Blood Pressure Improvement

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THE GREAT BLOOD PRESSURE SCAM

Ever since I first encountered the medical field, something struck me as “off” about the relentless focus on blood pressure. I noticed that the blood pressures that relatives or friends shared with me varied immensely. As I was ponder­ing this, an Eastern spiritual teacher shared their belief that the West’s fixation on blood pressure was due to it being much easier to measure than blood perfusion (healthy blood flow).

Next, I began to notice a consistent pattern. Whenever a drug existed that could treat a number or statistic, as the years went by, the acceptable number kept on being narrowed, making more and more people eligible to take the drug. For example, once statins entered the market, the acceptable blood cholesterol levels kept on being lowered, and before long, almost everyone was told they would die from a heart attack unless they started a statin—despite the fact that statins have an almost non-existent mortality benefit and cause often severe side effects for roughly 20 percent of users. Broadly recommending these drugs hence appears unconscionable, but as I showed in my article titled “The Great Cholesterol Scam and the Dangers of Statins,”¹ these unjustifiable guidelines were a product of clever pharmaceutical marketing and targeted bribery of public officials.

In fact, many of the dogmas that underlie popular drugs are actually sales slogans cre­ated by a marketing company. I’ve previously discussed how a chemical imbalance from low serotonin was never linked to depression² (in fact, patients who commit suicide have elevated brain serotonin); acid reflux is due to too little acid in the stomach,³ though medical school teaches that it is due to too much acidity; and “sleeping” pills are sedatives that block the re­storative phase of the sleep cycle.⁴ Each of these drugs is immensely harmful, but due to how solidly these myths were established (just like “safe and effective”), large numbers of people continue to use them. In this article, I will show how something similar happened in the field of blood pressure (BP).

CONVENTIONAL BP PERSPECTIVES

For a long time, I wondered whether rising blood pressure damages arteries—or instead, whether damage to the circulation raises blood pressure. Once the outflow from the heart gets obstructed (for example, through aortic stenosis), the heart’s left ventricle is known to become enlarged (this is called left ventricular hypertrophy or LVH), yet we typically ascribe the hypertension associated with LVH to being the cause of it rather than a result of it. Simi­larly, if the blood flow through the lungs gets obstructed (due to pulmonary hypertension), the right heart ventricle enlarges (called right ventricular hypertrophy or RVH) and eventually fails. In certain cases, this hypertension can be immediately reversed—for example, if it’s be­ing caused by chronic blood clots entering the lungs—at which point the heart immediately recovers. Another observation is that significant plaque within the artery that feeds the kidney raises blood pressure; if the kidney’s blood flow is restored, the blood pressure immediately drops.

Because blood vessels are elastic structures filled with fluid, that fluid holds them under pressure. Blood pressure, in turn, is typically measured by determining how much external force is needed to exceed the artery’s pressure and compress it so that blood no longer flows through it. Low blood pressure (hypotension) is a problem because it prevents blood from reach­ing the areas where it’s needed; for example, orthostatic hypotension or postural orthostatic tachycardia syndrome (POTS) describe a com­mon situation where people become lightheaded as they stand up due to insufficient blood being pushed into the brain. In most cases, though, medicine chooses to focus on the consequences of high blood pressure.

Within the existing model, one of the conse­quences of high blood pressure is that weakened blood vessels become more likely to break open and leak as higher blood pressure pushes against them. This is why emergency departments ag­gressively lower the blood pressure of patients who show up with symptoms of “hypertensive emergency” (such as a severe headache and a significantly elevated blood pressure). Likewise, whenever a critical blood vessel ruptures (such as the aorta or one in the brain), once the bleed has been confirmed, the first step in managing it is to lower the patient’s blood pressure so less blood leaks out, after which they are sent to surgery. Other consequences of high blood pressure—according to the conventional mod­el—include excessive pressure on the arteries (which strains and damages them, causing the lining of the vessels to become damaged and gradually develop atherosclerosis) and damage to the internal organs (“end-organ damage”), leading to premature failure and early death (for example, from a heart attack or kidney failure).

Because of these situations, high blood pressure is viewed as one of the greatest prevent­able causes of cardiovascular disease. Thus, a chief focus of all medical visits is ensuring that a patient achieves a sufficiently lowered blood pressure. Unfortunately, the chain of logic has quite a few gaps in it.

BLOOD PRESSURE VARIABILITY

Blood pressure is immensely variable. Pres­sures at the periphery (where BP is typically measured) have been found to vary by around 14 points.⁵ This frequently leads to individuals being erroneously diagnosed with hypertension and given a prescription for blood-pressure-lowering medications despite having normal blood pressures; those medications can then make them hypotensive. This phenomenon is so common (constituting 15 to 30 percent of hypertension diagnoses) that it is often referred to as “white-coat hypertension.”⁶ That name is derived from the fact that stress commonly el­evates blood pressure; because visiting a doctor can be stressful, many patients have temporarily elevated blood pressures in the doctor’s office. The guidelines suggest the need for multiple measurements to confirm a hypertension diag­nosis (for example, with home blood pressure monitoring), but unfortunately, this often does not happen in practice.

There are other common sources of error when measuring blood pressure. One is using the wrong-sized cuff, and another is that patients frequently have significantly different blood pressures in each arm.⁷ This helps to explain why it is estimated that 25 percent of those diagnosed with hypertension do not have it.⁸

Likewise, there is a surprisingly poor cor­relation between peripheral blood pressure and the central blood pressure inside the aorta. One large study found a significant difference between the blood pressure within the aorta and the arm, and the central aortic pressure had a much stronger correlation to the likelihood of cardiovascular disease.⁹ It should also be noted that different classes of blood pressure medi­cations have very different effects on central versus peripheral blood pressure.

WHAT AFFECTS BLOOD PRESSURE?

