Essential Hypertension is also known as Primary Hypertension or Idiopathic Hypertension. It is the most common type of hypertension affecting 85-90% of those with hypertension. Its physiological cause remains unidentified. It is generally asymptomatic. A doctor may perform an ECG and ECHO, but blood tests aren’t generally done. Allopathic/Conventional/Western medicine has no identifiable cause and a solution to it, though drugs generally target RAAS.  The Renin Angiotensin Aldosterone System (RAAS) Renin is a proteolytic enzyme(protease) synthesised by Kidneys. Angiotensinogen is an inactive peptide synthesised by the Liver.  Aldosterone is a steroid hormone made by the Adrenal Glands.  JG cells in Kidneys produce Renin when: Baroreceptors in Nephrons in the JG cells in afferent arterioles detect low blood volume thereby low water. Chemoreceptors in Nephrons in the Macula Densa of the Distal Convoluted Tubule detect low Sodium thereby low salt. The Left Common Carotid Artery has baroreceptors in the carotid sinus, they detect low blood pressure as they detect low blood flow. This also happens in the Aorta in the Aortic Sinus. It is done by the Vagus Nerve(more on this later). The liver makes Angiotensinogen and Renin converts it to Angiotensin 1, as it breaks the bond between Leucine and Valine.  Angiotensin 1 is a decapeptide and is inactive. It circulates in the blood and goes to the lungs.  Angiotensin Converting Enzyme1 (ACE1) present in the lungs, converts Angiotensin 1 to Angiotensin 2. ACE1 is prohypertensive and is a potent vasoconstrictor in itself. It further promotes fibrosis and inflammation.  ACE2 is counter-regulatory to ACE1. It is antihypertensive and a vasodilator. It is antifibrotic and antiinflammatory in nature. It does so as it breaks down Angiotensin 2.  Features of Angiotensin 2 Conventional Medicine treats it with drugs like  This is a limited view that Conventional Medicine takes for something that affects us throughout the body. Let’s look at the bigger picture. The Bigger Picture – Nutrition, Stress, Insulin, Cortisol and Sleep The Sympathetic Nervous System(SNS) through the Sympathomedullary(SAM) Pathway stimulates the release of Epinephrine(Adrenaline) – 80% and Norepinephrine(Noradrenaline) – 20%, in the Adrenal Medulla of Adrenal Glands. The SNS nerves act directly on the SA Node and the AV Node, thus increasing the Heart Rate and Blood Pressure. Also, the SNS nerves in the Thoracolumbar region go to the blood vessels, particularly the Tunica Media, the muscular layer of the blood vessels that is responsible for dilation and constriction, resulting in vasoconstriction, thus increasing the Blood Pressure. Epinephrine has a greater effect on the Heart and Norepinephrine has a greater effect on the Blood Vessels. Chemically, Epinephrine and Norepinephrine are very similar. Both Epinephrine and Norepinephrine work on Alpha and Beta receptors. However, Epinephrine has a greater effect on Beta receptors compared with Norepinephrine. Alpha receptors are only found in the arteries. Beta receptors are in the heart, lungs, and arteries of skeletal muscles Both Epinephrine and Norepinephrine can affect your heart, blood sugar levels, and blood vessels. However, Norepinephrine can also make your blood vessels become narrower, increasing blood pressure. At the same time, though slower than the SAM Pathway, after a  10 minute lag, the Hypothalamus Pituitary Adrenal(HPA) Axis signals the Adrenal Cortex of the Adrenal Glands to release Cortisol. The effects of the HPA axis are significant and long lasting.  Aldosterone, a mineralocorticoid and Cortisol, a glucocorticoid are made simultaneously in the body by the Adrenal Cortex of the Adrenal Glands. Aldosterone controls water and salt balance by reabsorbing Sodium and excreting Potassium.  Also Insulin increases Aldosterone activity. Sodium follows Water and Water follows Sodium. So water retention means sodium retention. The main culprit for water retention is the sugar in our diet. How? Kidneys have insulin receptors.  Whenever there is a low salt intake, the Kidneys hold on to the Sodium by signalling to raise insulin levels as a protective mechanism to preserve Sodium. Insulin directly stimulates Sodium reabsorption in the Distal Convoluted Tubules, hence retaining water. This goes to show that sugar retains water, not salt. Sodium and Salt retention increase the End Diastolic Volume which increases the Cardiac Output hence raising the Diastolic Pressure. Sodium, Calcium and SNS are involved in the depolarisation of the heart i.e. the contraction of the heart, increasing the heart rate. Further, inadequate Potassium intake or low amount of Potassium circulating in the blood also retains Sodium. Sodium functions inside the cells and Potassium does outside of it. Vagus Nerve is the longest running cranial nerve of the Autonomic Nervous System and holds as much as 75% of the Parasympathetic Nervous System(PNS) fibres. It is a PNS nerve that runs from the brain to the large intestine connecting all the major internal organs through the heart, lungs and the digestive tract. The Vagus Nerve is made from the visceral fibres. 20% are efferent fibres, which provide Brain to Body communication. 80% are afferent fibres, which provide Body to Brain communication. Hypothalamus is the centre of SNS and PNS. Acetylcholine is the major neurotransmitter of the PNS.  PNS repolarises the heart i.e. the relaxation of the heart. The right vagus innervates the SA Node and the left vagus innervates the AV Node. Potassium is also involved in the repolarisation of the heart. The Vagal response is a Neuro-Cardiogenic-Gastrointestinal. The Vagal response is dependent on 2 factors If any of these issues are there, the Vagus Nerve doesn’t respond and Low Blood Pressure doesn’t stimulate the Vagus Nerve getting the body in a negative loop by activating SNS. Another connection between the gut and hypertension comes from Bile Salts. Bile Salts are important for the absorption of dietary fat. The lesser-known function of bile salts is that it protects against hypertension. Fatty Liver inarguably plays a huge role in developing hypertension as Angiotensinogen is synthesized in the Liver by the visceral fat cells.   Some nutritional deficiencies and imbalance also cause hypertension. The deficiencies in Vitamins and an imbalance (too much or too little) of minerals contribute to it. They are :  It’s the stimulation of SNS that starts a cascade that eventually