1
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Bashing pharma
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2
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BP & HBP
explained, and distorted by pharma
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3
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HBP history ,
important compensatory mechanism which should not be tempered with
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4
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Primary &
secondary HP, syndrome of Microvascular disease, renal involvement; seven system
drugs
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5
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Fact about increase,
obesity definition of HBP 140/100, facts 5 fold increase since 1900
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6
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HBP Tweaked to promote sales
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7
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Infectious agents the
leading cause of AS
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8
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Preventing
atherogenesis the has health benefits lack by simply lowering with drug BP
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9
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HP seven bodily
systems, pharma story
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10
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contributing factors
according to pharma
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11
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Diuretics
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12
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Beta blockers ACE
inhibitors (angiotensin-converting-enzyme
inhibitor)
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13
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Calcium channel
blockers
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14
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ACE inhibitors
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15
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Angiotensin II
receptor antagonists
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16
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Renin inhibitors
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17
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Side effects
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18
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Pharma marketing
ploys listed
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19
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CoQ10
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20
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Natural treatments
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21
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Sorting it out
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22
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What drugs for HBP (Thiazides)
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23
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Bad pharma
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Hypertension & treatments -- 9 pgs -- JK
11/13/15 http://healthfully.org/rl/id1.html
1)
Quality evidence based conclusions are at variance with pharma1
“messaged” protocols. As
Harvard Prof. Marcia Angell has written
in her book The Truth about Drug Companies: “the
system is very good at marketing”—her lecture. Better treatments
are replaced by newer, patented,
often inferior ones. And in most
cases
the hawked drug is not worth the side effects and expenses. Over and over again drugs are tested for 6
weeks, on an ideal cohort, shown to be better than nothing at all (a sugar
pill), side effects are hardly considered by the FDA, and once patented hawked to a
much wider public.[1]
And pharma’s
sales reps and key opinion leaders (KOLs)[2] can
recommend the drug for new not approved uses, though not the company.
In a corporatist state & world we have
corporatist ethics. As Dr. Marcia
Angell wrote:
“We certainly are in a health care
crisis.... If we had set out to design the worst system that we could imagine,
we couldn't have imagined one as bad as we have.” Part of this nightmare is the system of reporting serious side effects; it
is a sham, pharma collects and reports side effects maybe. If you are shown a figure for a serious side
effect such as irregular heart beat or sexual dysfunction, a better “guesstimate”
would be to multiply that number by 5[3] Over and over again
the sum total of negative
consequences (side effects, cost, and diminished quality of life) entail that
there are better choices than what is hawked, and a better analysis of the biology
of the condition. The patient’s
informed
choice requires critical evaluation of the evidence which is not possible when
pharma manipulates the education of doctors and they own the clinical trials
that are designed for products promotion and for which they are written up with
an average positive bias of 32%--so
found when 74 journal articles were compared to the raw data for the clinical trials. The
controls & influence of
pharma—including treatment guidelines--has forced doctors to prescribe harmful
treatments. This
paper is about hypertension (HP): its -primary cause
& pharma’s spin, pharma’s standard treatments, side effects, and better choices.
2a)
Having stated shown that Pharma operates using tobacco ethics, we would
expect that pharma has control of the education of doctors and public, and that
they would promote drugs that maximize their profits, which would be taken
life-long, don’t prevent other medical conditions, cause decline in cognitive
function to create a dependence upon their doctor, and their side effects are
treated with other drugs. We would
expect that they have distorted the biology behind the pathology to promote
treating signs of the condition rather than the cause. All of these have occurred with
hypertension. Hypertension is caused
by atherosclerosis (AS), hard stiff, swollen arteries. AS is acknowledged as the result of an
inflammatory process. Though it
has been
known since the 1920 that pathogens living in the artery walls cause the
inflammatory process that develops into AS, pharma has chosen to blame AS on
cholesterol, saturated fats, cigarettes, and hypertension. And though the cholesterol theory has
thoroughly been rebutted (watch the Australian Broadcast Corporation exposure
of these myths at and
at.), but pharma
controls the education and marginalizes the critics. Hypertension is a sign of AS for 90% of cases.
Thus
lowering blood pressure has little effect upon the cause of strokes and heart
attacks because 85% of them are caused by atherosclerotic young plaque leaking
and causing a thrombus (clot). Young
plaque is like the pus in a pimple; when it leaks it can clog an artery to
cause an acute event. Old plaque
is
stiff with fibrous tissue, muscle cells, and calcium compounds, thus lowering
blood pressure doesn’t fix the hard mature boil. Except for diuretics, pharma’s most
popular drugs to treat hypertension will in general cause the heart to pump
with less force and the arteries muscles tissue to relax—lowering blood
pressure. Weakening the heart muscle
entails that during a heart attack the risk of death increases.
These antihypertensive drugs in combination
lower cognitive function, physical strength, libido, and thus quality of
life—three of them are often prescribed.
Since they don’t prevent young, unstable plaque from leaking, their long-term
usage is negative.
2b)
As to be expected with KOLs dominating the research and writing the
textbooks, that the basis of hypertension has been grossly distorted.
On point is the Wikipedia article on hypertension. Atherosclerosis is mentioned but once,
calcium zero times, though the calcification of arteries is a major contributor
to the hard stiff arteries that result in increased blood pressure.
The article goes on to point out that the
elderly have elevated blood pressure as though it is a normal part of aging,
but the elder in modern Paleolithic societies don’t develop hypertension. “Blood
pressure rises with aging and the risk of becoming hypertensive in later
life is considerable” Wiki. Stressed are neurotransmitters, kidney
hormones, and the risks for ischemic events.
“Hypertension is classified as either primary
(essential) hypertension or secondary
hypertension.
About 90–95%
of cases are categorized as primary hypertension, defined as high blood
pressure with no obvious underlying cause.[3] The
remaining 5–10% of cases are categorized as secondary hypertension, defined as
hypertension due to an identifiable cause, such as chronic
kidney disease,
narrowing
of the aorta or kidney
arteries,
or an
endocrine disorder such as excess aldosterone, cortisol, or catecholamine”
Wiki. In
journal articles insulin resistance and its
endpoint type-2 diabetes are considered as causal factors, and guidelines now
require the treating all type-2 diabetics with high-normal blood pressure for hypertension. This is what your doctor learns from
KOLs. Pharma doesn’t treat
atherosclerosis because it is not in their financial interest.
2c)
Each
cycle of cardiac contraction propels a bolus of 70 ml of blood into the
systemic arterial system, perfusing organs with oxygen and nutrients.
This propulsion imparts pressure on the
vascular wall [which stretch during peak pressure], the level of pressure
depending solely upon the cardiac output (the amount of blood pumped by the
heart) and the resistance to flow imparted by the vasculature. Because of the episodic ejection of blood from
the heart, pressure in the vessels shows periodic variation, being highest at
the peak of a passing bolus of blood; and lowest after its passage. These
respective peak and trough pressures correspond to the systolic
and diastolic pressures that can be measured intra-arterially
or more commonly by a blood pressure cuff. Population studies demonstrate that levels of blood
pressure (BP)
in the population show a continuous distribution. Blood
pressure must be tightly regulated to permit uninterrupted perfusion of all vital
organs. For example, even transient interruption in blood flow to the brain
will cause loss of consciousness, and longer interruptions will result in death
of unperfused tissues. Conversely, higher pressures that deliver flow exceeding
metabolic demand provide little or no metabolic gain. The morbid consequences of malignant
[systolic
above 200] high blood pressure (HBP) have been documented by
epidemiologic studies [systolic between 140 & 180 is a much different
condition--see 6]. HBP is “essential”
for perfusion of tissues through sclerotic and
narrowed blood vessels. The essential
role
of atherosclerosis (AS) in the development of HBP, and the subsequent pathogenic role
of HBP are now clear—though
pharma
distorts this relationship in its market-place manipulations.
Pharma has pulled a switch from
atherosclerosis, the cause to that of constriction of arteries which they
treat. It is like treating fever
instead
of bronchitis. In fact for 90% of
cases
atherosclerosis is the demonstrated cause of HBP. In a study of the
elder, for example, those with systolic hypertension were 3 times more likely
to have stenosis of the carotid artery than those with normal systolic blood
pressure, at. (Note,
this is only one location examined,
atherosclerotic occlusion occurs only in some of the arteries, thus there are
many cases of false negatives when measuring the carotid artery.)
The failure to treat the underlying
condition explains the minimal, if any, benefit from treating HBP with drugs that don’t treat AS.
Moreover pharma has through their KOLs gone after the most effective
interventions—all off patent—high-dose
aspirin, natural HRT, and testosterone, and they treat atherosclerosis
with what has been termed “the greatest medical scam in history”—watch documentaries on CVD section, mid
page.