If fluid at a set pressure tries to move through a tube, as the tube shrinks, the pres­sure it creates (for example, on the walls of the tube) will increase, while if the tube enlarges, the pressure it exerts will decrease. The body, in turn, continually controls where blood in the body goes by changing the heart rate and fully or partially constricting the arteries, allowing it to shunt blood to where it is most needed (such as by dilating arteries in that area).

Blood pressure is thus a product of two fac­tors: the amount of blood in the arteries and the constriction or relaxation of the arteries contain­ing it. Arterial BP is greater than venous BP and is what is measured externally; veins compress long before arteries do, and only arterial blood has a signature pulsatile wave created by the heartbeat. Because each beat of the heart pushes blood into the arteries and hence increases the pressure within them, two different blood pressure values exist—the baseline pressure (diastolic blood pressure or DBP) and the pressure when the heart contracts (systolic blood pressure or SBP) (Figure 1). The blood pressure values you see (such as 140/90) represent that maximum and minimum (the systolic over the diastolic). One reason why this stretching is important is because when the vessels contract back to their normal size once the systolic pressure fades, that recoil pushes blood further along into the circulation.

WHAT CAUSES HIGH BLOOD PRESSURE?

Most cases of high blood pressure (90 to 95 percent10) are known as “essential” or “primary” hypertension, which is a fancy (and rarely ques­tioned) way of saying “elevated blood pressure without a known cause.” The belief that there is no known cause for most cases of elevated blood pressure has been widespread in medicine for decades. For the remaining 5 to 10 percent of cases (“secondary” hypertension), recognized causes include reduced blood flow to the kidneys¹¹ (which sets off a signal to raise the blood pressure because the kidney believes there isn’t enough blood perfusion), sleep apnea¹² or having a rare tumor,¹³ which dumps large amounts of adrenaline into the blood, thereby constricting blood vessels and increasing the heart rate.

Note that a kidney (especially the left) being in the wrong position— which is quite common—can functionally compress the renal artery. However, until there is an actual stenosis (narrowing) of the artery, this can be quite difficult to identify with conventional measurements. Ad­ditionally, poor sleep is immensely damaging to cardiovascular health, and those effects extend to blood pressure.⁴ In one study, a single night of partial sleep deprivation raised SBP by 6 and DBP by 3.¹⁴ Another study found that a night of sleep loss raised SBP by 4.5 and DBP by 2.6, and functional magnetic resonance imaging (fMRI) showed that sleep loss also impaired the brain’s control of blood vessel function.¹⁵

Because the causes of most cases of hypertension aren’t known, medicine focuses on specific “risk factors” that are known to be associated with it, such as being over age sixty-five, having diabetes, insomnia, obesity, not exercising, stress, being an alcoholic, having other people in your family who have high blood pressure or “eating too much salt.” The latter is the one we tend to hear most about, despite the fact that the most detailed review of this subject showed that drastic salt reduction typically results in less than a 1 percent reduction in blood pressure.¹⁶ I and many of my colleagues believe that one of the most underappreciated causes of hypertension is anxiety; frequently, effectively addressing anxiety can resolve a case of high blood pressure, which would otherwise receive pharmacologic treatment, often indefinitely.

ATHEROSCLEROSIS AND BP

Many of us initially became suspicious of the existing blood pressure paradigm because we noticed that circulatory impairments would proceed or occur in tandem with elevating blood pressures, rather than happening long after an elevated blood pressure had had time to dam­age the arteries. Each of us came to a similar conclusion—the increased blood pressure must be a compensatory mechanism the body is using to counteract the fact that it can’t get enough blood to where it is needed (which, again, is recognized to occur with the kidneys).

I found a few ways to explain how this could be happening. First, if you consider the illustration of the circulatory cycle (Figure 1), it should be clear why calcification of the arter­ies (which stiffens them) also increases blood pressure, as they can no longer expand as ef­fectively and release the pressure within them. However, there are also three other reasons why this could occur.

First, measuring blood pressure utilizes an external cuff to pressurize the arteries until the blood flow cuts off. If the artery has stiffened, that is much harder to do. When patients have severe atherosclerosis, their blood pressure is no longer measured in the arm’s arteries, as those arteries won’t compress from the cuff.¹⁷ At the same time, however, there is most likely a gradual stiffening that leads to the measured blood pressure being higher than it actually is.

Second, the health of the cardiovascular system depends to a large extent on the lining of the blood vessels being able to secrete nitric oxide, which in turn dilates the blood vessels, locally decreasing blood pressure and regionally increasing blood flow. Defective production or activity of nitric oxide (endothelial dysfunction) typically precedes the development of athero­sclerotic plaques¹⁸ and is much more severe by the time they’ve formed, as the surface of the endothelium has calcified at that point. For this reason, many believe the core issue is not cal­cification of the arteries or high blood pressure but rather endothelial dysfunction, which in turn leads to abnormal growth of the endothelium and formation of harmful blood clots. Given that endothelial dysfunction happens to increase blood pressure, that again argues that the direction of causality for heart disease is incorrect.

Third, whenever the body is not getting enough blood, a sympathetic reflex will be triggered to increase the BP. For example, this is commonly seen in critically ill patients or those who have rapidly lost a significant amount of blood,¹⁹ at which point the blood vessels will tighten and the heart rate will increase.

BLOOD SLUDGING

Approximately a century ago, many Western researchers argued that blood cells clumping together—a condition that came to be known as “blood sludging”—was a root cause of many illnesses, particularly where a focal issue (such as burns or cancers) created a systemic problem. This theory became quite influential, especially once it was possible to directly observe the phenomenon by using the appropriate microscope to look at the blood vessels in the eyes. Sadly, the concept of blood sludging has largely been forgotten and persists today only through live blood cell analysis, which is not only widely disparaged by conventional medicine but is significantly more error-prone than the original method of looking into the eyes.

