Monday, August 17, 2009
Increasingly, however, it appears that many cases of hypertension may in fact be cases of high levels of inflammation in the body--in particular, cases of inflammation of the liver.
When large amounts of fat are stored in the liver, the liver becomes stressed. This raises the level of several liver enzymes, and has been strongly associated with hypertension.
Metabolic Syndrome, or Syndrome X, commonly has has high blood pressure as a key marker. The early stages of Metabolic Syndrome are characterized by high blood levels of insulin. Insulin raises blood pressure, so the linkage between Metabolic Syndrome and hypertension might seem to be obvious; but as Metabolic Syndrome progresses into Type II diabetes, the pancreas becomes unable to provide insulin, and blood insulin levels plummet. If it were insulin levels alone causing the hypertension, we would expect that as people became diabetic, their blood pressure would fall--but instead, the opposite occurs, and blood pressure usually worsens with the onset of diabetes.
The real culprit may be fatty liver, which is common in Metabolic Syndrome and in Type II diabetes (indeed, some researchers now feel that fatty liver is one of the hallmarks of Metabolic Syndrome). The mechanism by which fatty liver causes increases in blod pressure has only recently been discovered. As fat accumulates in the liver, the liver becomes inflammed. In response, it releases C-Reactive Protein (CRP). CRP is one of the classic markers of inflammation; for example, it rises sharply when the body is fighting an infection. CRP's role in cardiovascular disease is controversial, and CRP testing has been shown to be a poor predictor of heart disease or stroke. 
CRP is, however, intimately involved in hypertension, and recent research shows how CRP circulating in the bloodstream acts upon the arteries to raise blood pressure. 
Fatty liver disease is traditionally divided into two flavors--Alcoholic Fatty Liver Disease (AFLD), and Non-Alcoholic Fatty Liver Disease (NAFLD). The only difference between the two, however, is that NAFLD is not attributed to overconsumption of alcohol; the condition of the liver is indistinguishable in the two diseases. When the liver becomes highly inflamed, AFLD is called alcoholic hepatitis, while NAFLD progresses into Non-Alcoholic Steatohepatitis (NASH). NAFLD was only recently recognized as a specific disease, but it is widespread: in one major study, one-third of adults were discovered to have fatty livers (defined as a liver-fat content of 5.5% or more), although the prevalence varied considerably by ethnic group. 
NAFLD is considered by some to be mainly a metabolic disease--part of Metabolic Syndrome--while others consider it to be simply a disease of obesity. Since obesity is one of the hallmarks of Metabolic Syndrome, this may be a moot distinction.
Almost everyone is now familiar with the fact that those who accumulate fat around their stomachs are at greater risk for heart disease than those who accumulate fat around their hips--the so-called "apple" and "pear" patterns of fat storage. This turns out not to be quite accurate. Samuel Klein, a leading researcher on the connection between liver problems and cardivascular disease, says, "Abdominal fat is not the best marker for risk. It appears liver fat is the real marker. Abdominal fat probably has been cited in the past because it tends to track so closely with liver fat. But if you look at people where the two don't correspond — with excess fat in the liver but not in the abdomen and vice versa — the only thing that consistently predicts metabolic derangements is fat in the liver." 
Klein goes on to say, ""Fatty liver disease is completely reversible. If you lose weight, you quickly eliminate fat in your liver. As little as two days of calorie restriction can improve the situation dramatically, and as fat in the liver is reduced, insulin sensitivity and metabolic problems improve."
The linkage between fatty liver and hypertension is an important research result, because most cases of fatty liver can be cured--by the patient, without medication or medical intervention. Weight loss of five percent of body weight shows quick improvement in liver fat accumulation and insulin resistance, while a loss of nine percent of body weight or more appears to reverse liver damage. [6,7].
Even moderate levels of exercise also have a powerful and rapid effect on reversing fatty liver, even without substantial weight loss. [8,9].
I'll have more on this topic in my next post.