3) “Hypertension
as a medical condition came into being at the turn of the 20th
century when methods for its measurement were developed. Two types were
differentiated, malignant (very severe) and moderate. Malignant typically ran its course in a few
years and resulted in death from MI,
stroke, or kidney failure. Moderate
is
associated with a higher death rate. In
the 1931, John Hay, Professor of Medicine at Liverpool University, wrote that "there is some truth
in the saying that the greatest danger to a man
with a high blood pressure lies in its discovery, because then some fool is
certain to try and reduce it". This view was echoed by the
eminent US cardiologist Paul Dudley White in 1937,
who suggested that "hypertension
may be an important compensatory
mechanism which should not be tampered with, even when it’s certain that we
could control it". This is because hypertension is like fever
accompanying the flu, treating fever does not affect the course of the disease,
nor does lowering blood pressure affect the course of cardiovascular disease
(CVD). Charles Friedberg's 1949 classic textbook
"Diseases of the Heart", [10] stated
that "people with 'mild benign' hypertension ... [defined as blood
pressures up to levels of 210/100 mm Hg] ... need not be treated"[8] Wiki.
This is because to reduce blood
pressure entails weakening the heart’s ability to contract as it pumps blood,
and this ability is needed uncompromised to survive an MI. A number of studies, including those using insurance
actuaries, showed a correlation of HBP
with illness and death. The basic
underlying
cause for HBP is AS.
Drug treatments between 1890 and 1958 were of little value. “In 1958 the first thiazide diuretic became
available. It increased salt excretion
while preventing fluid accumulation”
Wiki. Since then pharma
has expanded the pool of
those to be treated and hawked in 7 categories of drugs over 100 drugs to lower
blood pressure. HBP has
become 6 fold more common since 1900, from 5-6% to 34% in 2008.
“64%
of men age 65-74 have high blood pressure and 69% of women, up from 54% and 53%
respectively for that age 55-64. About 7 in 10 U.S. adults (69.9%) with high blood
pressure use medications to treat the condition2” Wiki. The Merck Manual
P. 466, 1972 places the
figure at under 15% of the adult population, uses the medical name of “benign
essential hypertension”, and states that it is strongly associated with
atherosclerosis. “Patients
with
uncomplicated primary hypertension should be considered for therapy if the
diastolic pressure is >100 mm Hg in males or >115 in females” supra
470. Merck finds of value treating
malignant hypertension, but not benign hypertension. Moreover the often associated renal disease
is not directly attributed to hypertension but rather to ‘atheromatous plaque,
aneurysms, emboli, and thrombi occurring in the main renal arteries or their
branches” supra 620. How effective
are
drugs for HBP in prevent ischemic
events? Should those with moderate HBP be treated? And what
are the best treatments?
4) “Hypertension is classified as either primary
(essential) hypertension or secondary
hypertension; about 90–95% of cases are categorized as
"primary hypertension" which means HBP
with no obvious underlying medical cause.[2] [Pharma
BS, AS
is the main cause][4]. The remaining 5–10% of cases (secondary
hypertension) are caused by other conditions that affect the kidneys, arteries,
heart or endocrine system” Wiki. “BP varies markedly,
with minute to minute
variations largely determined by the tone of the sympathetic nervous system
(SNS) and the parasympathetic nervous system [1]. The cutoff of 140/90 mmHg was selected in the early 1900s based on the
fact that only 5−10% of the US
population had BP in that range.
In addition, it was recognized from the start that BP in the hypertensive range were
almost inevitably accompanied by small vessel disease of the arterioles
(arteriolosclerosis) as well as kidneys that were grossly contracted and
‘granular’ in appearance, with juxtaglomerularrular [tubular structure that
filters blood to form urine], and more commonly tubular, changes on microscopic
examination. This suggests that hypertension should not simply be defined by an
elevation in BP but rather should be considered a syndrome in which microvascular
disease and renal involvement are also key components. The vast majority of individuals [> 90%] with
essential HP had variable degrees
of
renal arteriolosclerosis and tubular changes consistent with ischemia” hypertension,
2009. Again pharma downplays the importance of AS to sell their drugs.
5)
“Hypertension, high blood pressure sometimes
called arterial hypertension
is a chronic medical
condition in which the blood
pressure in the arteries is elevated. This
requires the heart to work harder than normal to circulate blood through the
blood vessels. BP is summarized by
two measurements, systolic and diastolic, which depend
on whether the heart muscle is contracting (systole) or relaxed between beats
(diastole) and equate to a maximum and minimum pressure, respectively. Normal
blood pressure at rest is within the range of 100-140 mmHg systolic (top
reading) and 60-90mmHg diastolic (bottom reading). HBP is said to be present if it is persistently at or above
140/90 mmHg.[5] Currently one-third of the US population
is hypertensive, representing a three to six-fold increase since the early
1900s. Essential
hypertension is now also common in the pediatric population, where it tracks
with rising frequencies of obesity[6]
and metabolic syndrome. There are
a major environmental component driving
this process, all of which cause AS. Those who smoke are progressively
develop AS, and thus HBP.
Other causes include diet high in sugar and carbohydrates, high ration
of omega 6 fatty acids to omega 3, sedentary lifestyle, obesity, and metabolic
syndrome, which are discussed at
these links, and also estrogen mimics. Obesity
has increased from 3 to 5% of the US population in 1900 to over 30% today [123]”—j. hypertension, 2009. This
increase in dietary sugar causes liver damage and AS and it bypasses the hormone (leptin) regulation of appetite, and
thus causes obesity.
6) Given the
corruption worked by a profits-first system, what is taught about AS, cholesterol, and HBP is
tweaked to promote sales of drugs
by putting the cart of drugs that lower BP
before the horse of clogged, stiff
arteries (AS). “These anatomic lesions [atherosclerotic
plaque]
usually begin in some children younger than age one year and in
all children older than age 10
regardless of geography, race, sex, or environment” Wiki [7]
“This
yellow fatty streak seen in childhood is not
necessarily a precursor of adult AS
and occurs in populations in which AS
is uncommon: it is presumable reversible
at this stage. Around age 25 in
populations in which AS is common,
the fibrous plaque begins to develop. It
is white, elevated, and compromise the arterial lumen [where blood flows].
Reversibility is questionable when fibrous
tissue and intimal proliferation are present.
In the more advanced stages, deposition of fibrin and platelets and
necrosis of tissue with growth of new
vessels may occur” Cecil Essentials of Medicine, 1986, p. 62-3. At 12 years the BP range is 85-120 systolic and 50-80 diastolic, yet they form
fatty streaks. Since
few at the age of 25 have HBP, the process of fibrous plaque formation is not
initiated by HBP, but rather HBP is a result of the accumulation of plaque. As
macrophage cells die in the atheroma, calcification
occurs in mature plaque, a major contribution to the stiffness of the arteries
and further raising BP. Pharma sells the biological intervention that
fixes putative cellular imbalances,
and minimalizes the role AS—retain
this point, please. Most of their drugs alter normal levels of
calcium, sodium, or neurotransmitters to lowers BP. This creates an abnormally
low level neurotransmitters, calcium, & sodium not just in arteries,
but throughout the body. These drug
induced abnormal cellular states
cause
numerous side effects including cognitive impairment, some deadly, and some not
evident for years,[8] and they
don’t effect the cause for AS.
7) So
what causes AS? The
leading risk factor is infectious
agents living within the muscular wall of the arteries. These pathogens within the wall produce
toxins
and reactive chemical. HDL & LDL
besides transporting cholesterol and triglycerides have an immune function. LDL and HDL in their immune system
function have these toxins and reactive chemicals attach to their
surface. With the entry of white blood
cells into the tunica intimaa an immune system inflammation process beings. It
is acknowledged beyond dispute that AS
is an inflammatory condition. The
role of pathogens has been demonstrated
in hundreds of experiments that are published in journal articles (http://scholar.google.com/), yet the
research articles are essentially ignored by a pharma which functions to
maximize its profits by lowering cholesterol, LDL, BP with drugs. Prevention in
this case violates their fiduciary obligation.
The chorus of critics is ignored by pharma who controls the education of doctors including
the textbooks. Doctors are taught that
pharma’s drugs are safe and
effective. Blocking the production
of LDL and cholesterol not only doesn’t affect the inflammatory process, but
has numerous side effects, especially muscle pain and cognitive decline. Most
affected are senior, which constitute
2/3rds of the market. Numerous books and
documentaries are on the Cholesterol
Myth. Several factors accelerate
this process especially chronic infection, diabetes, insulin resistance, and
reactive chemicals such as those from smoking cigarettes (carbon
monoxide). Diabetes is associated with a
high level of blood sugar, and sugar is a reactive chemical; also the high
level of insulin is associated with other health issues including obesity by
promoting the storage of fat, increased appetite and lowering metabolism that
causes weight gain. Both also promote endothelia
dysfunction. Contra-pharma,
effective treatment starts with controlling atherogenesis, go to link for ways.
[1] “The aim of drug regulation
is to ensure that only effective
and safe treatments reach patients. Ideally, regulatory decisions are based on
good quality data from large trials measuring real world, patient centred
outcomes. Licensing agencies, however, routinely approve treatments on the
basis of small placebo controlled trials evaluating short term, surrogate
endpoints in selected populations. Consequently, medicines are commonly
prescribed without good quality data on their long term benefits and harms. Current licensing standards
are
inadequate to predict the real world therapeutic value of new medications.” Sept 9, 2015, British
medical Journal, Dr. Huseyin Naci http://www.bmj.com/content/351/bmj.h5260?etoc=
[2] Key Opinion leaders (KOLs) are renowned
specialists. They rise to prominence is though providing services for pharma,
such as research, for pharma, for which most receive 6-digit income. Their success
is dependent upon being
ppharma “friendly”. “Pharma” is short
for pharmaceutical companies, considered collectively, often also called “big
pharma” to refer to the corporate giants.
