Not all obese people have high blood pressure, and not all people with high blood pressure are obese. Nonetheless, there is a strong correlation between being overweight and developing hypertension--so much so that "you ought to lose some weight" is often the first thing a doctor says to a patient who has just been diagnosed with high blood pressure.
Of course, since the doctor doesn't expect that the patient will really make an effort to lose any weight, this advice is often uttered while the doctor is busy scribbling out a prescription for hypertension medication. What is ironic about this is that many anti-hypertensive drugs result in weight gain. (Weight gain is very common with beta-blockers. What is rather surprising is that, although diuretics typically result in an immediate drop in wieght owing to water loss, in the slightly longer term many people report ongoing weight gain from diuretics. Your doctor will no doubt scoff at this idea, but it makes good scientific sense given the fact that diuretics result in insulin resistance and many of the manifestations of diabletes.)
One of the puzzles about weight loss and blood pressure, though, is why losing weight tends to reduce blood pressure in the first place. There are many theories. In overweight people the renin-angiotensin-aldosterone hormone system appears to be overactivated--but this merely moves the question back one stage (since we don't know why being overweight would overstimulate the hypertensive hormonal system).
In overweight people, the sympathetic nervous system tends to be overactivated--but once again, this simply replaces one question with another, since we don;t know why extra pounds casue sypathetic overstimulation.
An appealing theory is one that might be called "the plumbing model." According to some calculations, every additional pound of fat requires about a mile of additional capillaries to supply adequate blood to the fat cells. According to this notion, pushing blood through this enlarged network of tiny blood vessels naturally requires a higher blood pressure leaving the heart. (I've been unable to discover what happens to all those miles of capillaries during wiehgt loss. I guess the body has some way of breaking them down--otherwise we'd end up spiderwebbed with miles of unneeded capillaries right under our skin.)
Much current thinking on the topic suggests that obesity doesn't actually cause hypertension; instead, hypertension and obesity have a common underlying cause, Syndrome X (or "Metabolic Syndrome.") In this model, it is insulin resistance, and high circulating levels of insulin, that cause weight gain and also raise blood pressure. According to this theory, taking dietary measures that begin to reverse Syndrome X and normalize insulin and glucose levels will both result in weight loss and in lower blood pressure--but it is not the weight loss that is causing the lowered blood pressure. (In another huge irony, the diets suggested by most doctors for weight loss--low-fat, high-carbohydrate diets--are exactly the diets that make Syndrome X worse, and often drive people from Syndrome X into full-fledged Type II diabetes.)
The newest theory is that the association of high blood pressure with obesity isn't caused by extra body fat per se, but only by extra fat stored in the liver.[1] (This isn't incompatible with the Syndrome-X theory, since fatty liver is associated with Metabolic Syndrome, and some researchers argue that it is one of the key elements.) In the past year, researchers have discovered that fatty livers secrete C-reactive Protein (CRP), a pro-inflammatory hormone, and CRP acts directly on the endothelium of the blood vessels to increase blood pressure.[2] The majority of--but not all--alcoholics and obese people have fatty livers; this could explain why the majority, but not all, alcoholics and obese people have high blood pressure. If correct, this would mean that blood-pressure researchershave been barking up all the wrong trees for several decades now. (CRP is also closely linked with arteriosclerosis and heart disease, and some researchers now believe that it is CRP, not cholesterol, that damages blood vessels. Yes, cholesterol forms the plaques in diseased arteries--but it is the inflammation caused by CRP that pulls cholesterol out of circulation and deposits it in the artery walls.)
[The recent research on fatty liver deserves a post of its own, and will get one soon.]
Whether extra fat causes hypertension, or obesity and hypertension are caused by a common underlying problem, taking steps that cause weight loss also usually cause a lowering of blood pressure. Different studies on the subject yield different results, which is hardly surprising, since some studies involve exercise programs, some caloric restrtiction, others anti-hypertensive drugs, and many of them employ some combination of those three.
There have been a number of "meta-studies" that use statistical analysis to tease out the effects of weght loss alone from the existing studies. The most recent of these, in 2003, established that in general the loss of one pound of body weight lowered both systolic and diastolic blood pressure by about a half point (to be more price, the numbers were 1.05 mm per kilogram systolic, and 0.92 mm per kilogram diastolic, which amounts to 0.48 mm per pound systolic and 0.42 mm per pound diastolic) [3].
A shy half point might not sound like much, but a pound of fat isn't much either. While losing ten pounds "only" knocks blood pressure down by about five points, losing twenty pounds would drop it by nearly ten points, which is as good as the drop achieved by most blood-pressure drugs.
