Introduction
A collection of disorders related to metabolism that increase the risk of cardiovascular disease is known as the cardiometabolic syndrome. Although the exact mechanism(s) behind the development of the cardiometabolic syndrome are unknown, multi-organ insulin resistance, a frequent hallmark of the syndrome, is most likely one of them. An essential risk factor for type 2 diabetes, insulin resistance can result in vasoconstriction and renal salt reabsorption, both of which raise blood pressure. The pathophysiology of insulin resistance includes changes in adipokine and adipose tissue fatty acid metabolism.
The capacity of insulin to promote muscle glucose uptake and inhibit hepatic glucose synthesis can be compromised by excessive rates of fatty acid release into the circulation. Insulin resistance may also be brought on by non-infectious systemic inflammation linked to the cytokine production of adipocytes and adipose tissue macrophages. Moreover, dyslipidemia can result from an increased supply of free fatty acids to the liver, which can drive the formation of very low-density lipoprotein triglycerides in the liver.
What Pathophysiology BehindCardiometabolic Syndrome?
Insulin resistance is another name for cardiometabolic syndrome, as it is thought to be the primary mechanism causing the metabolic abnormalities associated with the syndrome. The pathophysiology of dyslipidemia and hyperglycemia linked to the cardiometabolic syndrome most likely involves changes in the metabolism of free fatty acids. Insulin's capacity to promote muscle glucose uptake and inhibit hepatic glucose synthesis may be hampered by excessive release of free fatty acids from adipose tissue and elevated concentrations of free fatty acids in plasma. Additionally, hepatic very low-density lipoprotein triglyceride synthesis and plasma triglyceride concentration can also rise with increased transport of free fatty acids to the liver.
Triglycerides are transferred from very low-density lipoprotein to high-density lipoprotein more readily as plasma triglycerides rise. This phenomenon results in higher clearance of high-density lipoprotein and a lower concentration of high-density lipoprotein in plasma. Insulin is the primary physiological regulator of basal adipose tissue lipolytic activity because it suppresses lipolysis. Plasma-free fatty acids are primarily produced by the lipolysis of triglycerides in adipose tissue. Thus, increased lipolytic rate and bloodstream release of free fatty acids are caused by insulin resistance in adipose tissue. Insulin-resistant obese individuals have elevated basal lipolytic rates and plasma-free fatty acid concentrations because the usual rise in plasma insulin concentrations linked to obesity does not entirely offset adipose tissue insulin resistance.
How is Abdominal Adipose Tissue Linked to Insulin Resistance?
Insulin resistance is linked to increased visceral (intraperitoneal) fat in the abdomen. Visceral fat may or may not only be linked to insulin resistance; this is unknown. Visceral fat makes up a negligible portion of the quantity of fat in the body. In lean males, visceral fat makes up around 10 percent of total body fat mass, but in obese men, it makes up 15 percent. However, because these fatty acids reach the portal vein and go straight to the liver, it has been suggested that they constitute a major contributor to insulin resistance generated during the lipolysis of visceral adipose tissue.
How is Increased Blood Pressure Linked to Insulin Resistance?
There is ample evidence linking insulin resistance to hypertension. Vasoconstriction can be brought on directly by fatty acids. Furthermore, insulin resistance can raise blood pressure because hyperinsulinemia enhances renal salt reabsorption, and insulin is a vasodilator. The vasodilatory impact of insulin is often lost in insulin-resistant individuals, but the renal effect on sodium reabsorption is preserved. Additionally, individuals with cardiometabolic syndrome have enhanced salt reabsorption.
What Are the Criteria for Metabolic Syndrome?
If a person has three or more symptoms, they are considered to have metabolic syndrome.
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Excess Abdominal Weight: A circumference of around 40 inches for males and individuals designated male at birth (AMAB) and 35 inches for women and those assigned female at birth (AFAB) indicates excess abdominal weight.
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Hypertriglyceridemia: A high amount of triglycerides (150 mg/dL) in the blood is known as hypertriglyceridemia.
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Low HDL Cholesterol: 40 mg/dL or less in men and AMAB individuals, 50 mg/dL in women and AFAB individuals.
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Hypertriglyceridemia: A blood level of 150 mg/dL or above of triglycerides.
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Low HDL Cholesterol: Less than 40 mg/dL in men and individuals with AMAB blood type or less than 50 mg/dL in women and individuals with AFAB blood type.
What One Can Do to Improve the Cardiometabolic Health Scorecard?
The following are ways to improve the cardiometabolic health scorecard:
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Check the cholesterol, blood pressure, and blood sugar levels. If they are outside the optimal range, determine what actions may be taken to enhance them. To aid all three, for instance, getting enough exercise is beneficial.
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Increase daily physical activity and follow a nutritious diet to shed extra pounds and shed the extra weight.
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Give up smoking. Numerous cancers and other health issues, including poor cardiometabolic health, are greatly increased by smoking. The medical staff can assist a patient in developing a stop-smoking strategy that may involve taking medication or utilizing free smoking cessation tools.
How Cardiometabolic Health Can Be Managed?
The treatment of metabolic syndrome necessitates lifestyle modifications.
The following offers suggestions for an integrated strategy for metabolic syndrome lifestyle interventions:
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Physical Activity - Guidance on increasing physical activity, scheduling regular workouts, and incorporating more movement into everyday tasks (such as using the stairs rather than the lift).
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Diet: For medical nutrition counseling, a trained dietician should be referred.
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Weight Loss - Reduced waist circumference and body mass index (BMI) are the two main weight loss objectives.
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Quit Smoking - Helping people quit smoking: Offer counselling or suggest a smoking cessation facility.
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Reduce hba1c - Reduced fat, low carbohydrate, and low-calorie diets can help control high blood sugar levels. Suggested frequent physical activity, exercise, and a medication regimen containing medicines beneficial to metabolic syndrome should be considered.
Conclusion
An array of ailments, including dyslipidemia, insulin-resistant glucose metabolism, elevated blood pressure, and abdominal obesity, are collectively referred to as cardiometabolic syndrome. Changes in the metabolism of fatty acids, such as the increased release of fatty acids into plasma, probably cause metabolic anomalies.
Increased free fatty acids can cause decreased high-density lipoprotein concentrations and increased blood glucose concentrations by impairing the action of insulin in skeletal muscle and the liver; they can also stimulate the production of triglycerides from very low-density lipoprotein in the liver, increasing serum triglyceride levels and possibly raising blood pressure; and they can stimulate vasoconstriction and increase sodium reabsorption. Children and adults can avoid cardiovascular disease by receiving early diagnosis and treatment for cardiometabolic syndrome. Treatment for this condition should involve an integrated, multidisciplinary approach that includes lifestyle modifications and, if necessary, pharmaceutical treatments, as the symptoms are tightly linked.
