of MetS. Angiotensin II (AT II), produced as a result of angiotensin-converting enzyme activation, is also produced by adipose tissue. Obesity and insulin resistance are linked with the elevated formation of AT II. AT II, through activation of the Angiotensin type 1 receptor, activates Nicotinamide Adenine Dinucleotide Phosphate (NADP) oxidase leading to the formation of reactive oxygen species (ROS).[27]
ROS causes a lot of effects including “oxidation of LDL, endothelial injury, platelet aggregation, expression of redox-sensitive transcription factor nuclear factor-kappa-light-chain enhancer of activated B cells (NF-kB), and expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) on the endothelium and vascular smooth muscle cells”.[4]
RAAS, ROS, and LOX-1 have an interrelated positive feedback loop that initiate and sustains a vicious cycle of inflammation, endothelial damage, and fibroblast proliferation that leads to the development of hypertension, diabetes, dyslipidemia, cardiac hypertrophy, and CVD.[4]
C) Inflammation: the final common pathway
Activation of various pro-atherogenic pathways in MetS climaxes in a final common pathway of inflammation that eventually leads to clinical indicators of MetS. obesity and insulin resistance induces systemic oxidant stress that leads to an increase in activation of pathways that promote atherogenesis and tissue fibrosis.[4]
Inflammation plays a vital role in the pathogenesis of CVD and various inflammatory markers have been shown to be elevated in patients with MetS. The clinical significance of these markers - whether they play a role or are merely incidental in the pathogenesis of ongoing inflammation remains uncertain.[27] The macrophages in the adipose tissue are a vital player in immune response and energy metabolism. Pro-inflammatory (M1) macrophages encourage hepatic steatosis and adipogenesis, while anti-inflammatory macrophages (M2) do the reverse.[27]
Tumor necrosis factor-alpha: tumor necrosis factor-alpha (TNF-α) is secreted by macrophages within the adipose tissue and its production rises with an increase in the mass of adipose tissue. TNF-α causes phosphorylation and inactivation of insulin receptors in the adipose tissue and smooth muscle cells, the initiation of lipolysis increasing FFA load, and inhibition of adiponectin release.[18] Obesity and insulin resistance, two major components of MetS, are linked with elevated serum TNF-α levels.[17]
Interleukin 6 and C-reactive protein: Interleukin 6 (IL-6) is a cytokine produced by adipocytes and immune cells and has intricate regulatory mechanisms. IL-6 levels are positively correlated with an increase in insulin resistance and body fat. It acts on the liver, endothelium, and bone marrow, and causes augmented production of acute-phase reactants in the liver, including C-reactive protein (CRP).[27] Studies have shown a relationship between elevated CRP levels and the development of MetS, diabetes, and CVD.[3] IL-6 also results in elevated fibrinogen levels causing a prothrombotic state. IL6 also stimulates adhesion molecule expression by endothelial cells and activation of local RAAS pathways.[4]
High-sensitivity C-reactive protein (hsCRP) is a marker of inflammation that may also help to prognosticate in MetS. . hsCRP levels of less than 1, 1 to 3, and more than 3 mg/L are linked with lower, moderate, and higher cardiovascular risks, respectively.[29]
| RHEUMATIC, AUTOIMMUNE, AND AUTOINFLAMMATORY CONDITIONS ASSOCIATED WITH METS | | |
There is an interaction between the metabolic and immune systems. Metabolic Syndrome represents metabolic system dysfunction and results in a deleterious impact on the immune system, alteration in the gut microbiota, etc that is believed to mediate the other conditions associated with MetS.[30] Adipokines, discussed earlier in this review, have been discovered to contribute to the regulation of chronic inflammation and immune dysregulation linked to MetS.[26],[30],[31],[32]
Several rheumatic diseases (osteoarthritis (OA), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and ankylosing spondylitis (AS)) and autoinflammatory disease (eg. gout, Sjögren’s syndrome, psoriasis, psoriatic arthritis, lichen planus, Behçet’s disease, and inflammatory bowel disease (IBD), etc) have been associated with an increase in the prevalence of CVDs.[26],[33] This increase in CVD in patients with rheumatic and autoimmune disease is believed to be due to the impact of MetS, as the presence of traditional cardiovascular risk factors is not sufficient to explain their elevated risk of cardiovascular disease.[26]