When I learned of the blood sludging concept, I immediately won­dered whether it underlies high blood pressure. My reasoning was that if blood were to sludge together, it would (1) create a backlog in the circula­tion, which would increase the pressure on it (rather than being pushed forward, blood would instead push against the arterial walls); (2) signal the body to increase its blood pressure so that the pockets of sludged blood could be pushed along; and (3) directly stretch the smaller blood vessels, thereby increasing their pressure. It would also simultaneously “stiffen” the arteries because the clumps of sludge would have significantly more resistance to compression than dispersed blood cells.

I learned that the original pioneers of blood sludging had repeatedly observed that small arteries (namely, those in the eyes) would become stretched by larger sludges (see Figure 2). Additionally, they observed that once the pockets of sludge formed, the pressure build-up caused plasma (the non-cellular component of the blood) to begin leaking out into the tissues, leading to things like edema; the remaining blood thus became even more concentrated with these sludge pockets.

In a 1949 paper on the topic of sludged blood, the researchers looked at one hundred individuals with a SBP above 150.²⁰ In 50 per­cent of these individuals, they found Grade 1 clumping of red blood cells (they defined these as “fine granularities. . . which are rather uni­form and not too upsetting to flow rates”), Grade 2 clumping in 45 percent (“definite clumping which tends to hold together in larger collecting veins”), Grade 3 in 4 percent (“large agglutina­tions which completely block out normal flow”) and, in 1 percent, Grade 4 (“almost complete clumping of erythrocytes, which suggests the appearance of ’sludge’”). Of fifty normal adult controls, only one individual (2 percent) dis­played any intravascular pathology at all, rated as Grade 1. I have not been able to locate three additional papers cited by the primary authors in this field,²¹ which apparently show a relation­ship between blood sludging and blood pressure.

Given the observation that blood sludging disproportionately affects the smaller vessels (because it takes significantly smaller sludges to obstruct them), the primary effect of blood sludging would be injuries akin to microstrokes. However, because the larger blood vessels have their own small blood vessels (the vasa vasorum, which sustain the arteries), the early generation of researchers frequently observed blood sludging to obstruct the vasa vasorum in an identical manner to what happened in smaller sludged vessels. As clearly shown in a now-forgotten 1947 paper,²² once the blood supply in a vessel’s vasa vasorum is impaired, it causes the endothelial lining of the blood vessel to rapidly die and fall off, with total damage in proportion to how much the blood supply is interrupted and how long that interruption persists. Once this happens, those lost cells can no longer release the critical nitric oxide; as a result, clots frequently form, and the blood vessel is no longer protected from damage (as the endothelial cells create the primary protective layer of the blood vessels).

In the early 1960s, the engineer Thomas Riddick (1907–1975) helped popularize the con­cept of “zeta potential,”²³ a theory of coagulation and dispersion measured as the electrical charge difference between a colloidal particle and its surroundings. (Colloidal particles are small particles ranging in size from nanometers to mi­crons, dispersed in fluid.²⁴) A high zeta potential confers stability to colloidal systems, whereas conversely, colloids with low zeta potentials tend to coagulate. Vaccines—including the Covid shots and also the aluminum that many so-called “traditional” vaccines contain—are significant factors impairing zeta potential.²⁵

Riddick strongly believed that poor zeta potential increased blood pressure and likewise led to atherosclerosis. In fact, the findings of the blood sludging research pioneers suggest that poor zeta potential is a primary cause of arterial damage (and the inability of vessels to then repair themselves) and the lethal clots that damaged endothelium can form. Riddick and those who followed him frequently treated a variety of heart conditions by restoring the physiologic zeta potential.²⁶

Addressing the sludging phenomenon, Rid­dick observed:

“[I]t should be realized that each mobile agglomerate must be broken down into smaller sized particles as it flows along the arterial tree. The blood cells must eventually become completely discrete if they are to pass through the capillaries, whose small diameter permits the cells to pass only in single file. Considerable energy must be required to continuously break down these clumps ahead of each capillary—and then reform them past the capillary. Small wonder the workload of the myocardium is increased and blood pressure raised.”

Many holistic therapists have determined that impaired zeta potential and deformed red blood cells correlate with poor health. When research­ers in 2019 compared the zeta potential of four groups—hypertension patients, myocardial infarction (MI) patients, treated MI patients and healthy controls—they found “significantly reduced” zeta potentials in the first three groups compared to the controls.²⁷ Likewise, when they looked at study participants’ blood, they found significantly greater clumping, blood cell deformation and membrane fragility in cells from patients with cardiovascular disease (Figures 3 and 4, next page).

DOES HIGH BP ACTUALLY CAUSE HEART DISEASE?

Several observations originally led researchers to hypothesize that high blood pressure might be the cause of heart disease. First, high blood pressure has been observed to occur in association with heart disease. Second, significant vascular issues such as severe headaches, strokes and organ damage can occur when blood pressure is significantly elevated (such as, an SBP above 200) and improve once the blood pressure is rapidly lowered. Third, blood vessel damage never occurs in low-pressure areas of the body but does occur when blood vessels are suddenly transitioned to much higher pressures than normal, such as a vein being grafted onto the heart or the blood pressure suddenly being greatly elevated in the lungs.