Furthermore, what the median statistics don't show is the variation between studies, and the variation between individuals within any study. In one of the classic studies, when participants lost an average of twenty pounds, the average blood pressure drops were 30.5 mm systolic and 20.8 mm diastolic.[4] That's 1.5 mm per pound systolic and 1.0 mm per pound diastolic--which is triple the systolic drop, and double the diastolic drop, respectively, compared to the average found in the 2003 meta-analysis.
What these numbers mean is that a great many people with hypertension could normalize their blood pressure simply by normalizing their weight. Since obesity contributes to so many other medical problems, the benefits from weight loss go far beyond controlling hypertension.
Studies show that the vast majority of overweight people wish they could lose the fat they are carrying. Unfortunately, studies also show that the weight-loss recommendations given by most doctors result in only modest losses in many cases, and in the majority of cases result in no long-term weight loss at all, or even result in weight gain. The low-fat diet push that began in the 1970s and has been adopted as gospel by the medical establishment has been a dismal failure. Over the last four decades, Americans have dutifully cut down their intake of fat, both in absolute terms and as a percentage of daily calories--and the result has been an epidemic of obesity across the country.
If you have high blood pressure, then, as the doctor says, you probably ought to lose some weight. But you probably shouldn't take your doctor's advice about how to lose it.
[1] Stranges, Saverio, et al. Body Fat Distribution, Liver Enzymes, and Risk of Hypertension.
Hypertension. 2005;46;1186-1193.
[2]. CRP Liver Protein Induces Hypertension. Medical News Today (medicalnewstoday.com ). Feb. 22, 2007.
[3] Neter, Judith E., et al. Influence of Weight Reduction on Blood Pressure: A Meta-Analysis of Random Controlled Trials. Hypertension 2003;42;878-884.
[4] Reisin E, Frohlich. Effects of weight reduction on arterial pressure. J Chronic Dis. 1982;35:887–891.
Showing posts with label high blood pressure. Show all posts
Showing posts with label high blood pressure. Show all posts
Sunday, August 9, 2009
Sunday, July 26, 2009
Beta-Blockers: Benefits and Dangers
I caution you from the outset that I am biased against beta-blockers. My brief experience with them was horrible, and as far as I am concerned they are the devil's own drug.
Beta-blockers interfere with the body's beta-receptors. In some people, an overactive sympathetic nervous system is a factor in hypertension. High ongoing levels of sympathetic nervous system activity tends to raise the heart rate and increases the secretion of adrenaline and related hormones. Beta-blockers slow the heart rate, lower the secretion of stimulating hormones, and also block the effects of adrenaline. In short, the beta-blockers interfere with the "fight-or-flight" response of the body to stress or panic.
States of high sympathetic nervous system arousal tend to be self-reinforcing. If you are panicked, your heart is liable to race; and a racing heart tends to increase your feelings of panic. If the activity of the sympathetic nervous system is damped down by a beta-blocker, this positive-feedback loop is slowed down. A person may feel stress or fear at the mental level, but if the body fails to respond with an increase in heart rate, sweaty palms, and increased adrenaline, then the stressful thoughts will not result in the upward spiral of increased blood pressure and distress.
The way that beta-blockers interfere with the physical mianifestations of anxiety has made them popular for reasons that have nothing to do with treating cardiovascular disease. Although they are not FDA-approved for use in treating anxiety disorders, beta-blockers have been prescribed for various kinds of psychological problems, and they are especially popular for controlling performance anxiety in professional musicians [1].
Beta-blockers can be life-saving drugs for people suffering from heart failure or arrhythmias. They are also often prescribed for hypertension alone, even when high blood pressure is found without any accompanying heart discorders. Some doctors have achieved excellent results in controlling hypertension with beta-blockers, and some patients are very happy with the effects: not only do beta-blockers lower their blood pressure, but they lower feelings of anxiety as well--like Valium and a blood-pressure drug rolled into one.
But the side effects of beta-blockers can be severe. Weight gain, impotence, and reduced exercise capacity are frequently reported. Beta-blockers can interfere with sleeping patterns, and in some patients can cause nightmares. Depression, fatigue, and thougths of suicide are not uncommon.
In addition to the rather daunting effects listed above, beta-blockers can interfere with peripheral blood circulation and increase blood sugar levels, both of which can be dangerous, especially to diabetics. In fact, like thiazide diuretics, beta-blockers have been shown to be diabetogenic, causing diabetes in long-term users. [2] There is reason to believe that the diabetogenic effects are enhanced when beta-blockers and diuretcis are given together, and, unfortunately for the patients, this is very common; indeed, my former doctor had me on both of them.
