In part one (Jan. 22, 2013), I discussed how decades of psychosomatic research focused on anger and anxiety have not helped us understand or treat hypertension. Anger, anxiety and day-to-day stress do raise blood pressure in the moment, but with no lasting effect, just as interventions such as biofeedback, relaxation and meditation do lower blood pressure in the moment, but with little persisting effect.
In part two (Feb. 22, 2013), I discussed a different approach to understanding the psychological link of hypertension. Two important points: First, in most patients with hypertension, particularly ordinary hypertension, psychological factors are not a cause. Second, when they are a cause, it is usually repressed emotion, rather than the emotion we experience, that is at the heart of it. I described clues that suggest when hypertension is linked to psychological factors (see table).
Clues that your hypertension might be related to psychological factors:
In part three, I will discuss the unappreciated relevance of this mind/body understanding to the treatment, and drug treatment, of hypertension. The key point: If your hypertension is related to emotion, it will respond to different medications than if it isn't.
The Mind/Body Connection and Choice of Medication
In my book, Hypertension and You, I discuss the three main mechanisms that drive hypertension, and the drugs that target those mechanisms. The medication that is right for you is that which matches the mechanism or mechanisms driving your hypertension. The three mechanisms are (1) sodium/volume, (2) the renin angiotensin system (RAS), a hormonal trigger of arterial constriction triggered by the kidneys, and (3) the sympathetic nervous system (SNS), the link between brain and blood pressure.
The hypertensive mechanisms, and the drugs that target them:
(2)Renin-angiotensin system (RAS) (hormonal system triggered by the kidneys)
(3)Sympathetic nervous system (SNS) (the pathway that mediates the effect of the brain on blood pressure)
The first two mechanisms, sodium/volume and the RAS, are the drivers of hypertension in about 85 percent of people who have hypertension. The proof: treatment with a drug that targets sodium/volume, such as a diuretic, or one that targets the RAS, such as an angiotensin-converting enzyme inhibitor (ACEI or ACE inhibitor, for short) or angiotensin receptor blocker (ARB), or a combination of the two, will control hypertension in about 85 percent of people who take them.
In this 85 percent, the third mechanism, the SNS, is not prominently involved and does not need to be targeted. It is in the remaining 15 percent in whom the SNS is often the main driver of hypertension.
What causes the overactivity of the SNS? Hypertension researchers are still trying to figure that out, but this is where the mind/body connection fits in: In most cases of SNS-driven hypertension, it is emotion, even though repressed, that is driving the overactivity of the SNS. Just as the emotions we feel transiently stimulate the SNS and transiently elevate our blood pressure, the emotions we repress underlie more long-lasting stimulation of the SNS, and hypertension.
In other words, psychological factors are the trigger of hypertension in most cases of SNS-driven hypertension. And usually it is the emotions we are unaware of, which is why this link has gone unappreciated, while the study of the emotions we experience has failed to help our understanding.
If you are among the 85 percent with ordinary, mild or moderate hypertension, it is largely driven by genetics and health habits, and drugs that target sodium/volume and/or the RAS will likely control your hypertension. If you are among the remaining 15 percent (see clues listed above), particularly if your hypertension has not responded to a diuretic plus ACEI or ARB combination, it is likely driven by the SNS and linked to psychological factors, and likely to respond better to drugs that target the SNS. Of course, all three mechanisms could be contributory, in which case drugs to target all three mechanisms are needed.
Which drugs target the SNS? The main drugs are the beta-blockers, the alpha-blockers and the central alpha-agonists. Beta-blockers (e.g., metoprolol (Toprol), carvedilol (Coreg), atenolol (Tenormin)), can be effective in some patients when used alone, but in many need to be given in combination with an alpha-blocker (e.g., doxazosin (Cardura)). Central alpha-agonists (e.g. clonidine (Catapress)) are very effective, but I don't usually recommend them because of prominent side effects such as fatigue.
Is there a role for psychotherapy or other psychological intervention in treating hypertension driven by psychological factors? Usually no, because individuals whose hypertension is driven by repressed emotion, who aren't experiencing emotional distress, are unlikely to seek or benefit from psychological intervention. That is why you see fewer and fewer studies examining the role of relaxation techniques and psychotherapy in the treatment of hypertension. Also, with regard to repressed emotion related to trauma, it is often best to let sleeping dogs lie.
I believe repressed emotion is a factor in many patients with severe hypertension, or hypertension that has not responded to drugs that target sodium/volume or the RAS. I believe it is almost always the underlying cause in an uncommon but dramatic form of hypertension, episodic (paroxysmal) hypertension. Here, as I also discuss in Hypertension and You, dealing with what has been repressed, an alpha/beta-blocker combination, an anti-anxiety drug, and/or an antidepressant are the most effective treatment options, further demonstrating the underlying role of repressed emotion.
So there is very much a place for the mind/body connection in understanding and treating hypertension. But it is not the cause of hypertension in the 85 percent with ordinary hypertension, and the anger, anxiety and stress we experience are not at the heart of it.
Please feel free to pose questions in your comments.
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