 Stranges, Saverio, et al. Body Fat Distribution, Liver Enzymes, and Risk of Hypertension. Hypertension. 2005;46;1186-1193.
 Baker, S.L.. C-Reactive Protein Test for Heart Disease Found Useless. Natural News, Aug. 4, 2009.
 CRP Liver Protein Induces Hypertension. Medical News Today (medicalnewstoday.com ). Feb. 22, 2007.
 Prevalence of Non-alcoholic Fatty Liver Disease Varies by Ethnicity. Medical News Today (medicalnewstoday.com ). Dec. 8, 2004.
 Dryden, Jim. Apple or pear shape is not main culprit to heart woes — it's liver fat. Washington University St. Louis School of Medicine, Public Affairs News Release. Dec 3. 2008.
 Harrison, Stephen A., et al. Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial. Hepatology. 2009: 49(1); 80-86.
 Weight loss reverses fatty liver disease. Indo-Asian News Service. Feb 20, 2009.
 Exercise Helps Patients With Non-Alcoholic Fatty Liver Disease. Medical News Today (medicalnewstoday.com ). Jul. 3, 2009.
 Moderate exercise can reduce fatty livers in diabetics. Indo-Asian News Service. Sep. 20, 2008.
Sunday, August 9, 2009
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. (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. 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) .
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. 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.
 Stranges, Saverio, et al. Body Fat Distribution, Liver Enzymes, and Risk of Hypertension.
. CRP Liver Protein Induces Hypertension. Medical News Today (medicalnewstoday.com ). Feb. 22, 2007.
 Neter, Judith E., et al. Influence of Weight Reduction on Blood Pressure: A Meta-Analysis of Random Controlled Trials. Hypertension 2003;42;878-884.
 Reisin E, Frohlich. Effects of weight reduction on arterial pressure. J Chronic Dis. 1982;35:887–891.
Sunday, July 26, 2009
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 .
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.  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 . 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.
 Tindall, Blair. Better Music Through Chemistry. New York Times, Oct. 17, 2004.
 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.
 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.
Saturday, July 18, 2009
Despite having been widely prescribed for decades, the ways that diuretics lower blood pressure are still unclear. The most often cited effect is a simple lowering of the volume of blood circulating in the body; this allows the heart to work less, and with a lower total volume of fluid circulating the blood pressure "naturally" drops. Diuretics also tend to lower peripheral vascular resistence, allowing the blood to flow more easily to the extremities. Some researchers suspect that the extra excretion of sodium in the increased volume of urine may be a major factor. In many cases of hypertension, especially in obese patients, there is significant edema (swelling due to water retention), and relieving this condition may also have a major impact in lowering blood pressure.
There are a few varieties of diuretics, but only the thiazides are used to lower blood pressure. The powerful "loop" diuretics (such as Lasix) and "potassium-sparing" diuretics (such as Aldactone) are usually reverved for severe edema and conditions such as congestive heart failure; they have little effect on blood pressure. (Loop diuretics have powerful side effects, especially generalized nausea. My grandfather was prescribed Lasix in the last years of his life, and he often told me they made him feel so bad that he'd rather die than take another Lasix. I can well believe it.)
The long-recognized problem with thiazide diuretics is that they deplete the body of minerals and vitamins, which are flushed out in the urine. Among the minerals that are flushed are potassium and magnesium, both of which are important for keeping blood pressure low. (I'll have posts on both of these minerals some day in the future.) There is some recognition by doctors that potassium levels need to be monitored, but most doctors are happy enough with potassium levels even at the rock-bottom level of "normal," and I have yet to meet a doctor who worried about magnesium levels (probably because they are exceedingly hard to test). As to vitamins, few doctors seem to think that they are important.
Thiazide diuretics are prescribed casually, and some doctors don't seem to think that the patient's lifestyle makes much difference in whether or not a diuretic is appropriate. In my case, I was doing vigorous exercise every day (more on that in another post), including Bikram Yoga, which is a strenuous series of postures done in a room heated to about 105 F (40.5 C). I was also working out in a gym, and going for long walks.