Unfortunately for the “high blood pressure causes heart disease” hypothesis, there’s actually very little evidence that smaller elevations in blood pressure create issues. (Note: I obtained much of the research for this section from Scottish doctor Malcolm Kendrick.²⁸) Much of the current dogma is based on the long-standing Framingham Heart Study,²⁹ which “found” a linear relationship between blood pressure and the risk of death—meaning that continually lowering blood pressure decreases one’s risk of dying. That has been the basis for continual recommendations for lower and lower blood pressures (though the National Institutes of Health [NIH] also admits that an SBP below 90 is dangerous and unhealthy³⁰) as well as for a highly erroneous cardiovascular disease risk calculator later found to overestimate one’s risk of dying by 500 percent.³¹

Major problems with the paradigm include the following:

• It creates a situation where no optimal blood pressure can exist. (As Dr. Kendrick puts it in a blog titled “You absolutely cannot be healthy any more—it’s official,” “[W]e have reached a situ­ation whereby a [SBP] lower than 90mmHg increases risk; and a blood pressure higher than 90mmHg increases risk. I suppose you could say that anyone with a blood pressure of exactly 90mmHg is healthy, so the land of health still exists as a microscopically thin sliver of habitable area. But for all intents and purposes, health has gone.”³²)
• It’s exceedingly rare that things in biol­ogy follow a completely linear relation­ship.
• No one has ever done a study demon­strating that lowering blood pressure from 100 to 90 provides a benefit. Rather benefit is assumed from the linear model’s prediction.

Moreover, the original analysis of the Framingham study was flawed. Reanalysis of the data in 2000 instead found a relationship that was much more congruent with what’s typically seen in nature.³³ Specifically, rather than being a linear relationship, blood pressure had relatively little impact on mortality until a critical threshold was passed (going above 70 to 80 percent of the normal blood pressure for the person’s age and gender), at which point there was an exponential rise in their risk of death. A large number of people are diagnosed as having dangerous hypertension in the linear model but not in the more accurate threshold model.

The 2000 paper was mostly ignored. However, as quoted by Dr. Kendrick, it eventually received this response from the National Heart, Lung, and Blood Institute (NHLBI), illustrating how resistant medical dogmas are to evidence that refutes them: “After careful review of this study, the NHLBI finds that it does not offer a basis for changing the current hypertension guidelines.”³²

Recent research with more modern technologies has led to the same conclusions. A 2020 study of over four hundred thousand elderly patients above age seventy-five, obtained through their electronic health records, again showed that rather than being linear, an age-dependent threshold exists that is not recognized by the guidelines.³⁴ An SBP below 130 significantly increased the chance of death, and a DBP below 80 (a common consequence of blood pressure medications) made patients 8 to 19 percent more likely to die. A smaller study of eight hundred adults over age sixty found that a DBP below 80 made participants 90 to 190 percent more likely to die and, once again, an SBP under 120 was associated with a higher risk of death.³⁵

DOES LOWERING BP ACTUALLY IMPROVE SURVIVAL?

Given the hype around blood pressure, you would assume it had been clearly proven that lowering blood pressure improves survival. As best as I can tell, those studies don’t exist. In­stead, a universal assumption exists that lower­ing blood pressure is good; a related assumption is that if a drug can lower blood pressure, it must be good and should be approved. This may help to explain why there has been such a strong fo­cus on the theoretical benefit of lowering blood pressure versus actually proving a benefit exists.

One of the most pivotal studies began in 1973. With no studies offering proof that lowering a moderately elevated blood pressure reduced one’s chance of dying, researchers in the United Kingdom undertook a massive, decade-long, public study.³⁶ Ultimately, the study recruited over seventeen thousand patients between ages thirty-five and sixty-four who had blood pressures below 200 (averaging 158/98 in men and 166/99 in women) and randomly allocated them to take either a beta blocker, a thiazide diuretic or a placebo.

The study showed that treating high blood pressure made no real difference in the likeli­hood of a coronary event such as a heart attack (the rate went from 5.5 to 5.2 per thousand patient-years), and likewise, almost no difference in the death rate (two hundred fifty-three versus two hundred forty-eight deaths—or a 0.06 percent reduced chance of dying).³⁶ The study did show that lowering blood pressure made someone less likely to experience a stroke (probably hemorrhagic), as there were eighteen fatal and forty-two non-fatal strokes in the treatment groups versus twenty-seven fatal and eighty-two non-fatal in the placebo group; this led to a small overall reduction in those strokes (roughly one stroke delayed for around nine hundred years of treatment). On the other hand, roughly 25 percent of trial participants experienced side effects significant enough for them to withdraw from the study.

After this trial, the term “heart disease” was abandoned in favor of “cardiovascular disease.” This made it possible to create the perception that treating blood pressure stopped heart attacks while simultaneously concealing the actual benefit—a small reduction in vascular strokes. (In an April 2024 article, I described the use of the “skin cancer” label as another example of linguistic trickery.³⁷)

By 2009, a Cochrane review (considered the gold standard for evalu­ating scientific evidence) was reporting very little benefit from lowering SBP below 135 compared to having it below 140; this benefit, moreover, was likely outweighed by the margin of error created by unclear data and significant side effects in the trials.³⁸ A 2020 Cochrane review reconfirmed these results, again finding that the negligible benefit from aggressive blood-pressure-lowering targets was outweighed by the harms those drugs created.³⁹ Both reviews found a small increase in kidney disease (e.g., acute injuries or chronic kidney disease), which makes sense because the kidneys are damaged by insufficient blood reaching them; kidney disease creates heart disease and raises blood pressure.

MARCHING TOWARD MEDICATION

When the blood pressure craze took off, there was a rush to bring blood-pressure-lowering drugs to market before actual proof of their benefit (outside of a few short-term studies, which showed a small benefit for people with very high blood pressures). That mindset contin­ues to define this field. As the years have gone by, the blood pressure thresholds keep getting lowered without supporting evidence, and more people are put on medication—roughly sixty million American adults.⁴⁰ Originally, the focus was on treating DBP under the belief that the heart had to “work harder” if there was too much blood in the circulation; that this was believed for decades—but now is not—illustrates how arbitrary many medical dogmas are.

Because less elevated blood pressures are more common than the higher ones, each time the treatment target is lowered by a small amount, it results in a large number of people getting started on the drugs. Unfortunately, this is especially the case for the elderly, whose blood pressure rises to compensate for the decreased health of their arterial system; due to their calcified arteries, they have the least ability to tolerate insufficient blood pressure and simultaneously are the most likely to have elevated blood pressure.

In 2017, the American Heart Association and American College of Cardiology reformu­lated their guidelines, setting 130 (rather than 140) as the “new high” for SBP, eliminating a prior category of “prehypertension.”⁴¹ To quote the 2017 guidelines:

“Rather than 1 in 3 U.S. adults having high blood pressure (32 percent) with the previous definition, the new guidelines will result in nearly half of the U.S. adult population (46 percent) having high blood pressure, or hypertension.”

According to the revised guidelines, 79 percent of men and 85 percent of women over age seventy-five now have hypertension, and 71 and 78 percent of men and women in that age group, respectively, meet the threshold to start blood pressure medications.⁴²

What factors can explain this inexorable march toward putting every­one on these drugs? My best guess is that it is due to some combination of the following:

• Research funding is available for these areas (that is, from the drug manufacturers), meaning that it is a safe area for academics to explore.
• It illustrates the “if you have a hammer, everything looks like a nail” phenomenon and the medical profession’s desire to find more justifications for using its tools.
• “Experts” on guideline panels are paid to create recommenda­tions that result in more people taking the drugs. (In my article on “the great cholesterol scam,” I conclusively showed how this happened with statins1.)

SECONDARY EFFECTS OF HYPERTENSIVE MEDICATIONS

In many cases, the actual mechanism of a drug greatly differs from the purported one. For example, statins are sold on the basis of the claim that cholesterol causes heart disease and that they lower cholesterol. However, as I have shown, there is very little evidence that cholesterol causes heart disease, and more importantly, prior to statins hitting the market, there was no mortality benefit shown from other cholesterol-lowering medications.¹

Presently, four main types of antihypertensive drugs exist: diuretics (the oldest); beta-blockers; calcium channel blockers; and ACE inhibitors and related medications. Each drug works in a different manner, either by loosening the arterial walls, reducing the total blood in circulation or weakening the contraction of the heart (or a combination of all three), with very different degrees of benefits seen from their use despite them creating the same drop in blood pressure. This strongly argues that their effects are not due to lowering blood pressure but rather to how each one specifically affects the body.

A 1997 paper in JAMA reviewed the literature and found significantly different benefits from antihypertensive drugs, depending on which type was used.⁴³ To illustrate:

• A 1998 review found that the (known) cardiovascular benefits of ACE inhibitors were not seen with calcium channel block­ers, despite the latter having a more significant effect on blood pressure.⁴⁴
• A 2000 study of almost thirty-six hundred diabetics found that a specific ACE inhibitor, despite minimally reducing blood pressure (a 2.4 reduction in SBP and 1.0 reduction in DBP), had a massive effect (a 25 percent reduction) on the risk of a heart attack, stroke or cardiovascular death.⁴⁵
• An eight-year-long double-blind study published in 2007 and funded by NIH, involving over forty-two thousand subjects, found that when two different types of blood pressure medications were used, there was no differ­ence in their effect on blood pressure; however, their rate of preventing heart failure varied by 18 to 80 percent, depending on the drug, leading the in­vestigators to conclude, “blood pressure reduction is an inadequate surrogate marker for health benefits in hyperten­sion.”⁴⁶

HYPERTENSIVE MEDICATION HARMS

The typical management of blood pressure involves using a combination of drugs until they collectively achieve the desired blood pressure and simultaneously switching out drugs that cause more side effects than the patient can tolerate. This is a problem because, as just discussed, the drugs have very different effects on the body. On one hand, this is a good thing because it allows each of them to exert unique therapeutic benefits independent of their effect on blood pressure, but on the other hand, it means they each have unique side effects (see sidebar below). Each should be considered on the basis of whether their individual effects are appropriate for the individual patient’s situation, rather than whatever achieves the desired blood pressure—but as that would get in the way of drug sales, it never happens.

Typically, the most common side effect of blood pressure medications are complications of poor perfusion. For example, BP medications increase the risk of fainting by 28 percent47 and are notorious for causing older individuals (who have calcified arteries and hence difficulty get­ting blood to the brain) to become lightheaded and then suffer potentially devastating falls. Three of the more troubling side effects are an 18 percent increased risk of acute kidney injuries (affecting 1.5 percent of users); a 103 percent increased risk of hyperkalemia (high potassium), which can be quite dangerous and affects 4.8 percent of users; and a 19 percent increase in the risk of lung cancer.^47,48 (A 2022 study provides a more detailed summary of the rates of side effects from these drugs.⁴⁹)

To illustrate the problem with falls, a 2014 JAMA study of almost five thousand hyperten­sive adults over age seventy monitored three groups for three years: 14.1 percent received no antihypertensive medications, 54.6 percent were on moderate-intensity medical therapy and 31.3 percent were on high-intensity medical therapy.⁵⁰ Over the three-year period, 9 percent experienced falls, and 16.9 percent died. Those in the moderate-intensity treatment group were 40 percent more likely to have a fall that caused a serious injury, and 117 percent more likely to have a serious fall if they had a previous fall his­tory. The high-intensity group was 131 percent more likely to have a serious fall (which begs the question of why they were still on those drugs). The authors unfortunately did not report the rate of death between the groups but did find that calcium channel blockers had the highest rate of causing falls.

In 2007, an important Israeli study (titled “The war against polypharmacy”) found that discontinuing an average of 2.8 drugs per elderly patient reduced their one-year death rate from 45 to 21 percent and their hospitalization rate from 30 to 11.8 percent.⁵¹ The study did not provide specific data, but I am fairly sure that a signifi­cant degree of the benefit came from removing the antihypertensives that have become a core principle in geriatrics.

Emergency medicine recognizes that it is unwise to aggressively treat blood pressure in the emergency department (ED); the risk is that it will cause an ischemic stroke in the brain due to insufficient blood flow in the brain. It is worth quoting a review paper on this subject. Noting that “the majority of IV medications given to achieve immediate BP reduction in the ED are done so inappropriately,” the authors state:

“There are no evidence-based thresholds at which asymptomatic but markedly elevated BP in the ED benefits from immediate reduction. . . . [R]apid BP reduction can cause significant harm by impairing cere­bral blood flow, and it has not been shown to improve clinical outcomes except in hypertensive emergencies.”⁵²

Many serious diseases result from low blood pressure, especially in the organs most sensitive to a loss of blood flow. Low blood pressure is strongly linked to cognitive decline (the brain needs adequate blood to function).⁵³ Likewise, as you lower blood pressure, the kidneys start to struggle as they, too, require sufficient blood flow to function. As we already saw, hypertension drugs increase the risk of an acute renal injury by 18 percent.⁴⁷ In patients who had end-stage renal disease, those with blood pressures below 130 were 38.9 percent more likely to die compared to those with blood pressures between 130 and 149.⁵⁴

When one’s blood pressure is below 90, it is diagnosed as “hypotension.” Critical care medicine views blood pressures below 90 as dangerous because organs do not get enough blood.⁵⁵ The most common symptoms of hypotension are lightheadedness or dizziness. Other common symptoms include fainting (when it gets lower), blurry vision, confusion, nausea or vomiting, sleepiness, fatigue and weakness. Given the high inaccuracy of blood pressure measurements and the fact that patients often are put on excessive hypertensive medications (especially as they age and the body is less able to handle low blood pressures), these symptoms affect many blood pressure medication users to varying degrees. Stated another way, blood pressure medications can increase one’s risk of developing hypotension.

UNDERRECOGNITION OF SIDE EFFECTS

The concerning data I have presented about side effects probably underestimate the actual rate of side effects because much of the data comes from industry clinical trials that deliberately find ways to downplay their drug’s side effects. Independent patient surveys likely provide a far better perspective on the rate of symptomatic side effects. Consider, for example, a Swedish survey published in 2000, which found that roughly one in five users experienced side effects.⁵⁶

Because of side effects, patients frequently stop taking antihypertensives. In a large study of three hundred seventy thousand patients under age sixty-five conducted between 2007–2014, almost one in four participants (23.5 percent) stopped taking the drugs within roughly nine months of starting them, while 40.2 percent who continued taking them often skipped the medications.⁵⁷ Large studies have found that patients are least likely to stop using ACE in­hibitors (and the related angiotensin II receptor blockers or ARBs) and are most likely to stop using diuretics and especially beta blockers.⁵⁸ This is congruent with the rate of side effects we observe in practice.

Given such high discontinuation rates, it is surprising how little awareness exists regarding blood pressure drugs’ side effects, especially among doctors. (The article I just cited acknowl­edged side effects as a reason for discontinua­tion but insisted it was due to patient ignorance about the importance of the drugs.) This was illustrated in a 1982 study—which would not be repeated in today’s political climate—that compared how patients, their families and their doctors felt about the effects of these drugs.⁵⁹ Forty-eight percent of patients were taking beta blockers, 25 percent beta blockers plus diuretics and 12 percent diuretics only. When asked whether quality of life had improved, stayed the same or become worse on the blood-pressure-lowering drugs, 100 percent of doctors answered “improved” versus less than half (48 percent) of patients; meanwhile, 99 percent of relatives assessed their loved one’s quality of life as worse, and 9 percent of patients agreed with that assessment. Most relatives characterized the worsening as moderate (45 percent) or severe (30 percent), with commonly cited deterioration including an undue preoccupation with sickness, irritability and a decline in energy or general or sexual activity.

THE MATTER OF SALT

Patients diagnosed with high blood pressure are frequently advised to undertake aggressive salt lowering. I do not support this approach because significant salt reduction has almost no effect on blood pressure. Furthermore, many people don’t consider that hospital patients are routinely given large amounts of IV sodium chloride—receiving up to ten times the daily recommended sodium chloride—but their blood pressure does not rise.

Low sodium levels are strongly correlated with a risk of dying. Specifically, the salt consumption target we are told to follow increases one’s risk of dying by 25 percent.⁶⁰ A common reason for hospital admis­sions are symptoms resulting from low sodium levels; 15 to 20 percent of hospitalized patients have low sodium levels at admission.⁶¹ I presently believe many of the associations between salt and heart conditions are due to the effects on the zeta potential of the aluminum often contained in processed salt as a desiccant; this is something not found in natural salt products or in IV saline given at hospitals. Conversely, I believe many of the benefits from hospital care are a result of IV fluids being routinely given as they somewhat restore the physiologic zeta potential.²⁶

TREATING HYPERTENSION

Physicians I know who have reached conclusions similar to mine about the current hypertension paradigm’s flaws are much more conser­vative about when to directly treat blood pressure. They tend to focus on reversing the causes of high blood pressure rather than trying to treat it with medications. Nonetheless, there are still cases where treating hypertension has merit.

Given the probably pivotal role of poor zeta potential in hypertension, it makes sense that providing zeta aid²⁶ often causes a dramatic improve­ment in a person’s blood pressure. More potassium in the diet—partially switching from sodium chloride (NaCl) to potassium chloride (KCl) when salting foods—can also be helpful. A major problem with the war against sodium is that it ignores the vital importance of sufficient chloride.

