Why diabetic patients suffer from hypertension too?
Clinical Nutrition • • 1 minute to read • By Dr Aakash Bansal, INFS Faculty
Author- Dr. Aakash Bansal
Diabetes and Hypertension frequently occur together and there is an overlap between the two in disease mechanisms. They are the two leading risk factors for atherosclerosis and heart attacks and strokes. As per one of the studies done in Hong Kong, only 42% of people with diabetes had normal blood pressure and only 56% of people with hypertension had normal glucose tolerance.
Multiple factors play an important role in establishing a connection between the two diseases and knowing the common causes and mechanisms can help to plan the prevention and treatment better. Individuals with type 2 diabetes often display a cluster of metabolic disorders termed cardiometabolic or cardiorenal metabolic syndrome. This cluster includes cardiovascular disease risk factors including Type 2DM, hypertension, dyslipidemia , central obesity , and chronic kidney disease.
Causes of hypertension in diabetes
The causative factors can be the interaction between sedentary lifestyle and insulin resistance, autonomic nervous system, renal dysfunction as well as certain environmental factors.
Sedentary lifestyle and Insulin Resistance
Excess calorie intake along with a sedentary lifestyle can lead to increased obesity which has been associated with an increased risk factor for insulin resistance, leading to type 2DM in the future. This excess calorie intake along with IR also leads to spillage of fat in arterial walls thus increasing the chances of atherosclerosis which in turn elevates the blood pressure.
Premature vascular aging
Changes in the elasticity of blood vessels affect the ease with which blood flows through arteries. Patients with diabetes accelerate premature vascular aging by impairing endothelial relaxation, enhancing the contraction of smooth muscles, and increased vascular stiffness. These maladaptive changes in blood vessels contribute to the development of hypertension.
Autonomic Nervous System Dysregulation
Both the sympathetic and parasympathetic nervous systems are involved in the regulation of blood pressure. An Increased sympathetic system leads to an increase in heart rate, fluid retention, and force of contraction of ventricles of the heart. These actions promote BP elevation. The decreased parasympathetic system contributes more to the elevation of BP. Dysregulation of these pathways has been observed with central obesity and insulin resistance. Furthermore, dysregulation of these pathways promotes insulin resistance further and increases the risk for type2 diabetes.
Diabetic nephropathy (kidney damage) contributes to the development of hypertension. The reason is more volume of fluid because of increased renal sodium reabsorption and peripheral vasoconstriction because of endothelial dysfunction leading to elevated blood pressure.
- Reduce the salt intake
- Increase consumption of fruits and vegetables
- Limit intake of saturated fats
- Increase activity levels
- Reduction in 5-10% of body weight
- Pharmacotherapy for patients having BP <140/90 mm Hg
Diabetes is linked with an increased risk of cardiovascular disorder which becomes more complicated with hypertension. Controlling comorbidities, especially elevated blood pressure, and targeting modalities to promote vascular health becomes an important aspect to reduce the microvascular and macrovascular complications of diabetes.
- Cheung, B.M.Y. (2010). The hypertension-diabetes continuum. Journal of Cardiovascular Pharmacology, [online] 55(4), pp.333–339
- Cheung, B.M.Y. and Li, C. (2012). Diabetes and Hypertension: Is There a Common Metabolic Pathway? Current Atherosclerosis Reports, [online] 14(2), pp.160–166
- Khangura, D.S., Waqar Salam, M., Brietzke, S.A. and Sowers, J.R. (2000). Hypertension in Diabetes. [online] PubMed
- Petrie, J.R., Guzik, T.J. and Touyz, R.M. (2018). Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms. The Canadian journal of cardiology, [online] 34(5), pp.575–584
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