In these conditions, there is a higher proportion of MetS than in other members of the population ranging from 14% to 62.8%.[26],[34] Worthy of note also is that patients with these conditions also have an increased risk of type 2 DM, Hypertension, obesity, and hypertriglyceridemia.[34]
MetS is also linked with other coditions like cancer, infertility, and dementia.[35],[36],[37]
| Visceral obesity and ffas | | |
Elevation of visceral fat promotes an IR state, because, by its nature, it is more impervious to the metabolic effects of insulin than subcutaneous fat. Instead, it is more responsive to glucocorticoids, lipolytic hormones, and catecholamines.[24] The most obvious anomaly in the FFA metabolism of visceral fat is the failure to suppress FFA concentrations through adipose tissue lipolysis which usually occurs in response to hyperinsulinemia. This culminates in an increased CVD risk profile, with endothelial dysfunction, increased vascular smooth muscle cell proliferation, and alteration of circulating LDL-cholesterol and HDL-cholesterol.[24]
This persistently elevated release of FFA into the portal system also provides an augmented substrate for the hepatic formation of TAGs, a state that likely leads to the development of nonalcoholic fatty liver disease and IR.[2] In addition, FFAs themselves directly promote IR. The intracellular accumulation of FFAs in nonadipose tissues in high quantities may encourage the overproduction of damaging metabolites and structural abnormalities and ultimately induce necrosis and systemic inflammation, which again is associated with the development of CVD and T2DM.[2]
The Visceral Adiposity Index (VAI) is a dependable measure of visceral fat function associated with cardiometabolic risk.[38] VAI strongly correlates with MetS and cardio and brain events, correlating stronger the higher the VAI score.[38]
The calculation of VAI is different for men and women. VAI = (WC(cm)/(39,68+(1.88*BMI) *(TG/1.03) *(1.31/HDL) for men and VAI = (WC(cm)/(36,58+(BMI *1.89) *(TG/0.81) *(1.52/ HDL) for women.[38] VAI also correlates more strongly with cardiometabolic complications that individual components of MetS like WC, BMI, TG, or HDL.[38]
| NAFLD: A NOVEL COMPONENT OF METS | | |
The liver is an organ that is vulnerable to ectopic fat accumulation. Currently, the incidence of NAFLD matches the occurrence of obesity and MetS.[2] NAFLD is now one of the most common causes of chronic liver disease worldwide.[2] Because of the strong link to MetS, a recent consensus is to change the nomenclature of NAFLD to Metabolic Associated Fatty Liver Disease (MAFLD).[39],[40]
Approximately a third of the American adult population has NAFLD.[2] Recent estimates of prevalence in the USA are 20–30% for hepatic steatosis and 3.5–5% for non-alcoholic steatohepatitis, and up to 80% of people with type 2 diabetes may have NAFLD.[2] Worthy of note is that NAFLD is not a single disease entity, but describes a spectrum of liver disorders. The disorder ranges from simple fatty liver (steatosis) to more severe steatosis associated with severe inflammation called non-alcoholic steatohepatitis (NASH), which can lead to fibrosis, and thereafter to liver cirrhosis (15–17%), liver failure (3%), and hepatocellular carcinoma.[2]
Remarkably, all constituents of MetS correlate with liver fat, as assessed by H-magnetic resonance spectroscopy, and, even though these measures rise with obesity, they remain noteworthy even when adjusted for BMI. Therefore it is unsurprising that NAFLD is thought to be the hepatic manifestation of MetS.[41] This is similar to how visceral obesity correlates significantly with other components of MetS. In support of this, recent epidemiological studies have revealed that severe NAFLD is correlated to an elevated risk of CVD, independent of underlying cardiometabolic risk factors.[2] A prevalence of 40 – 60% of NAFLD in patients with T2DM in Caucasian, Indian, and Asian populations.[41] However the prevalence in the African population is significantly lower with 16.67% prevalence in T2DN populations and 6.25% in the general population.[41]
While some studies suggest that NAFLD may be involved in the development of CVD, possibly through the augmented release of pro-atherogenic factors from the liver (fibrinogen, CRP, plasminogen activator inhibitor-1, and other inflammatory cytokines). For instance, once substantial hepatic steatosis occurs, the liver develops insulin resistance and overproduces both glucose and VLDL, which in turn leads to hyperglycemia, hypertriglyceridemia, and low HDL concentrations.[2]
