07 Apr High Blood Pressure – The Hormone Connection
The incidence of high blood pressure in women increases dramatically after menopause, suggesting a connection to hormones. As the body’s chemical messengers, hormones orchestrate our metabolic processes by stimulating changes in cells—including those in our blood vessels. Hormones, which originate in various glands, circulate throughout the body in the blood, bathing our tissues. Receptors within our cells are sensitive to particular hormones, causing a reaction.
In our blood vessels, receptor cells are particularly sensitive to several hormones, including estrogens, progesterone, testosterone and cortisol. They are also very sensitive to a steroid hormone that acts as a precursor to all of these, called DHEA (dehydroepiandrosterone).
Cardiovascular problems have been linked to deficiencies in DHEA, thyroid, and other hormones, including Vitamin D. Both heart rate and arterial tone are controlled by the glands, “It is the disruption of glandular function that is at issue…when this system is dysfunctional, blood pressure disorders develop.”
Estrogens and Progesterone
For decades, estrogens have been thought to protect premenopausal women from heart disease. The theory was simple: estrogens lower “bad” cholesterol and raise “good” cholesterol, reducing atherosclerosis—the buildup of plaque in artery walls that causes them to harden, narrowing and restricting blood flow to the body’s tissues.
Researchers were so excited by this theory that they proposed that menopausal women consider hormone therapy solely to protect heart health. However, when the national Women’s Health Initiative (WHI) ran a large clinical trial to test this theory from 2002–2004, they found that participants taking Prempro, a combination of synthetic progestin and estrogens derived from horse urine (Premarin), actually showed a slight increase in heart attacks, stroke, blood clots and breast cancer. However, there were several limitations to this study, such as the fact that the progestin used in the WHI study was previously linked to coronary artery spasms, while bio-identical progesterone (i.e., not progestin) itself relaxes the arteries.
Research indicates that Premarin alone, or Premarin combined with biologically identical progesterone, may be more effective in increasing HDL (good cholesterol) than Prempro. In fact, results from an ancillary study of WHI participants, published by the New England Journal of Medicine in June 2007, found that women aged 50 to 59 who received estrogen (Premarin) had lower levels of calcified plaque in their coronary arteries, compared to participants who received a placebo. Further research is needed to determine if even better results can be achieved by using only biologically identical hormones.
Although the effects of various estrogen therapies on blood pressure have been controversial, sometimes contradictory, and often confusing, there is reassuring news. In 2006, a University of Wisconsin pharmacy student reviewed several studies and found that postmenopausal women taking biologically identical estrogens and/or progesterone did not have a statistically significant change in blood pressure. And, a 2006 editorial in Menopause: The Journal of the North American Menopause Society suggests that “the type of estrogen influences the hypertensive response,” such as estrone and estradiol showing reductions in blood pressure.
Testosterone and Cortisol
For over 40 years, scientists and practitioners have been debating the role of cholesterol in atherosclerosis. Dr. Jens Møller, the former President of the European Organization for the Control of Circulatory Diseases, argues that high cholesterol is a symptom of deterioration in circulation. Dr. Møller details how a deteriorated circulation system and high cholesterol levels can be treated with testosterone to decrease the “stickiness” of the plaque and reduce overall cholesterol levels.
Dr. Møller also reminds us that cholesterol is “the precursor of many hormones, including the vital substance testosterone itself. Decreasing the cholesterol level alone may in fact result in a decrease in the production of testosterone, which plays a vital role in maintaining a normal circulation.” The link between testosterone and the “stress hormone” cortisol provides the mechanism for Dr. Møller’s theory. The problem, he says, is that cholesterol is not a dietary problem, but a sign of a biochemical problem—how the body synthesizes cholesterol.
Excess cortisol is to blame, he says. It interferes with the normal metabolism of carbohydrates in food, which can lead to insulin resistance and plaque build-up, and eventually cardiovascular disease. The solution, he says, is to keep cortisol levels in check.
Dr. Broda Barnes concurs with the belief that cholesterol is not the cause of heart disease, but a symptom of another problem. In his view, thyroid deficiency is “firmly established as the cause of atherosclerosis.”
In Solved: The Riddle of Heart Attacks, Dr. Barnes reports how atherosclerosis is almost always accompanied by thyroid deficiency, whereas high cholesterol levels, even at an early age, do not necessarily result in a heart attack or cardiovascular disease.
Dr. Barnes claims that thyroid therapy, when given early enough in the course of the disease, prevents cardiovascular disease and increases life expectancy. There is a clear link between thyroid hormones and normal heart function. For example, the majority of thyroid deficient patients exhibit hypertension. There is also a relatively high incidence of heart attacks and strokes among patients with thyroid deficiencies, and an extremely high rate of atherosclerosis among patients who have had their thyroid removed.
The adrenal gland hormone DHEA (dehydroepiandrosterone) is a precursor of both testosterone and estrogens. It supports muscle growth and energy metabolism—the rate at which our body absorbs nutrients from our food.
Like testosterone, DHEA is a steroid hormone that acts to balance the effects of the stress hormone, cortisol. It is now well known that chronic stress leads to an outpouring of cortisol, and with that, a gradual depletion of DHEA.
Over time, this hormonal imbalance can lead to hardening of the arteries, thinning bones, increasing waistline girth, and impaired functioning of the immune system. By restoring proper DHEA levels, the normal balance between DHEA and cortisol can be restored.
DHEA may also help to reduce inflammation. Proper levels of DHEA promote a healthy immune system by helping to achieve the proper balance among the various types of cytokines.
Cytokines are proteins that act as chemical messengers in the body (much like hormones, except that they act locally). They are especially important for regulating inflammatory and immune responses.
As early as the late nineteenth century, a German physiologist proposed that heart disease was caused by inflammation of the heart and arteries. Rudolph Virchow, called the “father of pathology,” originated this theory.
Medicine has come back around to Virchow’s view, as there is now widespread acceptance of the role that inflammation plays in the development of atherosclerosis. Research in the 1980s led to the development of this now popular model: inflammatory immune-system cells burrow into an arterial wall, where they are fed by fat deposits.
“These cells form a plaque that is weakened by inflammation,” relates Nancy Appleton in Stopping Inflammation: Relieving the Cause of Degenerative Diseases, “Then the fibrous cap ruptures, spilling everything into the bloodstream, including cytokines that encourage blood clotting … thus changing a stable cholesterol plaque into an unstable lesion.”
Appleton also describes newer research linking high blood pressure to high cytokine production (indicating an inflammatory response) and also to allergens. By removing allergens, some people have been able to end their hypertension, possibly by eliminating the trigger to their body’s inflammatory response.