I didn't stay on my beta-blocker (Atenolol) for long, however. Although I did appreciate the anxiety-lowering effect for the first day or two, it immediately interfered with my sleep, making my rest uneasy and punctuated with terrifying dreams. By the end of my first week I was in a low-level state of despair round the clock, and by the second week I was sitting on the floor of distant rooms of the house where no one could hear me, sobbing. You say I should have told my doctor? Probably, but my mental state was so deteriorated after only two weeks that I couldn't face the prospect of dealing with him; I was sure that he would plunge me into more tests, more drugs, more procedures, and that I would end up even worse off. I thought constatly of suicide, and though I never came near to acting upon those thoughts, thee were moments where if I could have pushed a button and had everything be over I might well have done so.
You aren't supposed to quit beta-blockers cold turkey; you are supposed to taper them off gradually under medical supervision. Quitting suddenly, the pharmaceutical inserts tell you, can be deadly--althoug I suspect this applies to heart patients more than to people taking them for treatment of hypertension. In any case, after three weeks on Atenolol I decided to quit. I saw no downside, since the risk of dying seemed minor compared to the horror of spending another day on that drug.
Beta-blockers interfere with the body's beta-receptors. In some people, an overactive sympathetic nervous system is a factor in hypertension. High ongoing levels of sympathetic nervous system activity tends to raise the heart rate and increases the secretion of adrenaline and related hormones. Beta-blockers slow the heart rate, lower the secretion of stimulating hormones, and also block the effects of adrenaline. In short, the beta-blockers interfere with the "fight-or-flight" response of the body to stress or panic.
States of high sympathetic nervous system arousal tend to be self-reinforcing. If you are panicked, your heart is liable to race; and a racing heart tends to increase your feelings of panic. If the activity of the sympathetic nervous system is damped down by a beta-blocker, this positive-feedback loop is slowed down. A person may feel stress or fear at the mental level, but if the body fails to respond with an increase in heart rate, sweaty palms, and increased adrenaline, then the stressful thoughts will not result in the upward spiral of increased blood pressure and distress.
The way that beta-blockers interfere with the physical mianifestations of anxiety has made them popular for reasons that have nothing to do with treating cardiovascular disease. Although they are not FDA-approved for use in treating anxiety disorders, beta-blockers have been prescribed for various kinds of psychological problems, and they are especially popular for controlling performance anxiety in professional musicians [1].
Beta-blockers can be life-saving drugs for people suffering from heart failure or arrhythmias. They are also often prescribed for hypertension alone, even when high blood pressure is found without any accompanying heart discorders. Some doctors have achieved excellent results in controlling hypertension with beta-blockers, and some patients are very happy with the effects: not only do beta-blockers lower their blood pressure, but they lower feelings of anxiety as well--like Valium and a blood-pressure drug rolled into one.
But the side effects of beta-blockers can be severe. Weight gain, impotence, and reduced exercise capacity are frequently reported. Beta-blockers can interfere with sleeping patterns, and in some patients can cause nightmares. Depression, fatigue, and thougths of suicide are not uncommon.
In addition to the rather daunting effects listed above, beta-blockers can interfere with peripheral blood circulation and increase blood sugar levels, both of which can be dangerous, especially to diabetics. In fact, like thiazide diuretics, beta-blockers have been shown to be diabetogenic, causing diabetes in long-term users. [2] There is reason to believe that the diabetogenic effects are enhanced when beta-blockers and diuretcis are given together, and, unfortunately for the patients, this is very common; indeed, my former doctor had me on both of them.
I didn't stay on my beta-blocker (Atenolol) for long, however. Although I did appreciate the anxiety-lowering effect for the first day or two, it immediately interfered with my sleep, making my rest uneasy and punctuated with terrifying dreams. By the end of my first week I was in a low-level state of despair round the clock, and by the second week I was sitting on the floor of distant rooms of the house where no one could hear me, sobbing. You say I should have told my doctor? Probably, but my mental state was so deteriorated after only two weeks that I couldn't face the prospect of dealing with him; I was sure that he would plunge me into more tests, more drugs, more procedures, and that I would end up even worse off. I thought constatly of suicide, and though I never came near to acting upon those thoughts, thee were moments where if I could have pushed a button and had everything be over I might well have done so.
You aren't supposed to quit beta-blockers cold turkey; you are supposed to taper them off gradually under medical supervision. Quitting suddenly, the pharmaceutical inserts tell you, can be deadly--althoug I suspect this applies to heart patients more than to people taking them for treatment of hypertension. In any case, after three weeks on Atenolol I decided to quit. I saw no downside, since the risk of dying seemed minor compared to the horror of spending another day on that drug.
