Adrenal Support With DHEA for COPD And Related Breathing Disorders

Majid Ali, M.D.

COPD stands for chronic obstructive pulmonary disease. One would expect people who cannot breathe freely to be under chronic stress. This, of course, is true. Everyone with chronic stress needs adrenal support. Chronic oxygen deficit in the body creates chronic organic adrenal stress. Acute oxygen deficiency causes acute organic adrenal deficit. In it One would expect people who cannot breathe freely to be under chronic stress.

The best long-term adrenal support is personal spiritual realism (described fully in a companion article on the subject). This, of course, take time and people with COPD need a simpler, fasting acting remedies for adrenal function. Under these conditions, I commonly prescribe 25 to 50 mg daily of DHEA (dehydroepiandrosterone) for my male patients and a smaller dose (25 mg or less) for females. For information about other natural adrenal remedies, please go to a companion article on the website.

In February 2012, an article published in the journal Annals of Endocrinology published clear scientific evidence for the value of DHEA for patients with COPD who also develop high blood pressure in lung arteries ( pulmonary hypertension0. Below, I include the abstract of this article for readers with biology background.

* de LaRoque, ED, Savineau J-P, Mtivier An-C, et al. Dehydroepiandrosterone (DHEA) improves pulmonary hypertension in chronic obstructive pulmonary disease (COPD): a pilot study. Ann Endocrinol (Paris). 2012 Feb;73(1):20-5.

OBJECTIVES:

It was previously shown that dehydroepiandrosterone (DHEA) reverses chronic hypoxia-induced pulmonary hypertension (PH) in rats, but whether DHEA can improve the clinical and hemodynamic status of patients with PH associated to chronic obstructive pulmonary disease (PH-COPD) has not been studied whereas it is a very severe poorly treated disease.

PATIENTS AND METHODS:

Eight patients with PH-COPD were treated with DHEA (200mg daily orally) for 3 months. The primary end-point was the change in the 6-minute walk test (6-MWT) distance. Secondary end-points included pulmonary hemodynamics, lung function tests and tolerance of treatment.

RESULTS:

The 6-MWT increased in all cases, from 333m (median [IQR]) (257; 378) to 390m (362; 440) (P<0.05). Mean pulmonary artery pressure decreased from 26mmHg (25; 27) to 21.5mmHg (20; 25) (P<0.05) and pulmonary vascular resistance from 4.2UI (3.5; 4.4) to 2.6UI (2.5; 3.8) (P<0.05). The carbon monoxide diffusing capacity of the lung (DLCO % predicted) increased significantly from 27.4% (20.1; 29.3) to 36.4% (14.6; 39.6) (P<0.05). DHEA treatment did not change respiratory parameters of gas exchange and the 200mg per day of DHEA used was perfectly tolerated with no side effect reported.

CONCLUSION:

DHEA treatment significantly improves 6-MWT distance, pulmonary hemodynamics and DLCO of patients with PH-COPD, without worsening gas exchange, as do other pharmacological treatments of PH (trial registration NCT00581087).

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