I was flushing plenty of water through my system even without a diuretic. The common prescription for water consumption is "eight eight-ounce glasses of water a day"--64 ounces, or roughly two liters. When I was on diuretics there were days when I was drinking three times that amount--about 180 ounces (over five liters)--and still couldn't stay hydrated. I could almost feel the valuable nutrients in my body going down the toilet.
Lucky for me, I changed doctors, and at my very first meeting with the new doctor he took me off the diuretic. (I might add that my blood pressure in the ensuing days continued to go down rather than up. If you can discontinue a blood pressure medication and experience a drop in your blood pressure, you are clearly on the wrong medication.)
Diuretics, like any pharmaceutical, have a host of side effects. But there is one major side effect you won't find on the insert--a side effect that may not show up for many years: Thiazide diuretics can cause Type II diabetes.
It has been known since the 1960s that diuretics often caused changes similar to the early stages of adult-onset diabetes , but in the last few years the evidence has become overwhelming. "Diabetogenic" changes resulting from the use of thiazide diuretics over a period of only 12 weeks include the following :
1) Increased blood sugar levels (as measured by glycosylated hemoglobin)
2) Increased insulin resistance
3) Dangerous fat redistribution (migration of subcutaneous fat to visceral fat)
4) Accumulation of fat in the liver
5) Increased low-grade inflammation (as measured by increased C-reactive protein)
Even in cases where long-term administration of diuretics has not resulted in full-blown Type II diabetes, these changes predispose patients to metabolic syndrome (Syndrome X), weight gain, liver disease, and--because of the increased C-reactive protein levels--to a higher incidence of heart disease, cancer, and arteriosclerosis.
No one is quite sure why diuretics have these diabetogenic effects, though the depletion of potassium has been proposed as a possible cause . The common problem of low potassium levels from diuretics is one that has been shamefully neglected by many doctors, but with diuretics also causing the loss of a wide array of minerals and vitamins, there are many possible ways diuretics could cause long-term problems. To take a single--and counterintuitive--example, lower levels of sodium have many consequences, and one of them is increased insulin resistance . The lowering of salt retention, which most doctors think is one of the benefits of diuretics, may itself be part of the cause of diabetes.
Diabetes is generally slow to develop, so diuretics are not usually suspected: after all, the patient has been using them for years. Because of increased weight, high blood sugar and insulin, lower potassium levels, and fatty liver, over a period of years your blood pressure problems may worsen--but this takes so long to happen that the doctors are inclined to say, "Well, you're getting older." To be sure, you are; and in some cases, the older you get, the more time your medications have to make you sicker.
Diuretics are thought of as the front-line strategy in controlling hypertension, and they tend to be prescribed casually and are assumed by most physicians to be generally benign. But they can have grim long-term consequences for overall health. If you have hypertension accompanied by any of the signs of "Syndrome X" (high insulin, high blood sugar, visceral fat, abdominal obesity, or insulin resistance), you need to be aware that diuretics may make your condition much worse in the longer term--and, ironically, may over a period of years, increase your blood pressure problems. I am so thankful that my current doctor doesn't think I need to take them.
 Domenet, J.G. Diabetogenic Effect of Oral Diuretics. Br Med J. 1968; 3:188
 Ericksson, Jan W., et al. Hydrochlorothiazide, but not Candesartan, Aggravates Insulin Resistance and Causes Visceral and Hepatic Fat Accumulation. Hypertension. 2008;52:1030-1037
 Zillich, Alan J, et al. Thiazide Diuretics, Potassium, and the Development of Diabetes. Hypertension. 2006;48:219-224
 Alderman, Michael. A Pinch of Science. New York Times, Feb 6, 2009.
Sunday, July 12, 2009
Blood pressure readings can in principle be taken anywhere that the arteries can be compressed to the point where the flow is suppressed. But the vascular resistance to flow changes as you progress down an artery. If you think about it, this makes sense: if blood didn't flow more easily toward the extremities, it would be hard to ensure that blood reached the fingertips. The net effect is that, all else held equal, blood pressure will tend to be higher measured at the wrist than at the upper arm, and higher in the fingertip than at the wrist.