I felt better by the next day, with only minor crying jags. My blood pressure increased slightly for about two days and then declined. After a week my thinking was clearer and I was more-or-less back to normal. I also discovered that I wasn't alone; there are many reports of deep depression and suicidal thinking from beta-blockers, and one Danish study shows that users of beta-blockers have an increased rate of suicide compared to users of other anti-hypertension drugs [3]. I have to say I'm not surprised.
I'm probably not the person to ask about beta-blockers. Not only did Atenolol drop me into a severe depression, I found attempting to exercise while on Atenolol to be a horrifying experience--your effort increases but your heart refuses to keep up with the body's demands.
I've met other people who tolerate beta-blockers well, and even like them. Given the increased risk of diabetes from taking them long-term, they still seem like a bad bargain to me, but you may feel differently. In any case, be aware that beta-blockers can give you a highly distorted view of reality and even plunge you into a state that any professional would diagnose as a temporary mental illness. That's a hefty price to pay for dropping your blood pressure a few points.
[1] Tindall, Blair. Better Music Through Chemistry. New York Times, Oct. 17, 2004.
[2] Bangalore, S., et al. A meta-analysis of 94,492 patients with hypertension treated with beta blockers to determine the risk of new-onset diabetes mellitus. Am J. Cardiol. 2007 Oct 15;100(8):1254-62.
[3] Sorenson, H.K., et al. Risk of suicide in users of β-adrenoceptor blockers, calcium channel blockers and angiotensin converting enzyme inhibitors. Br J Clin Pharmacol. 2001 September; 52(3): 313–318.
Sunday, July 5, 2009
What Causes High Blood Pressure?
Alas, most of the time they have no idea.
Kidney problems can cause abnormal secretion of hormones and enzymes that raise blood pressure, and kidney problems can also interfere with electrolyte balances, altering the vital sodium/potassium/magnesium balances that govern the retention of water in the body. Thyroid problems can cause excess secretion of thyroid hormones, which can raise blood pressure. For these reasons, the first thing doctors typically do on detecting ongoing elevation of blood pressure is to request blood tests for kidney function and thyroid stimulating hormone. Adrenal gland diseases (the adrenal glands sit atop the kidneys) can also directly cause hypertension.
If the blood pressure problems stem from these identifiable problems, the condition is termed "secondary hypertension" (because the problem is secondary to another primary disease process). Secondary hypertension accounts for an estimated 5-10% of cases of high blood pressure.
And what of the other 90-95%, the cases of so-called "primary" or "essential" hypertension?
Nobody knows. There are a lot of associations, suspicions, and conjectures, but the origins of most high blood pressure are obscure, and multiple factors may be interacting to cause the condition.
There are three major interacting systems that directly govern blood pressure:
1) The barorecptor system. Baroreceptors (pressure receptors) aren't 'receptors' in the modern biological sense of the word, which usually means a chemoreceptor. Instead, baroreceptors are complexes of blood vessels and nerves located along major blood vessels. The high-pressure baroreceptors, located along the carotid arteries and the aortic arch, respond to increases in blood pressure, while the low-pressure baroerecptors, located in the right atrium of the heart and along major veins, respond to decreases in blood pressure.
2) The autonomic nervous system. The sympathetic nervous system is responsible for arousal, and prepares the body for exertion, stress, or emergencies. An overstimulated sympathetic nervous system can contract arteries, speed the heart rate, and steer blood away from the stomach and intestines to the muscles. All of these effects increase blood pressure. Signals from the sympathetic nervous system that cause jumps in blood pressure when someone is alarmed or frightened. The other half of the autonomic nervous system, the parasympathetic system, is responsible for lowering blood pressure. Neither system is under direct conscious control, but both of them respond to what is happening in the mind.
3) The renin-angiotension-aldosterone systems. The renin-angiotensin hormones, secreted by the kidneys, cause constriction of arteries. Aldosterone, secreted by the adrenal glands (in response to high levels of angiotensin, among other factors), causes sodium retention, fluid retention, and potassium excretion.
Here are a list of factors that may cause, or contribute to, high blood pressure:
High-pressure Baroreceptor Errors. Sometimes you need your blood pressure to increase. For example, when you stand up, blood pressure needs to rise somewhat or you will faint. If you need to lift a heavy object, sprint for a bus, or engage in hot sex, your blood pressure needs to climb suddenly and sharply. The high-pressure baroreceptors are designed to accomodate these kinds of transient changes, and then go back to monitoring the blood pressure against a more reasonable baseline. But when high blood pressure continues over a period of days, the barorecptors "reset," so that the higher blood pressure becomes the new normal. This, and other kinds of baroreceptor problems, are suspected of being involved in many cases of hypertension.