[3] It is the “responsibility” of the drug manufacture to
gather and disseminate information on side effects. For the best analysis of
that system and how
it really works, with examples, go to http://healthfully.org/rc/id9.html
and id1.
[4] AS as it progress
causes HBP, and HBP which increase
risk of hemorrhage strokes, renal damage and
blood clots that are a causal element of ischemic strokes and MI. This relationship
is argued for in Paragraph
6. Pharma can’t affectively treat AS,
so they stress causes that help
their drug sales.
[5] By lowering it to 140 from
150 a vast pool of people can be sold on 2 or 3 drugs to manage their blood
pressure. “… between the ages of 40 and
59, 40% of men and 50% of women. Almost 60%
of those older than 60 years, 70%of those older than 70 years, and 80% of those
older than 80 years have hypertension”
Conn’s Current Therapy 2012, p. 437.
That is quite a change from the early 1900s. “The
cutoff of 140/90 mmHg was selected in the early 1900s based on the fact that
only 5−10% of the US population had blood pressures in that range” at supra. The increase
in CVD has undone the benefits of modern
medicine with its success with many common reapers such as TB, syphilis,
operations for cancer: the life
expectancy of the mature male has since the 1871 UK census increased but 2
years, 75 to 77 years source
Wiki (US male life
expectancy is 75 years).
[6] “In turn, obesity has been shown to be associated with many
prohypertensive mechanisms, including SNS activation, insulin and leptin
resistance, endothelial dysfunction, elevations in plasma aldosterone, and
intrarenal fat accumulation [72,124]. Many
of these
findings can be associated with acquired renal microvascular and interstitial
injury, including endothelial dysfunction [91], SNS stimulation [89], and activation of the renin–angiotensin axis
[93].” The
author of this
article finds that fructose causes and elevation of uric acid as the main causes
of high blood pressure and metabolic syndrome (hypertension, raised fasting
glucose, and dyslipidemia)--j. hypertension, 2009.
[7] More pro-drug spin,
compare to the 1986 medical textbook account.
Without contrary evidence this older account has been dropped. So too
has the healing process of
revascularization. Pharma’s drugs does
the healing & children should be taking them.
[8] This is an important
principle to understand. To mess with a
process that occurs in many different types of cells throughout the body very
often has dire consequence. It is fairly
safe to take a compound such as penicillin that harms certain types of bacteria
or morphine that blocks pain signals from specialized nerves; but it is a bag
of snakes to mess with the norepinephrine system or ccalcium
ion levels,
or COX-2 prostaglandin as does Vioxx and Celebrex. For the latter to date over 200,000 Americans
have had strokes and MI attributed to this family of drugs. This is why in a
cost benefit analysis so few drugs rate high.
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8) Reducing major events is the purpose
of lowering
blood pressure with drugs so as to reduce risk of myocardial infarction (MI),
and strokes sufficiently so that
there is a significant net gain over costs and side effects; but does it?. About
85% of strokes, and all MIs are ischemic events (obstruction of
blood supply), caused by unstable soft plaque--before it hardens into matures stable
plaque. The occlusion is less than 50%, typically 20%, and thus not visible
with an angiogram. When the young stable
plaque over the decades hardens to form mature plaque that won’t leak the
artery looses flexibility. The lack of
expansion entails a rise in blood pressure, as too does the reduced internal
diameter of the artery. As the amount of
area affected by this process, the condition develops into AS. The BP rises as the heart pumps harder to supply adequate
blood to the
organs in the body. HBP is a result
of AS; not
the other way around that KOLs
teach. HBP is merely a marker of
AS
and its associated morbidity. Lowering
blood pressure with a drug doesn’t change the rate of atherogenesis, because
the process occurs within the tunica intima (artery wall—not were blood flows).
Nor does lowering BP reduce the risk of
plaque rupture. Lowering BP from 160
to 140 with drugs doesn’t reduce the amount of CVD; doesn’t place
that person in the group whose BP is naturally 140 and thus has very
little mature plaque in his arteries.[1] But it will lower modestly the risk of an
ischemic event. This is because an
ischemic event is a 2-step process. First
occurs when the leaking of young,
unstable plaque partially clogs downstream an artery (a thrombi forms). Young
plaque is too soft to clog a large artery.
The second step is the formation of a blood clot that further
occludes the partially plugged artery. As
blood pressure goes up, this second step (thrombi) occurs more frequently and thus
is more likely to occlude the artery totally or near totally. If this occurs
in a mid-size artery in the
brain a stroke results, in the heart an MI.
If it occurs in a small artery of the heart
or brain the event will go unnoticed, though eventually the accumulative effect
or repeated events can manifest itself as vascular dementia or angina. Similar
thrombus events can also occur in
other organs such as the kidney. Given
the real cause of HBP, the issue
before the patient is not how to lower BP,
but how to stop atherogenesis and allow through the body’s healing process for
the blood pressure to natural creep lower. See paragraphs 19 thorough 24 for
answers.
9) Hypertension pharma teach
is a
malfunction in 7 bodily systems: in
sodium retention, baroreceptors, elevated catecholamines, inappropriate
activation of the rennin-angiotensin system, over activated somatic nervous
system (and consequentially a reduction in the parasympathetic system), and
endothelial dysfunctions resulting in impaired nitric oxide release. For
each of these there are drug
interventions. But a drug that changes
the level of calcium in the cell to lower BP
doesn’t prove that there is an excess amount of calcium. Focusing
on these systems is not very
insightful.
10) Contributing factors (pharma’s spin): For pharma
there are currently 6 contributing process that result in hypertension, thus
reducing the role of AS and
promoting drugs to treat the remaining 5 processes. This is truly unfortunate
They are
interconnected variety of mechanisms that increases the BP. First is atherogenesis,
that the development of AS clogs the
blood arteries and makes them less elastic, and that this results in the heart
pumping with more force to provide an adequate blood supply to the brain and
other organs. Second is renal
arteriolar disease: hypertension
is strongly correlated with arteriolar changes in the kidney as opposed to other
organs such as the spleen. Third
there are several neural
mechanism: an activated
somatic nervous system[2]
(and a reduction in parasympathetic3
activity), including higher basal heart rate, increased BP in response to stimuli
and elevated plasma catecholamines.3 The
mechanisms
responsible for this activation is diverse, and includes defective baroreceptor[3]
autoregulation [29], increased hypothalamic response to environmental stimuli
[30], stimulation of renal afferent sympathetics that activate
central nervous system (CNS) adrenergic
pathways [31], and elevated thoracolumbar sympathetic activity [32]. Fourth systemic mediator systems have included
evidence for inappropriate activation of the renin–angiotensin system[4]
relative to the volume (sodium) status of the patient, perhaps triggered by
heterogeneous perfusion within the kidney [33]. “The system
can be activated when there is a loss of blood volume or a drop
in blood pressure (such
as in hemorrhage or dehydration)”
Wiki. “Angiotensin is a peptide
hormone that causes vasoconstriction and a subsequent increase in BP. It is part of the renin-angiotensin
system, Angiotensin
also stimulates the release of aldosterone, another
hormone, from the adrenal
cortex. Aldosterone promotes sodium
retention in the distal nephron, in the kidney, which also drives BP up”
Wiki. “The juxtaglomerular
cells in the kidneys secrete renin directly into circulation
when the blood
volume is low. Angiotensin is a potent
direct vasoconstrictor, increases the desire for salt. Increases thirst increases
the retention of salt and loss of potassium” Wiki. Fifth is the “endothelial
dysfunction associated
with impaired nitric oxide release resulting in inadequate vasodilation of
resistance vessels has also been shown to be present in many patients with
hypertension. It is a systemic
pathological state of the endothelium (the inner lining of blood vessels) and can be
broadly defined as an imbalance between vasodilating and vasoconstricting
substances produced by (or acting on) the endothelium.[1] Normal functions of endothelial cells include
mediation of coagulation, platelet
adhesion, immune function and control of volume and electrolyte content of the intravascular and extravascular
spaces. Endothelial dysfunction is a
major physio-pathological mechanism that leads towards coronary artery
disease, and other
atherosclerotic diseases.[5] It
can also result from environmental factors, such as from smoking tobacco
products and exposure to air pollution.[2] Sixth, nitric Oxide (NO) reduction[5] is
considered the hallmark of endothelial dysfunction.[8] Endothelial
dysfunction can result from and/or contribute to several disease processes, as
occurs in hypertension
& hypercholesterolaemia” Wiki. Because of
the many diverse contributing systems, there are six main categories of BP lowering
drugs, diuretics like thiazides,
beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-II
receptor antagonists, Renin inhibitors, and calcium
channel blockers.