If we view much of hypertension as being a disease of the arteries, there are a few different ways to restore their pliability and health. First, weakened and inflexible blood vessels can be the result of nutritional deficiencies—most commonly, not enough manganese or zinc; in both cases, we use Standard Process formulations (Manganese B12 taken every other day or Zinc Chelate taken daily) to effectively strengthen the blood vessels. In many other cases, the issue is a magnesium defi­ciency; magnesium allows blood vessels to relax, which makes it one of the most well-known natural blood pressure therapies. We often use the micronutrient test panel by SpectraCell Laboratories to identify these nutritional deficiencies.⁶²

Second, certain regions of the body are very sensitive to poor blood flow, and in some cases, this results not from an issue within the vessel but rather from an external compression. As already mentioned, a kid­ney being out of place and thus constricting a renal artery causes high blood pressure; moving it back into its correct position normalizes blood pressure. I know visceral body workers who have had success with this approach for hypertension, and it is specifically detailed in the primary textbook on the subject, Visceral Manipulation.⁶³ Carotid arteries can also have structural issues because they contain the baroceptors that monitor blood pressure.⁶⁴

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BLOOD PRESSURE LOWERING IN OLDER PATIENTS? NOT SUCH A GOOD IDEA?

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Third, I strongly support the hypothesis that damage to the arteries (which then causes clots to form) is the root cause of cardiovascular dis­ease.¹ If inflammation is a primary source of arterial damage, it makes sense to focus on doing whatever we can to reduce it, such as eliminating chronic infections or addressing inflammatory components of the diet.

Fourth, addressing any anxiety or excessive stress component of the condition can provide dramatic benefits. Although the approach will necessarily be patient-specific, in many cases, simple relaxation exercises (such as deep abdominal breathing through the nose) can help increase parasympathetic tone and relax the nervous system.

In most non-severe cases, simple lifestyle measures will eliminate high blood pressure and also address many of the underlying problems giving rise to heart disease in the first place. Such measures include getting out in the sun, fixing one’s sleep cycle,⁴ exercising, regularly practicing a relaxation technique and cleaning up the diet to reduce insulin resistance and high blood sugar and increase potassium and magnesium. Improving one will also often improve the others.

Other things we sometimes use to treat blood pressure (or to inadvertently treat blood pressure when using them for another condi­tion)1 include:

• Enhanced external counter pulsation (EECP) therapy: This is a method of rhythmically increasing the return of blood to the heart, which results in new blood vessels forming, the functions of organs such as the heart, brain and kidneys significantly improving and the blood vessels being much more able to do their normal func­tions (e.g., vasodilate). We often observe that EECP improves BP. However, in patients who have significant vascular compromise, EECP initially needs to be very gentle; otherwise, patients can’t tolerate it.
• EDTA chelation therapy: This approach repairs arteries (by re­moving calcification) and improves the physiologic zeta potential. Caveat: it should be an aluminum-free form and a low dose.²⁶
• Ultraviolet blood irradiation (UVBI): As I have discussed else­where,⁶⁵ UVBI often provides immense benefits to the cardio­vascular system and may significantly reduce blood pressure.

CASE BY CASE—NOT “ONE SIZE FITS ALL”

A continual topic of debate has to do with the threshold at which blood pressure management should be started. We all agree that “exces­sively high” blood pressure should be treated, but exactly what constitutes that threshold varies greatly from patient to patient. There are no clear thresholds to indicate which patients need something to be done about their blood pressure and which don’t. For example, if someone in their twenties has a blood pressure over 160, we probably would view that as an issue that needs to be addressed for their long-term health, whereas in an older patient, we would leave that same pressure alone.

Most often, finding the cause or using a natural method will be enough, but if patients are not willing to make the lifestyle changes, a third option is medication. When blood pressure medications are used, there are a few general rules. First, view blood pressure medications as adjunctive treatments rather than the primary strategy. Second, start with a lower dose. Third, evaluate one drug at a time to see how the pa­tient responds rather than stacking numerous ones on to lower the blood pressure incrementally. (Typically, ACE inhibitors are the best tolerated, but some patients still have issues with them.) In addition, the specific medication needs to be matched to the patient’s situation. For example, while I dislike beta blockers, for a younger “type A” individual who is burning their body out with excessive stress and overexertion, beta blockers do help. Likewise, some patients will have a specific medical illness that requires a specific antihypertensive (such as a calcium channel blocker for a heart arrhythmia), and that drug can also be used as their hypertension medication.

A good case can be made that phosphodiesterase (PDE) inhibitors are the safest and most effective blood pressure medications because they work by increasing nitric oxide. However, there are also issues with those drugs, so a lot of thought needs to go into their use. This class of drugs originally was developed to lower blood pressure but then was shunted to erectile dysfunction (a much more lucrative market). Most doctors will not be familiar with this application because they aren’t typically used to treat blood pressure.

CONCLUSION

Given that measuring and documenting blood pressure is one of the most routine pro­cedures administered during a medical visit, the perspective shared in this article may seem like a controversial position to take. I’ve done my best to present the evidence clearly so that you can make your own determination.

Editor’s note: The author published the original version of this article⁶⁶ on Substack [midwest­erndoctor.com] in July 2024; this edited version is republished here with permission.

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SIDEBARS

A NEPHROLOGIST CHIMES IN By Richard Amerling, MD (quoted by A Midwestern Doctor⁶⁶)

As a nephrologist of many years, I’m intimately acquainted with this topic. . .. Here are a few more [points]:

• In addition to blood volume and vascular tone, inotropy (contractile force of the heart) contributes to blood pressure. Beta blockers work mostly by reducing this, and the heart rate.
• The body is designed to maintain blood pressure! Any perturbations will immediately trigger counter-regulatory mechanisms. Reducing salt intake, or administering a diuretic, decreases blood volume and pressure and leads to activation of the sympathetic nervous system. This increases heart rate, inotropy, and vasoconstriction, all of which restore blood pressure (and hence organ perfusion), and can actually overshoot and cause hypertension.
• Decreasing sodium delivery to the kidney results in activation of the renin-angiotensin-aldosterone system, caus­ing vasoconstriction and sodium retention.
• Chronic salt depletion (which is rampant due to its demonization) causes quasi-permanent activation of these hormonal systems and is deleterious to health.