However, it is still unclear which comes first – IR or ectopic fat deposition.[2]
Another early marker of MetS is pancreatic fat content.[42] Patients with similar BMI and cholesterol levels differ in their risk of developing MetS based on their pancreatic fat. With high pancreatic fat being a significant risk factor in development of MetS and other cardiometabolic syndromes.[42] Remission of T2DM with some increase in Beta cell function has also been observed in patients who had decreased pancreatic fat regardless of cholesterol or blood glucose levels.[42] Reduction in liver fat content also correlates strongly with reversal in T2DM symptoms and recovery of β cell ability.[42]
| Management of mets | | |
MetS are linked with an elevated risk of both atherosclerotic and nonatherosclerotic CVD. As stated earlier, whether the risk is a sum of its components or if the conglomeration of these components induces a synergistic risk is still unclear. Studies have indicated that MetS doubles the risk of CVD outcomes and increases all-cause mortality by 1.5 times.[43]
Management of MetS involves a double approach that combines lifestyle changes and pharmacological mediations to decrease CVD and other complications.[3]
| Lifestyle modification | | |
As described earlier, MetS results from increased calorie intake more than metabolic requirements. Lifestyle modification is a prerequisite in the management of underlying risk factors. Weight reduction and preservation of ideal body weight are indispensable preventive and management strategies. Strategies include walking 6,000- 10,000 steps daily and dietary modification. The aim of weight reduction is a loss of 7–10% in baseline body weight over a 6–12 months period in addition to a reduction of caloric intake by 500–1000 calories/day.[43]
Dietary modification can also normalize other MetS components: reduced consumption of saturated fats, trans fats, sodium, cholesterol, and simple sugars is facilitate the reduction of dyslipidemia, hyperglycemia, and hypertension, for example, diets high or very low in fat content worsen atherogenic dyslipidemia, as such, 25– 35% of daily caloric intake in the form of fat is usually recommended.[4],[21]
Cautious use of bariatric surgery has shown benefits in the morbidly obese. Weight reduction helps with improvement in all components of exercise. Exercise increases calorie utilization, promotes weight loss, and reduces overall CVD risk: about 30–60 min of moderate-intensity exercise and deliberate efforts to change a sedentary lifestyle can be useful for the management of MetS.[3]
| Pharmacotherapy and natural remedies | | |
Along with altering the underlying risk factors, pharmacotherapy is another pathway for the prevention of CVD. Major pharmacological approaches include management of dyslipidemia with statins, using insulin sensitizers to decrease the risk of diabetes, and decreasing prothrombotic risk with antiplatelet drugs.[3],[9]
Metformin, angiotensin-converting enzyme (ACE) inhibitors, statins, and angiotensin receptor blockers are some of the most used drugs in the treatment of co-morbidities. In the last few years, novel drugs have been identified to be used in the treatment of MetS components. These drugs include sodium-glucose co-transporter 2 (SGLT2) inhibitors, glucagon-like-peptide 1 (GLP-1) agonists, dipeptidyl peptidase 4 (DPP4) inhibitors, and novel dual GIP and GLP-1 receptor agonist (tirzepatide).[44] These drugs have positive effects on more than a single MetS component (ie, weight control and hyperglycemia.[9],[45],[46]
No single drug therapy for MetS is available and currently available medications for MetS components require lengthy use of multiple medications, which is difficult for patients due to reduced compliance and polypharmacy. Thus, there is developing interest in the usage of complimentary alternative medicine (CAM) products. These are naturally occurring compounds which minimize the risk and progression of MetS, although their long-term effect on cardiovascular outcomes is unknown.[9]
Various natural compounds derived from plant extracts, herbs, essential oils, and spices have shown benefit in the management of patients with MetS. Examples of such natural compounds include Tumeric, garlic, cinnamon, neem, cumin, cardamom, ginger, grapes, fish oils (omega fatty acids), etc.[3]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1]
[Table 1]
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