Sympathetic Nervous System Overactivity. Overstimulation or overactivity of the sympathetic nervous system can raise blood pressure. Ongoing fear, stress, panic, or just plain tension can raise blood pressure directly (as well as speeding heart rate).
Too Much Stress. In addition to the sympathetic nervous system activity engendered by stress, various kinds of hormones (notably cortisol and noradrenaline) generated by stress and sympathetic nervous system activity act to raise blood pressure. Chronic elevation of these chemicals in the bloodstream can cause hypertension.
Oversecretion of angiotensin or other hormones. Attacking angiotensin (by means of drugs such as ACE inhibitors) is a common approach to lowering blood pressure, but the fact that this approach is taken doesn't necessarily confirm that the cause of a given case of hypertension was oversecretion. Since inhibiting Ancgiotensin Converting Enzyme lowers blood pressure, ACE inhibitors are often employed even though the hypertension might be unrelated to oversecretion.
Too Much Sodium. This topic requires a whole post of its own, but as almost everyone knows, too much salt can raise blood pressure in at least some people. (In some people, too little sodium results in overstimulation of the sympathetic nervous system, which raises blood pressure, but the medical establishment has chosen to ignore this inconvenient fact.)
Too Little Potassium. Potassium acts to lower blood pressure, and can be thought of as the counterweight to sodium. Recommended intakes of potassium are very high--three to four grams a day--but very few Americans eat enough fruits and vegetables to get anywhere near this amount. Because potassium is so potent at lowering blood pressure, however, the FDA has made potassium supplements above 99 mg (about 3% of the typical daily requirement) available by prescription only.
Too Little Magnesium. Magnesium also acts to lower blood pressure, and plays a vital role in cardiovascular health. Unlike sodium and potassium, however, where a simple blood test gives a good indication of any deficiencies or excesses, magnesium deficiencies are difficult to identify with serum tests. Most of the body's magnesium is sequestered in cells and bone, and these reserves can be called upon to keep blood levels reasonably stable. By the time blood magnesium drops, the total body deficit is very large. Furthermore, the body can only absorb so much magnesium at a time, so returning the body to magnesium balance can take months.
Sleep disturbances. Sleep apnea (interruption of breathing during sleep) has been shown to be a clear cause of some cases of hypertension. In addition, sleep deprivation unrelated to apnea also appears to raise blood pressure. Even in subjects with normal blood pressure, cutting back on hours of sleep raises blood pressure on the subsequent day, and many scientists now believe that prolonged sleep deficits may result in the development of hypertension.
Obesity. There is a high correlation between overweight and hypertension, but the relationship is far from perfect; there are many overweight people with normal blood pressure, and many trim people with hypertension. Losing weight can often lower blood pressure, sometimes dramatically, but since losing weight usually involves changing diet and exercise, it is unclear whether it is the weight loss per se that causes the reduction on blood pressure. The mechanisms by which obesity causes hypertension are unclear, although Syndrome X and/or liver problems (see below) may be the root causes.
Arteriosclerosis/atherosclerosis. Clogged arteries increase blood pressure by requiring the heart to pump harder to move blood around the body.
High cholesterol. High cholesterol, particularly high LDL cholesterol, is commonly assocaited with hypertension, but there is considerable doubt whether it directly causes hypertension. LDL is a building block involved in clogging arteries, which raises blood pressure, but the mechanisms of laying down arterial plaque now appear to be more complicated than the mere presence of high levels os LDL.
Sedentary lifestyle. Lack of exercise predisposes to the development of hypertension, and hypertension can sometimes be reversed by exercise. Once again, the mechanism is unclear. Exercise may help reset baroreceptors (see above), and can also reverse aspects of Syndrome X (see below).
Alcohol. The link between alcohol and high blood pressure has long been a puzzle to researchers. One or two alcoholic drinks per day is associated with lower blood pressure than found in abstainers, but higher levels of consumption are associated with increased blood pressure. Moreover, the blood-pressure-increasing effects of alcohol are reversible as soon as intake is reversed. Recent research suggests that the association between high alcohol consumption and high blood pressure may not be an effect of the alcohol as such, but rather an effect of developing a fatty liver [1], which is common with high levels of alcohol intake (see below).
Upper cervical spine problems. Recently it was discovered that misalignment of the top cervical vertebra, the "Atlas" vertebra, can cause high blood pressure, presumably by pressing on nerves in the brainstem. Techniques for adjusting this misalignment through procedures developed by NUCCA (National Upper Cervical Chiropractic Association) techniques have been decisively shown to normalize blood pressure in individuals with neck injuries[2].