In addition, the height at which the wrist or finger is held relative to the heart also affects the blood pressure. This also stands to reason: it is easier to cut off blood flow when it is pushing "uphill" than when it is flowing "downhill."
In principle, these factors can all be compensated for so that a measurement made at the wrist or finger can be translated back to an equivalent in upper-arm terms. In practice, this long proved difficult in the case of wrist monitoring, and has thus far proved impossible in finger monitors.
Recently, however, a few manufacturers have overcome the problems with wrist monitors, and a number of models have been validated by the two key certification agencies, the Association for Advancement of Medical Instuments (AAMI) and the British Hypertension Society. The better versions of these monitors will not take readings unless the wrist is supported at exactly the level of the heart--the position that ensures accurate results.
It is still possible to screw up a reading, even with the automatic monitoring of wrist position. If the cuff inflation begins and the user then moves their arm to another position, the result will be inaccurate. For this reason, no agency recommends wrist monitors over upper arm monitors. (Although you can also produce incorrect readings by moving your arm with an upper arm monitor, it is less easily done by accident--and you can't move your upper arm as far above or below your heart as you can move your wrist.) In other words, the powers that be don't want you using wrist monitors because they don't trust you to follow the directions.
Despite all that, I use a wrist monitor (though I started out on an upper-arm monitor.) Why? I think wrist monitors have a number of advantages:
1) Wrist monitors are easy to transport. You can slip them into a purse, briefcase, or the glove compartment of your car. Though they are much larger than a wristwatch, I've seen women wearing clunky bracelets that were about the same size as my wrist monitor.
2) Wrist monitors can be used almost anywhere. Well, anywhere you can sit down. Conventional upper-arm monitors require a table nearby to station the monitor and rest your arm, and the monitor is connected to the cuff by an inconvenient tube. I've used my wrist monitor to take my blood pressure in the locker room after exercise, in airport transit lounges while traveling, and sitting on the freeway stuck in traffic. Try doing any of those with an upper-arm monitor.
3) Wrist monitors don't make you feel as if you're being strangled. Upper-arm cuffs are huge. Most people find the massive crushing sensation on their upper arm to be unpleasant, and a substantial number of people respond to it with surges in blood pressure--whcih rather defeats the whole purpose. The squeeze from a wrist monitor isn't like a hug from your grandmother, but it's a whole lot easier to ignore than the full-arm crush of a standard monitor.
4) The better wrist monitors don't "overpressure." To measure blood pressure, the cuff needs to be inflated to the point where the sounds of blood flow are completely cut off, and then gradually deflated as the sounds of the pulse are restored. Most automatic upper-arm units inflate to some high value; pause; listen...and then if sounds are still heard, inflate to an even higher pressure, and repeat the process. This is slow (giving the panic-prone time to shoot their blood pressure through the roof), and well-respected research shows that an overinflated cuff in itself results in higher blood pressure readings . Most AAMI/BHS-validated wrist monitors are smarter, and use techniques (such as Omron's "Intellisense") to minimize overinflation. (Anti-overpressuring techniques are now also built in to some upper-arm monitors as well.)
I'm not in the business of recommending specific products, but, for the record, I use an Omron HEM-650 Wrist Monitor, and I'm very happy with it. It takes a little time to learn the proper technique, but after a few sessions the supporting and postioning of the arm becomes instinctive (and it also beeps to signal whether your wrist is too low, too high, or just right). It's good to calibrate/validate the readings against readings in a doctor's office or against an upper-arm monitor, but this sort of calibration is advised for all home-monitoring units.
