High blood pressure is a silent epidemic that threatens the lives of one in every three American adults. Of those taking blood pressure medications, control rates vary between less than half to only two-thirds (Lloyd-Jones 2009; Lloyd-Jones 2005). This means that the majority of those diagnosed with hypertension spend most of their day with blood pressure levels that are dangerously elevated. Since increased blood pressure is a major risk factor for heart disease, stroke, congestive heart failure, and kidney disease, it acts as an accomplice in millions of additional deaths each year (Roger 2011).
Mainstream medicine has fallen fatally short of relieving high blood pressure. A major problem is that mainstream medicine’s definition of what constitutes acceptable blood pressure levels is far too high. The medical establishment defines high blood pressure (hypertension) as over 139/89 mmHg. However, in 2006, researchers found that blood pressure levels ranging from 120-129 mmHg systolic/ 80-84 mmHg diastolic were associated with an 81% higher risk of cardiovascular disease compared to levels of less than 120/80 mmHg. Moreover, blood pressure levels of 130-139/85-89 mmHg were associated with a frightening 133% greater risk of cardiovascular disease compare to levels below 120/80 (Kshirsagar 2006). Worse yet, studies suggest that conventional physicians are unlikely to treat hypertension until levels exceed 160/90 mmHg, a level that dramatically increases the risk of disease and death (Hyman 2002).
Controlling blood pressure means radically reducing disease risk. Studies have estimated that reducing blood pressure by 10/5 mmHg, to no lower than 115/75, can reduce the risk of death due to stroke by 40% and the risk of death due to heart disease or other vascular causes by 30% (Lewington 2002). In individuals 40 to 70 years old, each 20/10 mmHg increment over 115/75 doubles the risk of heart attack, heart failure, stroke, or kidney disease (Lewington 2002; Chobanian 2003;). Based on this and other data, Life Extension recognizes that for many individuals, a target blood pressure of 115/75 mmHg yields the best benefits (Chobanian 2003).
The development and progression of high blood pressure is complex and multifactorial. Thus, effective management is rarely achieved through a single intervention. Instead, optimal management often requires a broad-based approach including lifestyle modification, nutritional components, pharmaceutical medication(s), and regular self-monitoring. These approaches will be discussed in detail throughout this protocol.
Blood pressure is a measurement of the force exerted upon blood vessel walls by blood as it flows through the arteries. High blood pressure occurs when there is an increase of force against the arterial wall, with potentially damaging consequences.
Since the heart has distinct “beats”, the pressure of oxygenated blood in the arteries is not continuous, but varies between two values, one when the heart is contracting, and one when the heart is relaxing. As the heart contracts, blood is expelled from the left ventricle under the greatest force; this upper pressure limit is the systolic blood pressure.
Following contraction of the heart, the aortic valve closes, which prevents blood from flowing backward into the heart, and helps to maintain the pressure in the arteries. This allows the heart muscle to relax and fill with blood. Unlike all other organs, which receive blood flow when the heart “beats” or contracts, the heart itself is unique in that it receives blood supply between heartbeats. As the heart contracts to pump blood to the rest of the body, circulation to the heart itself is impeded. Blood pressure during the heart’s “resting” period between contractions, called diastole, must be sufficient to deliver an adequate supply of oxygenated blood to cardiac tissue. In aging individuals with pre-existing coronary disease and/ or long-standing high blood pressure, overly-aggressive reduction of diastolic blood pressure can reduce the delivery of oxygenated blood to the heart. The diastolic blood pressure should be close to 75 mmHg for optimal health.
The alternation between systolic and diastolic blood pressure occurs with every heartbeat, some 60-80 times per minute in the average adult at rest. Clinically, blood pressure measurements are expressed, in millimeters of mercury (mmHg), as the ratio of systolic pressure over diastolic pressure (e.g. 120/80 mmHg).
For most aging individuals, Life Extension recommends an optimal blood pressure goal of 115/75 mmHg. However, those aging individuals with long-standing hypertension and/ or coronary artery disease should be aware that a rapid, overly-aggressive reduction of blood pressure, in particular diastolic blood pressure, should be avoided.
