The number of people with hypertension or high blood pressure has doubled globally in the last 30 years, increased from 650 million to 1.28 billion. Almost half of U.S. adults are now classified as having high blood pressure based on the updated definitions. But does this mean everyone with a diagnosis of hypertension needs medications?
A new study published in the Journal of the American Medical Association (JAMA), suggests the blood pressure guidelines go too far for low risk individuals, and the risk of harm outweighs the potential benefits. The JAMA study was an extensive chart review of over 38,000 patients at low risk for heart disease who had stage two hypertension (blood pressure between 149/90 and 159/99) and were treated with blood pressure medications. Over an average follow-up time of almost six years, they found no reduction in the risk of cardiovascular disease events or risk of death with medication use. They did, however, find an increased risk for low blood pressure, fainting, and acute kidney injury among those treated with medications.
In 2012 meta-analyses of anti-hypertensive drug treatment compared to placebo or no treatment trials up until the end of 2011 found that, antihypertensive drugs used in the treatment of adults (primary prevention) with mild hypertension (systolic BP 140-159 mmHg and/or diastolic BP 90-99 mmHg) at a period of four to five years follow up, no differences were seen in mortality, cardiovascular events, CAD, or stroke. Treatment caused 9% of patients to discontinue treatment due to adverse effects.
Based on these results, treating stage two hypertension in low risk patients tends to cause more harm than good.
According to TheNNT group, none were helped (preventing death, stroke, heart disease, or cardiovascular events) for those who received medication for the treatment of mild hypertension (systolic blood pressure 140-159 or diastolic blood pressure 90-99), but 1 in 12 were harmed (medication side effects and stopped the drug). Up to 40% of adults worldwide have hypertension, over half of which is classified as “mild.”
According to a recent randomized trial that enrolled 1,318 Australians from an online panel, ‘Hypertension’ and ‘high-normal’ labels may cause more harm than good in low-risk patients. Advising people that they are hypertensive or high normal when they have low risk of cardiovascular disease potentially may cause harm rather than engage them.
A 2015 study found that people on hypertension drugs can have stroke risk almost 2.5-times greater than those without high blood pressure. Their study involved 26,785 participants 45 and older.
The findings from all these studies are a timely reminder of the Hippocratic oath, ‘First, do no harm’. Since guidelines are evidence-based, they should also consider the increasing evidence of patients’ responses to having a medical label because words do matter to the patients. And this possibility for harm is only amplified if this may lead to initiating treatment with potential side effects.
A new 2021 Canadian study finds that for people who take thiazide diuretics — were associated with higher rates of keratinocyte skin cancers, including basal cell carcinoma, squamous cell carcinoma, advanced keratinocyte carcinoma and melanoma.
Calcium channel blockers reduce pancreatic insulin secretion and induce end-organ insulin resistance causing hyperglycemia.
Calcium channel blockers (CCB) and beta-blockers (BB) account for approximately 40% of cardiovascular drug exposures reported to the American Association of Poison Centers. However, Calcium channel blockers (CCB) and beta-blockers (BB) s represent >65% of deaths from cardiovascular medications.
Experimental models show that CCB toxicity shifts myocardial substrate preference to carbohydrates from free fatty acids; thus cardiac substrate delivery is impaired. Additionally, CCBs interfere with calcium-stimulated mitochondrial action and glucose catabolism; this results in lactate production and ATP hydrolysis contributing to acidosis.
All the above studies indicate, that drugs are not the solution. Actually, most drugs don’t benefit most of the patients who take them. Since we have no way of identifying those who will benefit, we are stuck treating the many to benefit the few. Its like buying a lottery ticket or buying insurance. Say, most of us pay for fire insurance for our homes, but not many houses burn down. We willingly pay premiums that may never benefit us because the cost of an uninsured disaster is so great. Paying premiums has no real harms apart from money spent while drugs inevitably have side effects.
The flaw of conventional approach to treatment is that the human body is seen as a car machine which can be repaired part by part. Whereas, the human body is a whole entity and should be treated in entirety. How else can one explain the side-effect of drugs used to treat one organ, affecting the other organs?
By the way, according to the research paper published in American Heart Association Journal (dated 9 March 2018) the mortality rate drops when the doctors are absent from the ICCU. This means the chances of survival of the heart patient increases because of the absence of doctors, responsible to take care of patient. Its shocking but true.
Researchers at Harvard Medical School found that when heart specialists are away at academic conferences, the survival rate at their hospitals actually improves. They believe that specialists who attend the meetings are more prone to using intensive interventions for their patients which may do more harm than good, rather than taking a more holistic approach.