Although most users find this device to be excellent (see the 200+ reviews at Amazon), a few reported discrepancies in validation or calibration. On the other hand, it's worth noting that many of the aneroid blood pressure monitors in clincal settings are out of whack: in the 1990s, one study found that 30-40% of all automatic monitors in use by physicians were out of calibration by 4 mm or more, and 10% were out of calibration by 10 mm or more. Since the majority of physicians and nurses don't follow the AHA guidelines for taking blood pressure, the combination of inaccurate monitors plus incorrect readings mean that a very large percentage of patients are probably misdiagnosed in clinical settings. It's disturbing that the medical industry considers the calibration of home monitors to be a major problem while ignoring the fact that a huge percentage--perhaps the majority--of measurements taken in clinics are also wrong. Apparently mistakes by professionals are somehow less worrisome than mistake by patients.
The truth is, blood pressure measurement isn't as exact as most people in the medical profession pretend. Take a few repeated measurements--at home, or in your doctor's office--and you'll see what I mean. Both systolic and diastolic numbers fluctuate considerably over the period of only a few minutes.
For that reason, I never put much faith in any single measurement. I record my blood pressure at least twice a day (in the morning, and 1-2 hours after exercise), but the number I record is the average of three measurments--one after five minutes of sitting quietly according to American Heart Association guidelines, and then two more, each after another wait of three minutes. (Some research protocols claim that a two-minute pause between measurements is sufficient.)
Doing it right--waiting five minutes before measuring and then taking two more measurements spaced apart by three minutes--ends up requiring about fifteen minutes of your time. But sitting quietly and relaxing for fifteen minutes twice a day isn't such a bad idea even for people who aren't taking their blood pressure.
 Sprafka, JM et al. The Effect of Cuff Size on Blood Pressure Measurements in Adults. Epidemiology. May 1991; 2(3):214-7.
 Campbell, Norman R.C., and McKay, Donald W., Accurate Blood Pressure Measurement: Why Does it Matter?, CMAJ. August 1999; 161 (3) 277
Sunday, July 5, 2009
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 , 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.
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 . 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.
 Stranges, S. et al. Body Fat Distribution, Liver Enzymes, and Risk of Hypertension. Hypertension. 2005;46:1186
 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.
 CRP Liver Protein Induces Hypertension. Medical News Today, Feb 22, 2007.
Sunday, June 28, 2009
What few people know--and scientists didn't know until the advent of ambulatory blood pressure monitoring--is how much blood pressure can be increased by normal, everyday activities. Chances are your doctor isn't aware of these facts, either (otherwise they wouldn't talk to you when they are taking your blood pressure).
Below is a table that lists the average change in blood pressure from everyday activities. Perhaps you won't be surprised that attending a meeting can raise your blood pressure by 20/15 (I've been to some that surely raised my blood pressure more than that). But the process of eating raises blood pressure by about 9/10. Getting dressed jumps it up by about 12/10.
Merely talking to someone raises blood pressure on average by 7/7 (and talking to doctors and nurses is probably a little more stressful than talking to, say, your grandmother). Talking on the telephone is even worse--a jump of about 10/7, even if you aren't talking to a telemarketer.
Unfortunately there is no data on what happens to your blood pressure when you have to listen to someone else yammering on their cell phone, but I'm guessing this gets as high as 30/20.
This underlines three major points. First, your blood pressure fluctuates a great deal during the course of a normal day. The idea that any single measurement tells you your average blood pressure is clearly incorrect. Blood pressure jumps around from moment to moment.
Second, since all of the scientific recommendations on hypertension are based on relaxed, resting blood pressure, without any of the seemingly innocous activities listed above, you need to be aware that blood pressure measurements taken without full relaxation, or while talking, or reading, or watching television, are probably too high to reflect the scientific benchmark.
Third, given all this varability, it is wise to be very suspicious of "trends" identified by your doctor. If your blood pressure is up, say, five points from your previous visit, does it really mean anything? Was your reading taken perfectly this time? Did you have time to relax, and five minutes without any distractions such as conversation?
This is the reason home monitoring is so important; a handful of measurements made under imperfect conditions at your doctor's office shouldn't be allowed to determine everything about the course of your treatment.
But it's your responsibility to make sure those home measurements are taken correctly.