Blood pressure in the circulatory system is controlled three ways: 1) The force and rate at which blood leaves the heart (cardiac output); 2) the diameter and flexibility of the blood vessels though which blood flows (peripheral resistance); and 3) the total volume of blood in the circulatory system. All three work in concert to maintain a steady long-term pressure, while allowing for short-term increases to address cardiovascular needs.
Increasing the rate at which the heart beats, and the force at which blood leaves the heart results in a greater flow of blood and an increase in pressure; thus allowing the short-term increase in circulation that may be necessary during exercise, or in adapting to stress. Increases in cardiac output can be triggered by signals from the brain, or in response to stress hormones, such as epinephrine (adrenaline).
Peripheral resistance describes the increase in blood pressure caused by blood vessels themselves. The more resistance to blood flow, the greater the amount of blood pressure needed to overcome this resistance. Arteries actively modulate their resistance by constriction, which decreases the diameter of the vessel (vasoconstriction) and increases blood pressure, or dilation (vasodilation), which lowers resistance and blood pressure. Vasoconstriction and vasodilation are also short-term mechanisms to regulate blood pressure, and are under the control of several hormones. Aging causes arteries to lose their elasticity, which explains why the majority of aging people have blood pressure readings that are higher than optimal. Since it is “normal” for people’s blood pressure to rise with age, interventions are usually required to keep it in safe ranges. People should not be surprised to learn that they need to take steps to bring their blood pressure under control – it is a part of normal aging for most of us.
The last mechanism for blood pressure regulation is through blood volume. Blood is a suspension of cells in an aqueous medium; its volume can therefore be modified by altering its water content. Increasing the amount of water in the blood increases volume and the pressure it exerts. Reducing water content lowers blood pressure. Changes in blood volume are long-term mechanisms for blood pressure control.
Aside from the influence of neural triggers on heart rate, much of blood pressure control is performed by the kidneys. By controlling the balance of water and salt, the kidneys influence blood volume, lending long-term blood pressure control. The kidneys also produce hormones that act remotely to increase blood pressure through vasoconstriction of arteries. Kidney function can become impaired as people age, which is another reason why blood pressure may increase as we grow older. A major reason for kidney impairment is hypertension, so those starting with mild kidney problems have elevated blood pressure that then inflicts more kidney damage resulting in still higher blood pressure readings. Excess blood glucose (above 99 mg/dL) is another major cause of kidney damage. Fasting glucose levels should be kept below 86 mg/dL for overall disease prevention (optimal range: 70 to 85 mg/dL).
Central to the kidney’s control of blood pressure is the renin-angiotensin-aldosterone system, a system of hormones that work together to control blood pressure. Renin is an enzyme produced in the kidneys in response to low blood volume, depletion of sodium chloride, and stress. The production of renin leads, in turn, to the production of angiotensin II, a hormone that increases blood pressure. Angiotensin II increases blood pressure in several ways; it:
Hypertension and Endothelial Dysfunction: A Deadly, Dual Threat to Vascular Health
In recent years, researchers have made tremendous strides in understanding the connection between high blood pressure and various cardiovascular diseases. It turns out that elevated blood pressure damages arteries at a basic level—the endothelium. Endothelial dysfunction is linked with the development of cardiovascular events.
Arteries are made up of three layers. The outer layer is mostly connective tissue that provides support to the inner two layers. The middle layer is smooth muscle that contracts and expands to facilitate circulation and maintain optimal blood pressure. The inner layer, or endothelium, is composed of a thin layer of cells that protects the integrity of the artery, promotes blood clotting in case of injury, and helps prevent damaging molecules such as low-density lipoproteins (LDLs) and triglycerides from penetrating the wall of the artery. When the endothelial layer is damaged, the result can be a thickened arterial wall and the abnormal aggregation of white blood cells. Sensing an injury, the endothelium stimulates a healing response that ultimately leads to an atherosclerotic plaque (Versari 2009; Rocha 2010).