P.S
The most recent update to the AHA hypertension guidelines refined how we classify hypertension. A systolic pressure between 120-129 and a diastolic above 80 is now classified as “elevated blood pressure.” A systolic pressure between 130-139 and diastolic 80-89 is now stage 1 hypertension, and a systolic greater than 140 or diastolic greater than 90 is now stage 2 hypertension.
Since people living with type 2 diabetes are at increased risk of heart disease, guidelines from the AHA and ACC recommend a blood pressure goal of 130/80. However, the ACCORD trial as well as a meta-analysis of randomized trials suggest aggressive treatment to this level does not reduce cardiovascular events but may increase significant adverse events. Thus, the latest recommendations from the American Diabetes Association set the target blood pressure for those with diabetes at 140/90.
The evidence supports that stage 1 hypertension and stage 2 in otherwise healthy individuals are best treated with lifestyle interventions.
High Blood Pressure in Middle Age Can Harm Your Brain
High blood pressure can begin to take a toll on memory and thinking skills as early as middle age, new Brazilian research warns.
And you won’t be spared simply by keeping high blood pressure at bay until you hit your golden years, because the study found that even those who hadn’t developed high blood pressure until becoming seniors still experienced a faster decline in thinking skills than those who continued to remain heart-healthy in their golden years.
“As a practical matter, this suggests that we must prevent hypertension at any age in order to avoid its deleterious effect on cognitive [thinking] decline,” said study author Dr. Sandhi Barreto, a professor of medicine at the Universidade Federal de Minas Gerais in Belo Horizonte, Brazil.
Whether or not high blood pressure directly triggers mental decline remains an open question, however, given that “proof of causation is very difficult,” said Barreto.
But even if it does, it’s not all bad news, she added, because the results also indicate that thinking skills can be preserved — or at least impairment slowed down — by getting high blood pressure under control through medication and lifestyle changes.
In the study, roughly 7,000 participants were drawn from six Brazilian cities and were about 59, on average, when they first enrolled in the study.
Blood pressure history was noted at the study’s launch. And during two testing periods — 2008/2010 and again in 2012/2014 — participants underwent repeated assessments (for an average of four years) designed to track changes in memory, language skills, concentration, attention, motor speed and mental “flexibility.”
The team ultimately found that middle-aged and senior participants whose top (systolic) blood pressure number and bottom (diastolic) number were deemed “high” experienced some form of accelerated decline in thinking skills, compared with those who maintained normal blood pressure readings.
Memory took a clear hit among all those with high blood pressure, whether initially diagnosed before or after the age of 55, as those folks saw their score on all tests of thinking skills collectively start to fall.
The speed with which thinking skills started to diminish seemed to have no relationship to how long a patient had been living with high blood pressure.
Yet there was an exception to the rule: Those who had brought their blood pressure down by taking meds or adopting helpful lifestyle choices experienced significantly slower decline in thinking skills than those who had not.
“Prevention of high blood pressure is always preferred,” stressed Barreto, but taking steps to address the issue once it takes hold can “avoid further damaging the cognitive function.”
There may, however, be a limit to how much lowering blood pressure can help preserve brain health, cautioned Dr. Gregg Fonarow, interim chief of the division of cardiology at the University of California, Los Angeles.
“Randomized clinical trials of systolic blood pressure reductions have produced mixed findings on whether lowering blood pressure can reduce the risk of mild cognitive impairment,” he noted.
For example, another recent study concluded that adults who brought their systolic high blood pressure back to normal range did not see their dementia risk fall compared to those with blood pressure as high as 139. They did, however, reduce their risk for mild cognitive impairment, Fonarow noted, but “further studies are needed regarding brain health and blood pressure.”
Meanwhile, getting high blood pressure under control is always a smart move, he said, given that it’s “been proven to lower the risk of heart attacks, heart failure, strokes and premature cardiovascular death.”
The findings were published Dec. 14 in the journal Hypertension.
Outdated High Blood Pressure Medications You Should Consider Upgrading
It’s natural for newer medications that work better and pose fewer risks to replace older ones. If you’re taking any of the following six outdated medications, it’s worth discussing with your doctor about a potential upgrade.
Atenolol
Except in cases of coronary artery disease (CAD) and heart failure, beta-blockers like atenolol are not used as first-line therapies to lower blood pressure. Even in these special cases, newer beta-blockers like bisoprolol (Zebeta), carvedilol (Coreg), and nebivolol (Bystolic) are preferred.
In general, atenolol doesn’t protect the heart as well as first-line blood pressure medications like ACE inhibitors and certain diuretics. (You can read more about these medications in my previous article here: Choosing Your Blood Pressure Medication.) Atenolol may also cause negative effects on blood sugar and cholesterol, which can increase your risk for diabetes and hyperlipidemia (or high levels of fat in the blood).