High insulin levels. Insulin causes high blood pressure in at least three ways. First, it instructs the kidneys to retain sodium and thereby retain body water. Second, it enlarges the smooth muscle cells of the walls of the arteries, stiffening them and also constricting them. Third, it stimulates the release of noradrenaline, which has many of the same effects as hyperactivity of the sympathetic nervous system.
Diabetes. When most people think of diabetes, they think of an insufficiency of insulin. But the most common form of diabetes, Type II diabetes, involves a long stage where there is a superabundance of insulin, co-existing with high blood sugar (a state called insulin resistance). About 70% of diabetics have hypertension. The exact link is not certain, but insulin is quite likely one of the culprits. In fact, diabetes may not be a cause of hypertension, but just another symptom of an underlying problem.
Syndrome X/Metabolic Syndrome. In the late 1980s, Gerald Reaven at Stanford University wrote a groundbreaking paper in which he contended that a whole host of health-damaging characteristics tended to occur in synchrony:
1) High insulin levels
2) Insulin resistance
3) High blood sugar
4) High blood pressure
5) Elevated VLDL cholesterol
6) Low HDL cholesterol
He dubbed this cluster of symptoms"Syndrome X" (though it is now often referred to as "metabolic syndrome"), and argued that insulin resistance was the real root of the problem. Syndrome X is a precursor to Type II diabetes, is associated with obesity and rapid weight gain, especially around the abdomen, and often is associated with fatty liver (see below). In effect, Reaven says that insulin resistance is a major cause of hypertension (as well as many other diseases).
Chronic inflammation. Inflammation has become the latest suspect in a great many diseases, ranging from arteriosclerosis to cancer to many autoimmune disorders. Recently it discovered, for example, that women with psoriasis (and inflammatory skin disorder) were far more likely to go on to develop Type II diabetes and high blood pressure.
Fatty liver. Fat accumulation in the liver causes the liver to become inflammed (and often progresses to hepatitis or even cirrhosis). An inflammed liver produces high levels of a protein called C-reactive protein (CRP). Although the exact role of CRP in the body is obscure, big jumps in CRP are seen during infections. Chronic elevation of CRP is associated with the development of arteriosclerosis; in fact, some medical scientists argue that CRP and another protein, homocysteine, rather than high cholesterol, cause atherosclerotic damage to arteries (the cholesterol is merely used as a building block). In any case, high CRP levels were recently shown to raise blood pressure directly by acting on the artery walls in some fashion [3]. Since fatty liver is associated with Syndrome X, obesity, high alcohol intake, and high cholesterol levels, fatty liver and elevated inflammation proteins may be the link between all of these conditions, and may point to the true root cause of many cases of hypertension.
[1] Stranges, S. et al. Body Fat Distribution, Liver Enzymes, and Risk of Hypertension. Hypertension. 2005;46:1186
[2] Bakris, G, et al. Atlas vertebra realignment and achievement of arterial pressure goal in hypertensive patients: a pilot study. Journal of Human Hypertension (2007), 1–6.
[3] CRP Liver Protein Induces Hypertension. Medical News Today, Feb 22, 2007.
Kidney problems can cause abnormal secretion of hormones and enzymes that raise blood pressure, and kidney problems can also interfere with electrolyte balances, altering the vital sodium/potassium/magnesium balances that govern the retention of water in the body. Thyroid problems can cause excess secretion of thyroid hormones, which can raise blood pressure. For these reasons, the first thing doctors typically do on detecting ongoing elevation of blood pressure is to request blood tests for kidney function and thyroid stimulating hormone. Adrenal gland diseases (the adrenal glands sit atop the kidneys) can also directly cause hypertension.
If the blood pressure problems stem from these identifiable problems, the condition is termed "secondary hypertension" (because the problem is secondary to another primary disease process). Secondary hypertension accounts for an estimated 5-10% of cases of high blood pressure.
And what of the other 90-95%, the cases of so-called "primary" or "essential" hypertension?
Nobody knows. There are a lot of associations, suspicions, and conjectures, but the origins of most high blood pressure are obscure, and multiple factors may be interacting to cause the condition.
There are three major interacting systems that directly govern blood pressure:
1) The barorecptor system. Baroreceptors (pressure receptors) aren't 'receptors' in the modern biological sense of the word, which usually means a chemoreceptor. Instead, baroreceptors are complexes of blood vessels and nerves located along major blood vessels. The high-pressure baroreceptors, located along the carotid arteries and the aortic arch, respond to increases in blood pressure, while the low-pressure baroerecptors, located in the right atrium of the heart and along major veins, respond to decreases in blood pressure.
2) The autonomic nervous system. The sympathetic nervous system is responsible for arousal, and prepares the body for exertion, stress, or emergencies. An overstimulated sympathetic nervous system can contract arteries, speed the heart rate, and steer blood away from the stomach and intestines to the muscles. All of these effects increase blood pressure. Signals from the sympathetic nervous system that cause jumps in blood pressure when someone is alarmed or frightened. The other half of the autonomic nervous system, the parasympathetic system, is responsible for lowering blood pressure. Neither system is under direct conscious control, but both of them respond to what is happening in the mind.
3) The renin-angiotension-aldosterone systems. The renin-angiotensin hormones, secreted by the kidneys, cause constriction of arteries. Aldosterone, secreted by the adrenal glands (in response to high levels of angiotensin, among other factors), causes sodium retention, fluid retention, and potassium excretion.
Here are a list of factors that may cause, or contribute to, high blood pressure:
High-pressure Baroreceptor Errors. Sometimes you need your blood pressure to increase. For example, when you stand up, blood pressure needs to rise somewhat or you will faint. If you need to lift a heavy object, sprint for a bus, or engage in hot sex, your blood pressure needs to climb suddenly and sharply. The high-pressure baroreceptors are designed to accomodate these kinds of transient changes, and then go back to monitoring the blood pressure against a more reasonable baseline. But when high blood pressure continues over a period of days, the barorecptors "reset," so that the higher blood pressure becomes the new normal. This, and other kinds of baroreceptor problems, are suspected of being involved in many cases of hypertension.
Sympathetic Nervous System Overactivity. Overstimulation or overactivity of the sympathetic nervous system can raise blood pressure. Ongoing fear, stress, panic, or just plain tension can raise blood pressure directly (as well as speeding heart rate).
Too Much Stress. In addition to the sympathetic nervous system activity engendered by stress, various kinds of hormones (notably cortisol and noradrenaline) generated by stress and sympathetic nervous system activity act to raise blood pressure. Chronic elevation of these chemicals in the bloodstream can cause hypertension.
Oversecretion of angiotensin or other hormones. Attacking angiotensin (by means of drugs such as ACE inhibitors) is a common approach to lowering blood pressure, but the fact that this approach is taken doesn't necessarily confirm that the cause of a given case of hypertension was oversecretion. Since inhibiting Ancgiotensin Converting Enzyme lowers blood pressure, ACE inhibitors are often employed even though the hypertension might be unrelated to oversecretion.
Too Much Sodium. This topic requires a whole post of its own, but as almost everyone knows, too much salt can raise blood pressure in at least some people. (In some people, too little sodium results in overstimulation of the sympathetic nervous system, which raises blood pressure, but the medical establishment has chosen to ignore this inconvenient fact.)
Too Little Potassium. Potassium acts to lower blood pressure, and can be thought of as the counterweight to sodium. Recommended intakes of potassium are very high--three to four grams a day--but very few Americans eat enough fruits and vegetables to get anywhere near this amount. Because potassium is so potent at lowering blood pressure, however, the FDA has made potassium supplements above 99 mg (about 3% of the typical daily requirement) available by prescription only.
Too Little Magnesium. Magnesium also acts to lower blood pressure, and plays a vital role in cardiovascular health. Unlike sodium and potassium, however, where a simple blood test gives a good indication of any deficiencies or excesses, magnesium deficiencies are difficult to identify with serum tests. Most of the body's magnesium is sequestered in cells and bone, and these reserves can be called upon to keep blood levels reasonably stable. By the time blood magnesium drops, the total body deficit is very large. Furthermore, the body can only absorb so much magnesium at a time, so returning the body to magnesium balance can take months.
Sleep disturbances. Sleep apnea (interruption of breathing during sleep) has been shown to be a clear cause of some cases of hypertension. In addition, sleep deprivation unrelated to apnea also appears to raise blood pressure. Even in subjects with normal blood pressure, cutting back on hours of sleep raises blood pressure on the subsequent day, and many scientists now believe that prolonged sleep deficits may result in the development of hypertension.
Obesity. There is a high correlation between overweight and hypertension, but the relationship is far from perfect; there are many overweight people with normal blood pressure, and many trim people with hypertension. Losing weight can often lower blood pressure, sometimes dramatically, but since losing weight usually involves changing diet and exercise, it is unclear whether it is the weight loss per se that causes the reduction on blood pressure. The mechanisms by which obesity causes hypertension are unclear, although Syndrome X and/or liver problems (see below) may be the root causes.
Arteriosclerosis/atherosclerosis. Clogged arteries increase blood pressure by requiring the heart to pump harder to move blood around the body.
High cholesterol. High cholesterol, particularly high LDL cholesterol, is commonly assocaited with hypertension, but there is considerable doubt whether it directly causes hypertension. LDL is a building block involved in clogging arteries, which raises blood pressure, but the mechanisms of laying down arterial plaque now appear to be more complicated than the mere presence of high levels os LDL.
Sedentary lifestyle. Lack of exercise predisposes to the development of hypertension, and hypertension can sometimes be reversed by exercise. Once again, the mechanism is unclear. Exercise may help reset baroreceptors (see above), and can also reverse aspects of Syndrome X (see below).
Alcohol. The link between alcohol and high blood pressure has long been a puzzle to researchers. One or two alcoholic drinks per day is associated with lower blood pressure than found in abstainers, but higher levels of consumption are associated with increased blood pressure. Moreover, the blood-pressure-increasing effects of alcohol are reversible as soon as intake is reversed. Recent research suggests that the association between high alcohol consumption and high blood pressure may not be an effect of the alcohol as such, but rather an effect of developing a fatty liver [1], which is common with high levels of alcohol intake (see below).
Upper cervical spine problems. Recently it was discovered that misalignment of the top cervical vertebra, the "Atlas" vertebra, can cause high blood pressure, presumably by pressing on nerves in the brainstem. Techniques for adjusting this misalignment through procedures developed by NUCCA (National Upper Cervical Chiropractic Association) techniques have been decisively shown to normalize blood pressure in individuals with neck injuries[2].
High insulin levels. Insulin causes high blood pressure in at least three ways. First, it instructs the kidneys to retain sodium and thereby retain body water. Second, it enlarges the smooth muscle cells of the walls of the arteries, stiffening them and also constricting them. Third, it stimulates the release of noradrenaline, which has many of the same effects as hyperactivity of the sympathetic nervous system.
Diabetes. When most people think of diabetes, they think of an insufficiency of insulin. But the most common form of diabetes, Type II diabetes, involves a long stage where there is a superabundance of insulin, co-existing with high blood sugar (a state called insulin resistance). About 70% of diabetics have hypertension. The exact link is not certain, but insulin is quite likely one of the culprits. In fact, diabetes may not be a cause of hypertension, but just another symptom of an underlying problem.
Syndrome X/Metabolic Syndrome. In the late 1980s, Gerald Reaven at Stanford University wrote a groundbreaking paper in which he contended that a whole host of health-damaging characteristics tended to occur in synchrony:
1) High insulin levels
2) Insulin resistance
3) High blood sugar
4) High blood pressure
5) Elevated VLDL cholesterol
6) Low HDL cholesterol
He dubbed this cluster of symptoms"Syndrome X" (though it is now often referred to as "metabolic syndrome"), and argued that insulin resistance was the real root of the problem. Syndrome X is a precursor to Type II diabetes, is associated with obesity and rapid weight gain, especially around the abdomen, and often is associated with fatty liver (see below). In effect, Reaven says that insulin resistance is a major cause of hypertension (as well as many other diseases).
Chronic inflammation. Inflammation has become the latest suspect in a great many diseases, ranging from arteriosclerosis to cancer to many autoimmune disorders. Recently it discovered, for example, that women with psoriasis (and inflammatory skin disorder) were far more likely to go on to develop Type II diabetes and high blood pressure.
Fatty liver. Fat accumulation in the liver causes the liver to become inflammed (and often progresses to hepatitis or even cirrhosis). An inflammed liver produces high levels of a protein called C-reactive protein (CRP). Although the exact role of CRP in the body is obscure, big jumps in CRP are seen during infections. Chronic elevation of CRP is associated with the development of arteriosclerosis; in fact, some medical scientists argue that CRP and another protein, homocysteine, rather than high cholesterol, cause atherosclerotic damage to arteries (the cholesterol is merely used as a building block). In any case, high CRP levels were recently shown to raise blood pressure directly by acting on the artery walls in some fashion [3]. Since fatty liver is associated with Syndrome X, obesity, high alcohol intake, and high cholesterol levels, fatty liver and elevated inflammation proteins may be the link between all of these conditions, and may point to the true root cause of many cases of hypertension.
[1] Stranges, S. et al. Body Fat Distribution, Liver Enzymes, and Risk of Hypertension. Hypertension. 2005;46:1186
[2] Bakris, G, et al. Atlas vertebra realignment and achievement of arterial pressure goal in hypertensive patients: a pilot study. Journal of Human Hypertension (2007), 1–6.
[3] CRP Liver Protein Induces Hypertension. Medical News Today, Feb 22, 2007.
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