Elevated blood pressure has been shown to contribute significantly to endothelial dysfunction. High blood pressure causes functional alterations in the endothelium that, in turn, are associated with decreased arterial mobility and increasing stiffness in the arterial wall (Hausberg 2005). When the arteries become “stiff” or hardened, and can no longer contract and dilate sufficiently, additional stress is placed on the heart's main pumping chamber, the left ventricle. As a result, the left ventricle may be enlarged (left ventricular hypertrophy) (Palmieri 2005). Left ventricular hypertrophy is often the first sign that damage from uncontrolled high blood pressure has started to occur (Kannel 2005). If left untreated, ventricular hypertrophy may evolve into congestive heart failure.
The degree of endothelial dysfunction correlates with target organ damage (Xu 2009). As a result, physicians measure the effects of high blood pressure by looking at target organ damage. In other words, treatment decisions are based on how much damage high blood pressure is causing to organs such as the kidneys, eyes, or heart.
The intimate relationship that exists between high blood pressure and endothelial dysfunction highlights the need to address both of these phenomena as separate, yet unified contributors to cardiovascular disease. In fact, the network of interrelated cardiovascular risk factors includes a myriad of additional components that must be addressed to truly reduce cardiovascular risk. More information on the multifactorial nature of cardiovascular disease can be found in the Life Extension Magazine article entitled “How to Circumvent 17 Independent Heart Attack Risk Factors”.
While increases in blood pressure from the resting rate are expected under certain conditions such as excitement, stress or physical exertion, a prolonged elevation in blood pressure can be detrimental. Sustained high pressures within the cardiovascular system compromises the integrity of vessels, leading to vascular damage and failure of the organs that the vessels supply (Schmieder 2010). Short of this, even modest, sustained increases in blood pressure elevate the risk of several diseases, including arteriosclerosis, stroke, chronic kidney disease/failure, peripheral arterial disease (PAD), aneurysm, and vision loss. Hypertension is a more important risk factor for coronary heart disease than high non-HDL cholesterol, elevated C-reactive protein, high serum triglycerides, or even obesity (Kones 2010; Kaptoge 2010; Schnohr 2002). Even so, one cannot completely reduce cardiovascular risk without controlling all of their risk factors.
The current definition of hypertension is based upon the risk of serious complications and the methods of their management (Chobanian 2003). While the threshold used to define hypertension has been >139/89 mmHg for decades, several published studies reveal that blood pressure should be kept around 115/75 mmHg in order to truly protect against cardiovascular disease (Basile 2008; Bakris 2007; Russell 2006).
Hypertension is classified as Primary and Secondary based on underlying cause. Primary hypertension, the most frequent and preventable type, arises from a number of underlying contributing factors (Chiong 2008; Carretero 2000). Inadequate intake of nutrients including potassium, magnesium, vitamin D and vitamin K may also play a role. Secondary hypertension represents only about 5-10% of hypertension cases, and results from an underlying condition, usually associated with diseases of the kidneys, endocrine, vascular, or central nervous system. Although antihypertensive drugs are sometimes used to manage secondary hypertension, correcting the underlying cause can often lead to a cure (Chiong 2008).
Prehypertension is a “predisease” state, which carries an increased risk of progression to hypertension. Those in the 130/80 to 139/89 mmHg blood pressure range (which is already dangerously high) are twice as likely to develop clinical hypertension (which means much higher blood pressure readings) as those with lower values (Viera 2011; Vasan 2001). Despite the availability of studies which indicate that individuals within this blood pressure range are at increased risk of developing clinical hypertension as well as heart disease, mainstream medicine usually opts not to treat blood pressure with pharmaceutical drugs at this level.
Stage 1 and stage 2 hypertension, defined as 140-159/90-99, and greater than 160/100 mmHg respectively, carry the greatest risk of cardiovascular disease. The two stages of hypertension differ in their conventional medical treatments, with stage 2 hypertensive patients usually requiring the most aggressive intervention using combinations of anti-hypertensive drugs.
Some causes of Secondary Hypertension (Chiong 2008; Chobanian 2003)
Hypertension induced by drugs: