Thiazide diuretics are a popular first-line treatment for hypertension among the primary care set.
This practice became especially well-established with the 2002 publication of the ALLHAT Study (Major Outcomes in High-Risk Hypertensive Patients Randomized to Angiotensin-Converting Enzyme Inhibitor or Calcium Channel Blocker vs Diuretic:The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)).
ALLHAT showed that an inexpensive diuretic like chlorthalidone (a weak diuretic in the thiazide class, similar to hydrochlorothiazide) as first-line treatment for hypertension achieved equivalent reductions in cardiovascular events (cardiovasular death and heart attack) as non-thiazide antihypertensives, lisinopril (an ACE inhibitor) and amlodipine (a calcium channel blocker, better known as Norvasc).
After 7 years of treatment, there was 14% death or heart attack among all three groups--no difference.
This was interpreted to mean that inexpensive thiazide diuretics like chlorthalidone offer as much benefit as other blood pressure medications at reduced cost.
On the surface, that's great. Anything that detracts from the ubiquitous pharmaceutical industry propaganda of bigger, better, more expensive drugs to replace old, inexpensive, generic drugs is fine by me.
But you knew there'd be more to this issue! If we accept that thiazides are equivalent to other single-drug treatments for high blood pressure, what do we do with the following issues:
--Thiazides deplete body potassium -This effect can be profound. In fact, built into the ALLHAT mortality rate is an expected death rate from potassium depletion. When potassium in the body and blood go low, the heart becomes electrically unstable and dangerous rhythms develop.
--Thiazides deplete magnesium --Similar in implication to the potassium loss, magnesium loss also creates electrical instability in the heart, not to mention exaggeration of insulin resistance, rise in triglycerides, reduction in HDL.
--Thiazides reduce HDL cholesterol
--Thiazides increase triglycerides
--Thiazides increase small LDL particles --You know, the number one cause for heart disease in the U.S.
--Thiazides increase uric acid --Uric acid is increasingly looking like a coronary risk factor: The higher the uric acid blood level, the greater the risk for heart attack. Thiazides have long been known to increase uric acid, occasionally sufficient to trigger attacks of gout (uric acid crystals that precipitate in joints, like rock candy). (Fully detailed Special Report on uric acid coming this week on the Track Your Plaque website.)
What about the advice we commonly give people to hydrate themselves generously? Yet we give them diuretics? Which is it: More hydration or less hydration? You can't have both.
Do thiazides exert an apparent cardiovascular risk reduction in a society due to its flagrant sodium obsession?
Thus, there are a number of inconsistencies in the thinking surrounding thiazides. In my experience, I have seen more harm done than good using these agents. While I cannot fully reconcile the reported benefit seen in ALLHAT with what I see in real life, all too often I see people having to take another drug to make up for a side-effect of a thiazide diuretic (e.g., high-dose prescription potassium to replace lost potassium, allopurinol to reduce uric acid, etc.). I have seen many people get hospitalized, even suffer near-fatal or fatal events from extremely low potassium or magnesium levels.
My personal view: ALLHAT or no, avoid thiazide diuretics like the plague. Sure, it might save money on a population basis, but I suspect that the ALLHAT data are deeply misleading.
What's better than a thiazide, calcium blocker, or ACE inhibitor? How about vitamin D restoration, thyroid normalization, wheat elimination?