I recently consulted on two cases where healthy seniors were prescribed not one, not two, but three (!) antihyper­tensive medications for BP of 140/90. One developed acute kidney failure; the other had near-syncope and onset of atrial fibrillation. This is medical malpractice but now considered standard of care!

ZETA POTENTIAL

Zeta potential is an immensely important concept for human health and vitality, which can explain the benefits behind many renowned and easy-to-implement holistic therapies.^26,67 Biological systems generally rely on particles hav­ing a sufficiently negative zeta potential to repel the particles they are surrounded by. The kidney is the primary organ responsible for maintaining the physiologic zeta potential.

If the net charge of a colloidal system is made more negatively charged, particles will become more dispersed; if, on the other hand, the net charge becomes more positively charged, particles will begin to clump together, form­ing successively larger colloidal agglomerations. Because the body depends on the continual circulation of fluids, this clumping can be extremely problematic. For example, once red blood cells clump together, microstrokes often follow.

CHINESE MEDICINE AND HYPERTENSION

In Chinese medicine, one of the foundational diagnoses is “blood stasis,” and many modern practitioners argue that it is a primary cause of illness. Interestingly, the emphasis on blood stasis is relatively new in this ancient medical tradi­tion, beginning around the same time as China’s introduction of the smallpox vaccine. Many of the injuries caused by that extremely harmful vaccine mirror the effects that Chinese medicine attributes to blood stasis.⁶⁸ Vaccines are highly effective at destroying the negatively charged physiologic zeta potential. After I read a 1947 paper linking blood sludging to obstruction of the vasa vasorum (the blood microvessels in large blood vessels),²² I began to suspect that a significant degree of the vascular damage caused by the Covid injections might be due to microclotting within the vasa vasorum.

The school of thought within Chinese medicine that emphasizes blood stasis frequently associates the condition with hypertension. An acupuncturist I know finds two common patterns in high blood pressure. He characterizes the first pattern by the same process described by “blood sludging” researchers, where blood stasis leads to fluid leaking out of the vessels (extravasation), which in turn inflames the area. This is often seen in diabetics with high blood sugar (which also impairs zeta potential); the pulse in the wrist feels stagnated, and (according to this school of thought) blood pressure then rises because the brain and kidneys are triggering a reflexive response to ensure they have enough perfu­sion. This pattern is treatable (including with Chinese herbs, blood sugar normalization, weight loss and exercise), but it takes a while, as the body needs time to return to its normal homeostasis.

In the second pattern, the pulses have a more active, stronger and full quality, which Chinese medicine practitioners believe is due to the heart or kidney not getting enough blood (due to narrowed arteries) and the heart then pumping harder to overcome that obstruction. My colleague finds that this pattern is the most common in African-American men and matches a diagnosis that used to exist within conventional cardiology called the “water hammer pulse.”⁶⁹ Using hypertensive medicines, according to this practitioner, is often a bad idea because it directly opposes the body’s compensatory mechanisms for blood flow.

Another acupuncturist tells me that correctly targeted releases of blood stasis (done by bleeding specific points in the body) can be very helpful for hypertension. He frequently sees dramatic results for hypertension with this approach.

FOUR TYPES OF ANTIHYPERTENSIVE DRUGS AND THEIR SIDE EFFECTS

DIURETICS: Diuretics lower BP by blocking the reabsorption of sodium in the kidneys and thereby increasing urination. Many different types exist with slightly different side-effect profiles and effects on different electrolytes, but generally:

• These drugs cause a wide range of symptoms from electrolyte imbalances, particularly of sodium and potassium. Low sodium levels are a common cause of weakness and hospital admissions, while low potassium (resulting in muscle weakness, cramps and digestive disorders) affects 8.2 percent of the drugs’ users—occurring at a rate 973 percent greater than those not on the drugs.⁴⁷
• Diuretics cause many of the side effects associated with dehydration (because they effectively dehydrate you).
• Depending on the class, they can sometimes create sulfa sensitivities or allergies.
• They cause many of the general effects associated with low blood pressure (such as lightheadedness).
• Some of them (such as the thiazides) also increase uric acid levels, which may explain⁷⁰ why the drugs increase the risk of diabetes⁷¹ or why they cause a 358 percent increase in the risk of gout (which affects 2 percent of users).

BETA BLOCKERS: Beta blockers slow the heart and make it pump less forcefully. This has been found to be very helpful for heart failure patients, but simultaneously, beta blockers have a variety of common side effects, such as constricting the peripheral arteries. Typically, patients have the greatest difficulty tolerating beta blockers and frequently report a worsened quality of life. Some of the drugs’ most common side effects include mood swings, depression, extreme tiredness and fatigue, dizziness or lightheadedness, low blood pressure (hypotension), sexual dysfunction, an excessively slow heart rate, weight gain, cold hands or feet, nausea, trouble sleeping and shortness of breath.

CALCIUM CHANNEL BLOCKERS: These reduce the force of contraction of the heart, dilate arteries by relaxing the smooth muscle in them and somewhat slow the heart rate. The major issues are that the drugs cause edema (swelling) throughout the body (affecting between 5.7 and 16.1 percent of users depending on dosage⁷²) and frequently cause dizziness, lightheadedness or constipation. Calcium channel blockers are often quite helpful for resetting an abnormal heart rhythm but also can cause symptoms such as tiredness, headaches, abnormal heart rates and shortness of breath.

ACE INHIBITORS: When the kidneys do not have enough blood, they release a hormone that sets off a cascade to raise blood pressure.⁷³ ACE inhibitors block that cascade—which can often be quite helpful, as parts of the cascade can be damaging to the body. The most common side effect is a chronic dry cough, which patients often develop over time as they become sensitized to the drugs. Estimates of its frequency range from 3.9 to 35 percent of users; one review determined it was 8 percent.⁴⁹ Other common side effects include headaches, lightheadedness and a loss of taste.

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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Winter 2024

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