Furosemide (Lasix)
Like atenolol, furosemide (Lasix) is not a first-choice medication when it comes to lowering blood pressure, although the diuretic is useful for leg swelling as a result of heart failure. Instead, chlorthalidone is our currently preferred diuretic medication because it’s been proven to reduce heart disease risk and stays active for a long time. Hydrochlorothiazide (HCTZ) is another good diuretic choice, but again, chlorthalidone is preferred.
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Nifedipine (Adalat, Procardia)
Nifedipine (Adalat, Procardia) belongs to a class of drugs called calcium channel blockers, which lower blood pressure by relaxing the muscles of the heart and blood vessels. It was one of the most widely used medications to treat high blood pressure, but has since fallen out of favor because of concerns about safety and the fact that newer blood pressure medications with fewer risks have been developed. There are better options now.
Terazosin (Hytrin) and Prazosin (Minipress)
Terazosin (Hytrin) and prazosin (Minipress) are alpha-blocker medications that cause blood vessels to relax and dilate. They’re old-school drugs that were used to treat high blood pressure along with symptoms related to enlarged prostate (like difficulty urinating). If you’re only taking these medications for high blood pressure, make a change. They’re associated with low blood pressure when standing (aka orthostatic hypotension), which can result in fainting episodes.
Hydralazine (Apresoline)
Hydralazine (Apresoline) is known as a “direct-acting vasodilator”, which means it acts directly on blood vessels to relax and dilate them. Because hydralazine also causes salt and fluids to accumulate in blood vessels, it has to be used with a diuretic and beta-blocker to counteract the increased volume. There are very specific cases when hydralazine should be used, but not as a first- or even second-line treatment to lower blood pressure.
Clonidine (Catapres)
Unless you’ve tried several other medications and your doctor needs a last resort, stay away from clonidine (Catapres). Possible side effects include drowsiness, dry mouth, and slowed heart rate. Discontinuing clonidine treatment may result in rebound hypertension, which can make your blood pressure become dangerously high. For this reason, do not stop taking clonidine abruptly.
Time to upgrade…
Hepatic injury from calcium channel blockers
The calcium channel blockers act by blocking the influx of calcium ions into vascular smooth muscle and cardiac muscle cells during membrane depolarization. Because muscle contraction is largely dependent upon influx of calcium, its inhibition causes relaxation, particularly in arterial beds. Thus, the major effects of the calcium channel blockers are relaxation of vascular and arterial smooth muscle cells resulting in arterial vasodilation. The major use of the calcium channel blockers is for hypertension and angina pectoris (variant, exertional, and unstable). Some calcium channel blockers are also used for supraventricular arrhythmias and heart failure. Off label uses include migraine headaches. The major calcium channel blockers used in the United States include amlodipine, diltiazem, felodipine, isradipine, nicardipine, nifedipine, nimodipine, nisoldipine, and verapamil. While all affect the L type voltage gated calcium channel, the structure and site of interaction within the channel varies among the agents. Verapamil blocks the phenylalkylamine site and diltiazem the benzothiazepine site, while the remaining agents (exemplified by amlopidine and nifedipine) bind to the 1,4 dihydropyridine site. These agents are also commonly referred to as being first generation (verapamil, diltiazem, nifedipine) or second generation (amlopine, felodipine, isradipine, nicardipine, nimodipine and others) calcium channel blockers. Several of the calcium channel blockers are now available in generic forms and some are available as combinations with diuretics and lipid lowering agents.
Many of the calcium channel blockers have been linked to rare instances of idiosyncratic drug induced liver disease. Hepatic injury from calcium channel blockers is usually mild and reversible, but rare symptomatic and severe instances have been reported. Agents most clearly linked to liver injury are verapamil, diltiazem, amlodipine and nifedipine, probably because these agents have been most widely used. The pattern of injury varies somewhat among the different agents, so that the hepatic injury appears not to be a class effect or the result of inhibition of calcium channels, but rather due to hypersensitivity (verapamil) or metabolic injury that usually results in a mixed hepatocellular-cholestatic pattern (diltiazem, amlopidine, nifedipine). These four agents have different chemical structures and interact with different sites or different calcium channels, so that different patterns of idiosyncratic adverse events and different hepatic reactions might be expected. However, repeated instances of liver injury from different calcium channel blockers have been reported, so that switching from one calcium channel blocker that has caused liver injury to another in this class should be done with caution. Several of these agents can also cause minor elevations in serum aminotransferase levels that are often transient and resolve even with continuation of the agent or can be persistent, resolving only once the agent(s) are discontinued. Common, minor class specific side effects of the calcium channel blockers include headache, dizziness, flushing, nausea, fatigue, diarrhea, peripheral edema, palpitations, bradycardia and rash.