11) Diuretics
(13 diuretics listed with
links in Wiki, divided
into 4 classes): any substance that
promotes the production of urine. They are used to treat heart failure, liver
cirrhosis, hypertension,
and
certain kidney
diseases. The antihypertensive actions
of some diuretics (thiazides and loop
diuretics in particular) are independent
of their
diuretic effect and are given at lower doses than that required to produce
diuresis.[6]. Only the thiazide and thiazide-like diuretics have good evidence of
beneficial effects on important endpoints of hypertension, and hence,
should usually be the first choice when selecting a diuretic to treat
hypertension. The reason why thiazide-type diuretics are better than the others
is (at least in part) thought to be because of their vasodilating
properties. Thiazide diuretics also
increase calcium reabsorption at the distal tubule” Wiki. “One of the
most important decisions in treating people with elevated BP is what drug class
is used first. This decision has enormous
consequences in terms of health outcomes and cost. In this review health
outcomes resulting from 4 drug classes are summarized. Most of the evidence
demonstrated that first-line low-dose thiazides reduce mortality and morbidity
(stroke, heart attack and heart failure). No other drug class improved health
outcomes
better than low-dose thiazides;
beta-blockers and high-dose thiazides were inferior. Low-dose thiazides should
be the first choice drug in most patients with elevated BP. Fortunately, thiazides are also very inexpensive” Cochrane Review.[7] The
National Institutes of Health’s National Heart, Lung and Blood Institute
recommends beginning treatment with a mild water pill (diuretic) at a low dose.
The safest and best studied of the diuretics is hydrochlorothiazide (ESIDRIX,
HYDRODIURIL, MICROZIDE). T he
starting dose should be low: 12.5 to 25 milligrams per day or even every other
day. Confirming the advice we have been giving since 1988 is a large definitive
study (named ALLHAT) involving more than 33,000 patients aged 55 or older that
found “compelling evidence that thiazide diuretics (such as hydrochlorothiazide
or chlorthalidone) should be the initial drug of choice for patients with
hypertension. For older adults, in general, the rule for treating high blood
pressure, as with so many other drug treatments, is “start low [1/2 dose] and
go slow.” Worst Pill. “Diuretics
pose special problems with the elderly due to depletion of sodium and calcium
and the poor efficacy as to creatinine clearance, decreased baroreceptor
responsiveness, reduced cerebral, renal, and splanchnic blood flow, and a
tendency to electrolyte depletion (calcium, sodium, and magnesium)” Braunwald,
Heart Disease 5th Ed, p.
499. “The most worrisome effects of
diuretic therapy have revolved around hypokalemia (depletion of potassium) and
its relationship to cardiac arrhythmias and sudden death,” AHA
summation on diuretics for hypertension.
Again pharma is killing the competition with scare tacks, big
advertising dollars, and continuing education where they get the danger message
out to the prescription writers. Thiazides are
“associated with an increase in bone mineral density and reduction in fracture
rates attributed to osteoporosis” Wiki As Cochrane, Worst Pill, and the FDA point out
thiazides are the prudent drug choice.
12) Beta blockers (26 listed in Wiki with links): They are andrenergic receptor
antagonists consisting of non-selective and B1, B2,,B3 selective agents.
“(β-blockers,
beta-adrenergic blocking agents, beta antagonists, beta-adrenergic antagonists,
beta-adrenoreceptor antagonists, or beta adrenergic receptor antagonists) are a class
of drugs. Beta blockers target the beta receptor. Beta
receptors are found on cells of the heart muscles, smooth muscles, airways,
arteries, kidneys, and other tissues that are part of the sympathetic nervous
system and lead to stress responses, especially when
they are stimulated by epinephrine (adrenaline). Beta blockers interfere
with the binding to the receptor of epinephrine
and other stress hormones [neurotransmitters], and weaken the effects of
stress hormones” Wiki. “Although beta blockers lower BP,
they do not have a positive benefit on
endpoints as some other antihypertensives”[12]—Wiki. “Beta-blockers are not recommended as first
line treatment for hypertension as compared to placebo due to their modest
effect on stroke and no significant
reduction in mortality or coronary heart disease” Cochrane. Beta blockers inhibit CoQ10
(Q10), which depending on degree must have dire, long-term consequences. “Adverse drug reactions (ADRs) associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold
extremities, exacerbation of Raynaud's syndrome, bradycardia
[low heart beat], hypotension, Hypoglycemia, heart failure, heart block
[irregularity of
nerve regulation of
heart], edema fatigue,
abnormal
vision, dizziness, alopecia(hair loss), hallucinations, insomnia,
nightmares, sexual dysfunction, erectile dysfunction and/or alteration
of glucose
and
lipid metabolism. Glucagon
is the specific antidote for beta-blocker poisoning, because it increases
intracellular cAMP and cardiac
contractility. [32][33] Other antidotes for beta blocker
poisoning are salbutamol and isoprenaline.” Wiki. Warning avoid because they don’t reduce mortality (Cochrane),
blocking
neurotransmitters that effect mental (brain) functions it should be avoided (a
downer) plus its inhibition of CoQ10 entails serious long-term consequences including
atherogenesis, neuropathy, and fatal MI. Norepinephrine, epinephrine, and dopamine
are
major neurotransmitters; affecting their action has serious consequences poorly
understood, and ignored by beta blocker manufacturers. Beta
blockers are used to treat anxiety disorder—another way to sell a downer.
With the elderly the psychotropic effect is
far more pronounced and can lead to a diagnosis of Alzheimer’s disease.
13) “Calcium
channel blocker (CCB)
(30 listed in Wiki with links) is a chemical that disrupts the movement of calcium (Ca2+) through calcium
channels [in neurons].[1] Calcium channel blockers are used as antihypertensive
drugs, i.e. as
medications to decrease BP in patients with hypertension. CCBs are particularly effective against
large vessel stiffness, one of the common causes of elevated systolic BP in elderly
patients.[2] Calcium channel blockers are also frequently used
to alter heart rate, to prevent cerebral vasospasm, and to reduce chest pain caused by angina
pectoris. They reduce the flow
of calcium ions into the cells by blocking the L-typevoltage-gated calcium
channel”[5] Wiki. “Twenty
trials lasting an average of 7 weeks were found in the world
scientific literature to answer this question. The data showed that the
addition of a beta-blocker to thiazide diuretics or calcium channel blockers
reduced BP by 8/6 mmHg when given at doses 2 times the recommended starting
dose” Cochrane. “Warning: This drug is much worse than diuretics,
not
merely because of various side effects, but also because of increased mortality”
Worst Pill,
and. This occurs primarily by making the cardiac muscle weaker; and thus the heart is less
likely to survive the stress from an MI.
Side effects include fluid buildup in the legs and ankle edema, rapid
heart rate, slow heart rate,
constipation, gingival overgrowth, nausea, confusion, nystagmus (involuntary
eyeball movement), headache, weakness, myalgia, new or worsening depression, bipolar
disorder, paranoia, disorientation,
acute renal failure, atrial fibrillation, sepsis, etc, plus overdose due to
poor liver & renal clearance mostly in the elderly. And of course there
is the risk of drug
interactions. Warning
avoid because of increased mortality (Worst Pill)[8]. The reason is that they weaken the heart
muscle, thus during an acute MI, the risk of death increases.
14) “ACE
inhibitor (angiotensin-converting-enzyme inhibitor) (12
are listed in Wiki with links): is used
primarily for the treatment of hypertension
and
congestive heart
failure. This group of drugs causes dilation of blood
vessels, which results in lower BP.
In treating heart disease ACE inhibitors are usually used with other
medications. ACE inhibitors inhibit angiotensin-converting
enzyme (a component of the BP-regulating renin-angiotensin
system), thereby
decreases the tension of blood vessels and blood volume, thus lowering BP. They thereby: lower arteriolar resistance and increase venous capacity; decrease cardiac
output, cardiac index, stroke work,
and volume; lower
resistance in blood vessels in the kidneys; and lead to increased natriuresis (excretion of sodium in the urine)“ Wiki. “The
trials followed participants for
approximately 6 weeks (though people are
typically expected to take anti-hypertension drugs for the rest of their lives).
Most of the trials in this review were funded by companies that make ACE
inhibitors and serious adverse effects were not reported by the authors
of many of these trials. Due to incomplete reporting of the number
of participants who dropped out of the trials due to adverse drug reactions, as
well as the short duration of these trials, this review could not provide a good
estimate of the harms associated
with this class of drugs. The BP
lowering effect was modest.
There was an 8-point reduction in the upper number that signifies the systolic
pressure and a 5-point reduction in the lower number that signifies the
diastolic pressure. Most of the BP
lowering effect (about 70%) can be achieved with the lowest recommended dose of
the drugs. No ACE inhibitor drug appears to be any better or worse than
others in terms of BP lowering
ability” Cochrane. Common side effects include renal impairment,
headache, dizziness & falls, fatigue, nausea, cough, inflammation related
pain, rash, taste disturbance hyperkalemia (elevated blood potassium) which can
cause arrhythmia that can be fatal. “In 2011, there were 164 million ACE
inhibitor prescriptions (fifth highest-selling of any drug class)” Worst Pill.
15) “Angiotensin II
receptor antagonists, also known as angiotensin
receptor blockers (ARBs), AT1-receptor
antagonists or sartans (9
listed with links in Wiki)., are a group of
pharmaceuticals that modulate the renin-angiotensin-aldosterone system. Angiotensin II, through AT1 receptor
stimulation, is a major stress hormone and, because (ARBs) block these
receptors. Their main uses are in the
treatment of hypertension (HP), diabetic nephropathy (kidney damage due to diabetes) and congestive heart failure. They
used primarily for the treatment of hypertension where the patient is intolerant of ACE inhibitor therapy….
A 2011 systematic review of 58 trials in patients
with micro- and macroalbuminuria found there was no significant reduction in the risk of all-cause
mortality or
cardiac–cerebrovascular mortality with ARB versus placebo ”
Wiki. The trials followed participants
for only 7
weeks (though people are typically expected to take anti-hypertension drugs for
the rest of their lives). The BP
lowering effect was modest. There was an 8-point reduction in the upper
number that signifies the systolic pressure and a 5-point reduction in the
lower number that signifies the diastolic pressure. Most of the BP lowering
effect (about 70%) can be
achieved with the lowest recommended dose of the drugs. No ARB appears
to be any better or worse than
others in terms of BP lowering
ability” Cochrane, who attached the same warning about results that they provided for
ACE inhibitors (see above); they don’t
save lives. “In 2011, 86 million ARB prescriptions (16th
highest-selling) were dispensed U.S.
16) “Renin inhibitors
(1 listed with links in Wiki) are a group of pharmaceutical
drugs used
primarily in treatment of essential hypertension (HBP).
These drugs inhibit the first and rate-limiting
step of
the renin-angiotensin-aldosterone
system (RAAS), namely
the conversion of angiotensinogen to angiotensin I.
Renin (/ˈriːnɨn/ ree-nin), also known as an angiotensinogenase, is an enzyme that participates in the body's renin-angiotensin system (RAS)—also known as the renin-angiotensin-aldosterone
axis—that mediates extracellular
volume (i.e., that of
the blood plasma, lymph and interstitial fluid), and arterial vasoconstriction. Thus, it regulates
the body's mean arterial BP. Renin is secreted by
the kidney from cells of the juxtaglomerular apparatus in response to three stimuli:
decrease in arterial BP,
decrease in sodium chloride; sympathetic
nervous system activity, which also controls BP, acting through the beta1 adrenergic
receptors” Wiki. l
issued in Dec. 2012 a warning not to take with ACE inhibitors. Aliskiren is also widely used,
with 2.4 million prescriptions dispensed in 2011. ARBs
alone generated $7.6 billion in revenue in
2011. Side
effects include stroke, renal complications, hyperkalemia, and hypotension in
patients with diabetes and moderate renal impairment, also angio-edema,
diarrhea and other GI symptoms, headache, rash gout, and renal stones” Worst Pill.
[1] The common deception is to show their drug
reduces strokes by selecting those in the highest risk group, with diastolic BP of 180 or above, malignant
hypertension. They have over 5-fold
risk compared to normal
BP for hemorrhagic stroke, which
is
only 15% of all strokes. Pharma includes them in their clinical trial,
then concludes that everyone over 140 diastolic BP will benefit with reduced risk of stroke and MI. Moreover these trials have positive bias over
30%; the flaws are buried in the raw data which they own.
[3] Baroreceptors
are sensors
located in the blood vessels that are excited by the stretch of the blood vessels. Increase in blood pressure causes their
activation of the central nervous system which in turn influences cardiac
output and response by the vascular smooth muscles to influence total peripheral
resistance.[1] They
as
part of a negative feedback system called the baroreflex,[2] as soon as there
is a change from the usual mean arterial
blood pressure, returning
the pressure toward a normal level. There are distinct receptors for both high
and low blood pressures..
[5] NO has the following physiological effects that contribute
to the inhibition of AS: 1) NO is
released and produces vasodilation after shear stress in the vessel; the
vasodilation NO mediated-response in turns decreases the shear stress. If the
shear stress is chronically induced it leads to the upre gulation
of and release of inflammatory cytokines [10] 2) NO decreases
LDL oxidation; 3) NO reduces platelet
aggregation to the endothelium 4) NO Inhibits smooth muscle cell proliferation
5) NO prevents leukocyte adhesion and infiltration into the vessel.[11] Wiki.
[7] “The Cochrane Collaboration is an international
network of more than 31,000 dedicated people from over 120 countries. We work together to help healthcare practitioners,
policy-makers, patients, their advocates and carers, make well-informed
decisions about health care, by preparing, updating, and promoting the
accessibility of Cochrane Reviews– over 5,000 so far, published online in the Cochrane
Database of Systematic Reviews, part of The
Cochrane Library”.
They attempt to weed out marketing science.
17) Side
effects: There are numerous adverse side effects is long & without
quantification, thus burying the common and serious. “Adverse
drug reactions (ADRs) associated with the use of beta
blockers include nausea, diarrhea,
bronchospasm,
dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual
dysfunction, erectile
dysfunction and/or alteration of glucose and lipid metabolism. Mixed α1/β-antagonist
therapy is also commonly associated with orthostatic
hypotension. Carvedilol therapy
is commonly associated with edema.[23] Due to the high penetration across the blood–brain
barrier, lipophilic
beta blockers, such as propranolol and metoprolol, are more likely than other, less
lipophilic, beta blockers to cause sleep disturbances, such as insomnia and
vivid dreams and nightmares.[24]
Adverse effects associated with β2-adrenergic receptor
antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of
glucose and lipid metabolism) are less common with β1-selective
(often termed "cardioselective") agents, however receptor selectivity
diminishes at higher doses. Beta blockade, especially of the beta-1 receptor at
the macula densa, inhibits renin release, thus decreasing the release of aldosterone. This causes hyponatremia and hyperkalemia. Beta blockers are contraindicated in
patients with asthma” Wiki. Missing
from the list is cancer, causes of mortality,
Alzheimer’s disease[1], and gastrointestinal
bleeding; and in studies the reason why volunteers dropped out. PhARMA does
test short-term trial (typically 7
weeks, see beta blockers above) to assure the best results, often in an
atypical younger & healthier population.
What is written of
beta blockers essentially applies to the other types of hypertension drugs, and
also Cochrane criticism of the PhARMA funded studies (see ACE inhibitors above)
applies to all HP drugs.
Many of the side affect go unreported
because of polypharmacy and a very imperfect system of reporting. And polypharmacy
is the norm: “A typical treatment plan will often include
an ACE inhibitor, beta
blocker,
a long-acting nitrate and a calcium
channel blocker in combinations that are adjusted to
the
individual patient's needs” Wiki. If doctors knew
of the risks associated, and warned patients, if
protocols were not set up by PhARMA, then cows could fly. A well constructed
study journal article
based on raw data submitted to the FDA and obtained under the Freedom of
Information Act found positive bias averages 32% in 74 clinical trial (from 11
to 69% bias). There are over 100 drugs
to treat hypertension, in 7 categories, and the lack of scientific studies; selection
by even a specialist is a crap shoot. With
marketing science, very few honest head-to-head studies, and treatment protocols,
the physician can only provide what pharma’s thought leaders teach. As
Prof Marcia Angell said above (1st
paragraph) “we have a system that is worse than we could imagine.” Benefits
created by every trick in an
essentially unregulated industry. These
cooked benefits are not worth the side
effects .[2]
18) Pharma is very good at marketing;
they dress marketing science as medical science. A partial discussion of their sales ploys is
in order. First don’t be fooled by the use of bio-markers, in this case the
lowering of BP as a surrogate for
lives saved per hundred treated per year.
There are many ways to sell a drug by hiding the details such as a
comparison in a population study for hemorrhage strokes of those with very high
blood pressure to an untreated group and then running with the results as
though it applies to MI, etc. Strokes are often used to prove the
treatment’s worth, but heart problems are 4 fold[3] more likely to be a
cause of death than a stroke.[4] Another is using
a marketing science study
with manipulated results (see Side
Effects discussion of statins in the IDEAL study as an example). Positive bias in journal
articles averages 32%. Brochure
from a
pharma lap dog is a sales tool. The
physician will create numbers when trying to fulfill a quota and follow the protocol. Through a well rehearsed script, he can be
very convincing. His earnest belief
is
founded upon continuing education classes given by pharma. Another ploy is the basket effect, putting a
group who shouldn’t be included into the study.
To find out how life-threatening HBP
is the study needs to be controlled for confounding variables especially
renal disease, lifestyle, age, & AS
by doing a matching study. For many
studies the published results don’t support the written conclusion at the end
of the journal article. Unfortunately
it
is the conclusion that is presented in continuing education classes by thought
leaders. Pharma’s percentage figures are misleading. A
33% reduction in deaths from strokes sounds significant. For high blood pressure, a placebo group age
60 to 70 with 3 fatal stroke per
100
patents treated 5 years compared to a group placebo with 2 fatal strokes is a 33%
reduction in deaths , but this requires 500 year of drugging patients with side
effects and other causes of death to prevent 1 fatal stroke.
Total deaths is the important fact, but it is
rarely included in a pharma trail. Most favorable results are listed in journal
articles while unfavorable results and side effect are often missing or
misleading given. Most important
figure is
total mortality for assessing value, but its usually missing. A common deception is to compare in a
population two groups based on blood pressure.
For example, a study found that those age
60 and above with a BP of 160 or higher had a 26% higher mortality rate than
those who BP that was 10 mg lower-another study similar for CVD.
This results do not entail that
by lowering BP 10 mg that mortality would be reduced deaths by 26%.
Years of being in the
higher group entails, on
an average, the higher group has more advance AS; that doesn’t vanish by lowering the BP. Thus going down 10 mg
doesn’t entail a 26% drop in mortality from stroke, because the underlying
cause hardening of the arteries is still there.
There are many other ways to hide bias in studies and exaggerate
benefits and burry Side Effects. And
there are many ways to promote sales, Protocols (guidelines)
set standards of treatment by organizations that are “pharma friendly”; and
violating a protocol can result in a law suit[5] (2
main reason why doctors push drugs). Guidelines
are repeated in brochures published by organization such as the American Society of Hypertension and the Pulmonary Hypertension Association that are
“pharma friendly”. The
purpose of drug intervention
is to not lower BP, but to lower
overall risk of death[6] by
taking a drug that does not have a major negative impact upon quality of life. Such essential information is often not
available because pharma won’t do what is not in their financial interest. Our marketing-driven system is morally
bankrupt.
19) “Coenzyme
Q10 (CoQ10) has been studied as a potential treatment for hypertension, a common medical condition. However,
there is not enough reliable evidence to show whether or not it can be a useful
medication to lower BP. A systematic
review was conducted to try and use all available data to answer this question.
Databases of clinical trials were searched for any studies that tested the
effects of coenzyme Q10 on patients' BP
compared to a placebo. The test medications could be added to participants'
regular anti-hypertensive medications or be used alone. Three trials with a
total of 96 participants were found
in which coenzyme Q10 was used in patients with HBP. The patients took coenzyme Q10 or a placebo daily for up to
8-12 weeks. Weighted data analysis showed that the systolic BP was. [This is more than the average
for most big pharma drugs.] However
there
are questions about the reliability of the available studies. Therefore, it is
still uncertain if coenzyme Q10 could be a useful hypertension treatment, and
more studies are needed” Cochrane,
also. However,
the evidence is stronger than
Cochrane review indicates. “After
treatment with Q10, 90% improved by 1 or 2 New York Heart Association
classes. Mean Q10 rose from 0.855
Ug/ml
to 2.086 Ug/ml on varied dosage programs…” at. An excellent
review[7] of
the literature on CoQ110 with section on hypertension found at p 264-5 an
average reduction is 17/10 (systolic/diastolic BP, 392 participants). “Iwamoto et al identified a deficiency
in the
activity of succinate dehydrogenase Q10 reductase in leucocytes which results
in decreased levels of Q10 in human subjects (and rats) with chronic
hypertension (39% versus 6% in the
healthy control).” Five mechanisms
were positive affected by supplementation:
(1) vascular endothelium inducing vasodilatation; (2) antioxidant
properties quenching of free radicals causes inactivation of endothelium
derived relaxing factor and/or fibrosis of arteriolar smooth muscle; (3) the
improved diastolic function leads to an adaptive reduction in catecholamine;
(4) decreased in blood viscosity; and (5) reduces aldosterone secretions
lowering sodium retention.” To
dispel
doubts about Q10 as to its role in treating congestive heart failure,
hypertension, ischemic heart disease, arrhythmias, side effects from statins
and read the article in Pharmacology and
Therapeutics, 2009. “Coenzyme
Q10 is
critical adjuvant therapy for patients with cardiac diseases due to its
beneficial effects on cellular bioenergetics, regulation of cell membrane
channels and its antioxidant effect, at p. 267.” Since statins block the synthesis of Q10, numerous
articles have called for the use of CoQ10 with statins, especially among the
elderly because myopathy, neuropathy, cognitive decline, and heart
failure are issues. As a potential
treatment for Parkinson, it was tested at 2,400 mgs per day, long term and it
was with side effects
19)
20) Natural
treatments: “Major lifestyles
modifications including weight reduction and low sodium diet have been shown to
lower high blood pressure.5, 6 In addition, sodium reduction and a diet
rich in vegetables, fruits, and low-fat dairy products lowers blood pressure in
both those with and without hypertension.7, 8 For example, a 1,600 milligram sodium
restriction has effects similar to treatment with a single
blood-pressure-lowering drug.9 Exercise10 and moderate alcohol intake are also
beneficial in maintaining a healthy blood pressure.11 A
study of nutritional therapy showed that over one-third of people who
previously needed drug treatment for high blood pressure were able to
adequately control their blood pressure with nutritional therapy alone.12 In addition, these methods are safer than
using medication, since they have no adverse effects. Trying them will often
make other beneficial contributions to your health. Most obese people who lose
weight can reduce their blood pressure by 15%.... Treating systolic blood
pressure below 160 is controversial…. Are many people being given antihypertensive
drugs unnecessarily? One study found that 41%
of patients 50 and older who were carefully taken off their high blood pressure
medications did not need them, having normal blood pressure 11 months after the
drug was stopped.18 Worst Pill. Worst
Pill should also recommend Q10 (affirmed by Cochrane
Review, and others), CoQ10
(see #19) should be started immediately and continued for life.
.
21) Improving outcome, lowering BP and risks
associated with AS: In over 90% of
cases it is AS that causes
hypertension and the associated renal damage.
While AS can’t be reversed the risk can be reduced by reducing the
formation of young unstable plaque. “In developed countries, the two leading
causes of death, myocardial
infarction , and stroke, may each
directly result from an arterial system that has been slowly and progressively
compromised by years of deterioration”
Wiki. But pharma stresses HBP as a cause of this, and then sells drugs to lower BP as though that somehow affects the
plaque formation that coronary heart disease.
There is no quick fix for the damaged kidneys or clogged, stiff
calcified arteries. Encapsulated
plaque with fibrous matrix cannot be removed with drugs. Any chemical that can dissolve plaque will
cause major damage to epithelium cells that line the arteries and veins and
affect various vital processes. An
effective treatment thus would slow or stop the process of atherogenesis and
allow the body’s revascularization process to improve outcome and lower BP.
Statins use is based
upon the cholesterol myth; they fail to work because they don’t treat the cause.
For AS
there is a better approach: long-term
program of life-style changes including strenuous exercise/labor and healthful diet are
beneficial. 325 mg aspirin[8]lowers
the risk of clotting (the low dose is ineffective within 1 year due to
tolerance). Taking 325 mg or more
with
each meal is sufficient for aspirin’s
anti-inflammatory effect, and thus slows or prevents atherogenesis. At the 325 mg it reduces all cancers over
30%, and at a higher dose will promote
cancer survival. For
those who
believe the cholesterol myth, rather
than take a statin a safer way to lower cholesterol is to take 250 mg Niacin or inositol upon retiring
(if niacin use slow release). Take
omega-3
oils to reduce the immune response, and CoQ10 function to protect the
body from reactive chemicals, because both slow or stop atherogenesis.
Natural estrogen (estradiol with
progesterone)[9] in HRT reduces MI by 50%
by preventing atherogenesis through a variety of way and has many other health
benefits including preventing osteoporosis.
Testosterone strengthens
myocardial muscles, promotes healing, & reduces risk of metabolic syndrome,
diabetes, and aggressive prostate cancer.
These hormones will stop atherogenesis and promote healing. All of these
drugs have additional major health benefits, and thus are attacked by pharma
with tobacco science.
22) What drugs for HBP: There is no pressing need to start right away
drug therapy except when systolic pressure is over 180. The majority of people should NOT be taking blood pressure medicines,
because for mild hypertensive (systolic 140-159 and diastolic 90-99) Cochrane
review based on a meta-analysis of the best studies: “Drugs for mild HPB have not been proven to
benefit patients” also. “Absolute
risk increase (ARI) 9%” Cochrane. After
2 years of natural treatments the systolic
BP remains above 160: “Only the thiazide and thiazide-like diuretics have good
evidence of
beneficial effects on important endpoints of hypertension, and hence,
should usually be the first choice when selecting a diuretic to treat
hypertension. The reason why thiazide-type diuretics are better than the others
is (at least in part) thought to be because of their vasodilating properties. They are the recommended
first-line treatment in
the US (JNC VII) [5] guidelines for hypertension and a recommended
treatment in the European (ESC/ESH) [6] guidelines…. Thiazide diuretics also increase calcium re-absorption
at the distal tubule” Wiki. Thiazides are “associated with an increase
in
bone mineral density and reduction in fracture rates attributed to
osteoporosis” Wiki. And
their cost is under $100/year. However
there are no benefits
for those over 80 years. Don’t
confuse
the surrogate endpoint of lower blood pressure with reduction in acute ischemic
events, the reduction is minor.
23) Bad Pharma: Pharmaceutical
corporations should not be doing research, owning the results including raw data,
controlling its publication, give continuing education to physicians taught by
pharma’s KOLs (key opinion leaders). Pharma
head the FDA, influencing treatment
protocols (guidelines), and misinform the public about drugs on television and
through physicians who have been taught by KOLs.
Forty years ago, medical text books did a
reasonable good job of providing information; that has all changed, since they
are written by pharma’s KOLs. Before
Regan’s Presidency, clinical trials
were ran by universities, now pharma is involved in all stages of clinical
trials, often through corporations whom they hire to run the trials and right
the journal articles. Their influence in
universities over research determines who becomes KOLs and thus write textbooks.
Ghost writing has become the norm
for clinical trial. The extent of
intrusion has been meticulously documented in Prof. Ben Goldacre’s Bad
Pharma. Harvard prof. Marcia
Angell has an equally excellent book on How
Pharma deceives us. There is a fundamental conflict between
short-term profit maximization and the public’s health, I call this tobacco
ethic. The articles written for
the recommend section of healthfully.org make adjustments for the marketing
distortions of pharma. A quality study
of 74 published articles comparing raw data to published results determined
that positive bias averages 32%. Thus what
seem to work based on the published
evidence base, in the vast majority of cases doesn’t. And it gets worse
because side effect weren’t
considered—how could they given the reporting system is broken. Healthfully.org/rc
adjust for our broken system and thus provides the information for informed
choices in the best patient’s interest. As
of November 2014, 18 areas of treatment and
drugs have been published. An important new section is on diet and its
role in CVD, metabolic syndrome, and obesity.
These articles are regularly updated. In that new section are links to a
number of on-point YouTube videos. Included there are videos on bad pharm, SSRIs,
cholesterol myth, the use of statins, diet, and diabetes—and there are books
listed. Unfortunately there aren’t quality
videos on exposing hypertension,
arrhythmia, acetaminophen, anticoagulants, chemotherapy, bypass operations, polypharmacy,
SSRIs, Nor are there quality videos on
the health benefits of aspirin, CoQ10, and hormones, but there are books on their
benefits.
[1] A retrospective
analysis of five million patient records with the US Department of Veterans Affairs system found different types of commonly used
antihypertensive medications had very different Alzheimer’s Disease outcomes (AD). Those patients taking angiotensin
receptor blockers (ARBs) were 35—40% less likely to develop AD than those using
other antihypertensives.[10][11] Given
the dramatic rise in Alzheimer’s and
the lack of placebo comparison, I suspect
that some, if not most HBP drugs
increase the risk.
[2] Most
side effects go
unreported because with multiple drugs the cause as to which drug cannot be
singled out, and reporting is voluntary to the manufacturer, who is required to
periodically submit reports after they evaluate it—a requirement hardly
enforced.
[3] Death
stats for 2005:
446,000 CHD +151,000 MI = 597,000
death. Strokes account for 143,600 that 597.,000/143.600 = 4.2 more deaths from
CHD, source AHA. CHD
is coronary heart disease.
[4] This is a very important point about evidence and missing
evidence. I find over and over again
that obvious end points are not used in a majority of studies, it is most
likely because the results are or would be unfavorable, or marginally
favorable. Thus pharma turns to
a
biomarker and/or lesser benefits to market their drug.
When a study includes critical end points,
it is likely based on a manipulation of the raw data. The
reason for leaving out MI is that some types of hypertensive drugs
weaken the heart muscle, and thus lower blood
pressure, but this can prove fatal during an heart attack. Thus they push the reduction in strokes and
don’t include heart attack
in their
clinical trial. Remember, the mindset of pharma and their fellow followers:
it is all about product promotion.
[5] [5]
Treatment protocols and legal exposure for violating them is the primary cause
for being over medicated. Three
good
sources on the morass created by corporate medicine are Side Effects, Corporate Medicine; Prof.
Marcia Angell’s book The Truth About the Drug Companies,
How they
Deceive Us and What to do About It;
and
Are Your Prescriptions Killing You? Armon
B. Neel Jr, PharmD
[6] Total mortality is
preferred to events because it includes all side effects, even ones like
suicide and cancer that are often missed.
[7] The review
cardiac benefits of CoQ10 found
at p. 260 that it “is useful
in arterosclerosis, ischemic heart disease, chront heart failure, hypertropic
cadiomyopathy, cardiovascular surgery, hypertension, arrhythmias, valvular
heart disease, toxin-induced cardiomyopathy including statin cardiomyopathy and
Meniere’s disease.“ At p. 364, better results than Cochrane Review, (see 8
lines above) as to number of participants, and lowering of BP.
[9] Synthetic pill forms are very significantly inferior, for most
progestins interfere with the protective action of estradiol.
19) What
drugs for HP: it depends upon risk factors.
The majority of people should NOT be taking blood pressure medicines,
because for mild hypertensive (systolic 140-159 and diastolic 90-99) Cochrane
review based on a meta-analysis of the best studies: “Drugs
for mild HPB have not been proven to
benefit patients” also. “Absolute risk increase
(ARI) 9%”
Cochrane. After 2 years of natural treatments the
systolic
BP remains above 160:. “Only
the thiazide and thiazide-like
diuretics have good evidence of
beneficial effects on important endpoints of hypertension, and hence,
should usually be the first choice when selecting a diuretic to treat
hypertension. The reason why thiazide-type diuretics are better than the others
is (at least in part) thought to be because of their vasodilating properties. They are the recommended first-line treatment
in
the US (JNC VII) [5] guidelines for hypertension and a recommended
treatment in the European (ESC/ESH) [6] guidelines…. Thiazide diuretics also increase calcium re-absorption
at the distal tubule” Wiki. Thiazides are “associated with an increase in
bone mineral density and reduction in fracture rates attributed to
osteoporosis” Wiki. And their cost is under $100/year.
21) Pharma
is very good at marketing; they
dress marketing science as science. A partial
discussion of their sales ploys is in order.
First don’t be fooled by the use
of bio-markers, in this case the lowering of BP as a surrogate for lives
saved per hundred years. There are many ways to sell a drug by hiding the
details such as a comparison in a population study for hemorrhage strokes of
those with very high blood pressure to an untreated group and then running with
the results as though it applies to MI, etc.
Strokes are often used to prove the treatment’s worth, but heart
problems are 4 fold more likely to be a cause
of death than a stroke. Another is using a marketing science study
with manipulated results (see Side
Effects discussion of statins in the IDEAL study as an example).
Positive bias in journal
articles averages 32%. Brochure from a
pharma lap dog is a sales tool. The
physician will create numbers when trying to fulfill a quota and follow
protocol. Through a well rehearsed
script, he can be very convincing. His
earnest belief is founded upon continuing education classes given by
pharma. Another ploy is the basket
effect, putting a group who shouldn’t be included into the study. To find
out how life-threatening HBP is the study needs to be controlled
for confounding variables especially renal disease, lifestyle, age, &
atherosclerosis by doing a matching study.
For many studies the published results don’t support the written
conclusion at the end of the journal article.
Unfortunately it is the conclusion that is presented in continuing
education classes by thought leaders. Percentage figures are misleading. A
33% reduction in deaths from strokes sound significant. For high blood pressure,
a placebo group age 60
to 70 with 3 fatal stroke per 100 years
compared to a group treated with diuretics that has only 2 fatal strokes has a
33% reduction in deaths from strokes, but only 1 fewer stokes per 100 patients
per year. And if they don’t list total deaths,,
there is a significant chance that the treated group died at a higher rate or
same rate as the untreated group. Most
favorable results are listed while lest
favorable and side effect are often missing, misleading. Most important is total
mortality to
assessing costs, but there are few such published. A study found that those age
60 + with a BP of 160 or higher had a 26% higher mortality rate than those who
BP was 10mg Hg lower-similar
for CVD. This
doesn’t entail that by lowering BP 10 mg that mortality would be reduced deaths
by 26%,. Years of being in
the higher group entails on
an average very significantly greater
atherosclerosis, the main cause for MI and strokes. There are many ways
to hide bias in studies
and exaggerate benefits and burry Side Effects. Protocols set standards of treatment by
organizations that are “PhARMA friendly” and violating a protocol can result in
a law suit which
is main reason why doctors push drugs. Their
advice is often repeated in brochures
published by organization such as the American
Society of Hypertension and the Pulmonary
Hypertension Association that are “pharma friendly”. The purpose
of intervention is to not lower BP, but to lower overall risk of death by
taking a drug that does not have a major negative impact upon quality of life,
and its side effects are always grossly under estimated. Know these ploys and
that our marketing-driven
system entails an incredible amount of harm occurs. Informed choice based on
sound science is
nearly impossible. Healthfully.org/rc is attempting to provide the information
for
informed choices in the best patient’s interest.
CoQ10 lowers blood pressure
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
http://www.sciencedirect.com/science/article/pii/009829979490037X
Treatment of essential hypertension with
Coenzyme Q10
Abstract
A
total of 109 patients with symptomatic essential hypertension presenting to a
private cardiology practice were observed after the addition of CoQ10 (average dose, 225 mg/day by
mouth) to their existing
antihypertensive drug regimen. In 80 per cent of patients, the diagnosis of
essential hypertension was established for a year or more prior to starting CoQ10 (average 9.2 years). Only one patient was dropped from analysis
due to noncompliance. The dosage of CoQ10 was not fixed and was adjusted
according to clinical response
and blood CoQ10 levels.
Our aim was to attain blood levels greater than 2.0 μg/ml (average 3.02 μg/ml
on CoQ10). Patients were followed closely with frequent clinic visits to
record BP and clinical status and
make necessary adjustments in drug therapy. Echocardiograms were obtained at
baseline in 88% of patients and both at baseline and during treatment in 39% of
patients. A definite and gradual improvement in functional status was observed
with the concomitant need to gradually decrease antihypertensive drug therapy
within the first one to six months. Thereafter, clinical status and
cardiovascular drug requirements stabilized with a significantly improved
systolic and diastolic BP. Overall
New York Heart Association (NYHA) functional class improved from a mean of 2.40
to 1.36 (P <
0.001) and 51% of
patients came completely off of between one and three antihypertensive drugs at
an average of 4.4 months after starting CoQ10. Only 3% of patients required the addition of one
antihypertensive drug. In the 39.4% of patients with echocardiograms both
before and during treatment, we observed a highly significant improvement in
left ventricular wall thickness and diastolic function. We observed no side
effects or drug interactions from CoQ10.
The time course to improvement in functional class, BP control and myocardial
function is in keeping with an
improvement in myocardial bioenergetics by CoQ10 and not a pharmacological effect.
The reduction in BP seems likely to be
secondary to a decrease in the neurohumoral response to an early
impairment in myocardial function [adrenergic neurotransmitters are
released in response to poor cardiac function] which is primarily diastolic in
nature. The gratifying improvement in patients' quality of life was enhanced by
a marked reduction in their need for antihypertensive drugs along with the
substantial medical and financial burden that these drugs entail.
Hypertension: First choice
is Q10 (300 mgs),
exercise, sodium restriction, and weight control. Over half of those who follow
this program
will have normal blood by 1 year.
Moreover, the prestigious Cochrane review concluded that: “Drugs for mild hypertension have not
been proven to benefit patients.” Mild
hypertension is a systolic 140-159 and diastolic 90-99. If after 2 year there
isn’t sufficient
progress at lowering blood pressure below 160 over 100, then the second choice is “thiazide and thiazide-like
diuretics [lowers the
amount of water in the body]. [They]
have good evidence of beneficial effects on important endpoints of hypertension
… [and
they] also
increase calcium re-absorption at the distal tubule” Wiki, and they
are among the cheapest drugs. They are
widely recommended as first line in treatment guidelines. Treating hypertension
with pharma’s drug
arsenal (over 100 drugs of which 3 are typically prescribed at one time) has
serious side effects including drowsiness, cognitive impairment, ED, and low
libido. Moreover, pharma’s régime of
drugs when taken long-term doesn’t extend life.
For example the very popular group of calcium channel blockers cause a
“higher mortality rate over extended periods of use” Wiki.
The first approach (Q10, diet, etc) is the
only reasonable choice. Long term
prevention of further development of hardening of the arteries through aspirin
325 mgs, Q10, and estrogen will in most cases result in a gradual lowering of
blood pressure, and a significant long-term reduction in mortality.
^^^^^^^^^^^^^^^^^^^^^^^
The most common way that pharma expands a treatment
is
through using a high risk group with a lower risk group. And of course they
under-report (if at all)
side effects, and don’t include in their articles total mortality. Below
is an example of such, exposed in a
Cochrane meta-analysis that fails to bring up the issues of accurate accounting
of side effects including total mortality.
Informed choice and informed recommendations by physicians requires an
accurate appraisal of harm done.
http://www.bmj.com/content/345/bmj.e5511?etoc=
Cochrane review finds no proved benefit
in drug treatment for patients with
mild hypertension
BMJ 2012; 345 doi: 10.1136/bmj.e5511
(Published 15 August 2012)
Treating patients
with stage 1
(mild) hypertension has no benefit, a Cochrane review of studies conducted in
the United Kingdom, Australia, and the United States has found.1
Data from four
randomised controlled
trials, involving 8912 patients with stage 1 hypertension (systolic blood
pressure 140-159 mm Hg or diastolic 90-99 mm Hg, or both) and treated for four
to five years, found that drug treatment did not reduce total mortality (risk
ratio 0.85 (95% confidence interval 0.63 to 1.15)), coronary heart disease
(1.12 (0.8 to 1.57), or stroke (0.51 (0.24 to 1.08)). Patients with
pre-existing cardiovascular disease were excluded from the study. [They didn’t
include all causes of mortality or quality of life or side effects]
David Cundiff,
one of the reviewers,
said that he believes that the analysis should lead to dramatic changes in the
way doctors treat mild hypertension, allowing patients to throw away their
blood pressure pills and focus instead on far more effective as well as
evidence based approaches, such as exercising, smoking cessation, and eating a
DASH (diet against systolic hypertension) or Mediterranean diet.
Cundiff told
the BMJ that “in
light of the negative results of the trials in the literature” further clinical
trials of drug treatment for mild hypertension should be conducted only if
patients first undergo lifestyle changes and those efforts fail.
James Wright,
coordinating editor of
the Cochrane Hypertension Group, told the BMJ that until now it has
simply been assumed that treating mild hypertension, which is what most
hypertensive patients have, is beneficial. He said that doctors and guideline
writers have based their opinions on a combination of assumptions and data from
clinical trials in which patients with mild hypertension were not analysed
separately.
The
reviewers were able to
obtain patient level data for three of the four trials and conducted a pooled
analysis of those patients with mild hypertension {viz. raw data}. They then combined those data with a fourth trial that
enrolled participants who almost exclusively had mild hypertension. [Indicates
that by pooling high risk the
studies were able to extend treatment to the mild hypertension category—again total
morality excluded.]
The lack of benefit
is perhaps even
more significant, because the Cochrane review did not exclude patients with
risk factors such as diabetes and probably included patients with target organ
damage or a 10 year risk of cardiovascular disease of 20% or more, as these
parameters were not recorded.
Guidelines on
treating hypertension
differ among countries, but practice may be the same.
A spokesperson
for the US National
Heart, Lung, and Blood Institute, which appoints experts to the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure (known as the JNC), told the BMJ in a written statement that
its previous guidelines (JNC7) recommend lifestyle modification and drug
treatment to achieve a target blood pressure goal below 140/90 mm Hg for
patients with stage 1 hypertension. The spokesperson said that the committee is
“currently reviewing the evidence and deliberating on various topics, including
blood pressure treatment thresholds and goals.”
The institute
plans to pass the
Cochrane analysis along to the committee for consideration.
Professional
US and European
guidelines are more aggressive in recommending drug treatment for
uncomplicated, mild hypertension than UK guidance, which recommends treatment
for stage 1 hypertension only if the patient has additional risk factors.2 3 4 However,
according to the Cochrane
reviewers and others, prescribing in the UK and Europe is likely to be similar
to that in the US, as many doctors do not follow guidelines.
Des Spence, a
general practitioner
in Glasgow, told the BMJ, “Risk is abstract, and doctors and patients
struggle with the concept and may not follow the guidelines. Doctors see a
blood pressure of 156/98 and they prescribe. It’s
easier to treat than not treat—you never get blamed for over-treating.”
A spokesperson
for the UK National
Institute for Health and Clinical Excellence told the BMJ that it was
unable to comment on how many patients with stage 1 hypertension without the
risk criteria specified by NICE are currently taking antihypertensive drugs.
Jerome Hoffman,
emeritus professor
of medicine at UCLA and an expert in critical appraisal of medical literature,
said, “We’ve long known that almost all benefit from treating severe
hypertension comes with lowering BP [blood pressure] just a little. On the
other hand, efforts to lower BP to ‘normal,’ typically requiring multiple
drugs, are not only usually unsuccessful but produce more harm than good, since
adverse effects of intensive treatment outweigh the minimal marginal benefit of
a little more BP ‘control.’ Drug treatment of mild hypertension, like intensive
treatment of severe hypertension, may be of great value to drug makers, but it
was almost predictable that it would provide little or no benefit for
patients.”
However, not
all doctors are
convinced that these results should change practice. Mark Ebell, associate
professor of epidemiology in the University of Georgia’s College of Public
Health, told the BMJ that most patients came from a single study and
that many of the patients in that study were taking only a β blocker. Recent
systematic reviews have indicated that β blockers do not provide the same
mortality benefit as other antihypertensives. Also, the total number of events
in the studies was relatively small, suggesting that a large, well designed
study comparing thiazides or angiotensin converting enzyme inhibitors (or both)
with placebo is needed to definitively answer this question.
Wright said that
he agrees that a
well-designed trial is needed. However, he added, “The fact that we don’t know
hopefully should change practice.” He said that doctors should explain to
patients the lack of evidence supporting drug treatment for mild hypertension
and engage the patient in choosing whether to continue the pills or not.
Notes
Cite this as: BMJ 2012;345:e5511
References
Diao D, Wright JM, Cundiff DK, Gueyffier F.
Pharmacotherapy for mild hypertension. Cochrane Database Syst Rev2012;(8):CD006742. Joint National Committee on Prevention
Detection, Evaluation, and Treatment of High Blood Pressure. Seventh report of
the Joint National Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure: complete report 2011. www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.htm. Mancia G, De Backer G, Dominiczak
A, et al.
2007 Guidelines for the management of arterial hypertension: the task force for
the management of arterial hypertension of the European Society of Hypertension
(ESH) and of the European Society of Cardiology (ESC). J
Hypertens2007;25:1105-87.
CrossRefMedlineWeb
of Science
National Institute for Health
and Clinical
Excellence. Hypertension: clinical management of primary hypertension in adults
2011. CG127. Aug 2011. www.nice.org.uk/nicemedia/live/13561/56008/56008.pdf
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