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Does Blood Pressure Decrease in Late Life, and Why Would this Happen?

Blood pressure tends to increase with age, ultimately producing clinical hypertension in a sizable fraction of the population. This is driven by the progressive stiffening of blood vessels, which breaks the finely tuned feedback system that reacts to and controls blood pressure. Stiffening of blood vessels is in turn caused by factors such as calcification and inflammation resulting from cellular senescence, as well as cross-linking in the extracellular matrix that degrades tissue elasticity, and dysfunction of the muscle tissue that controls contraction and dilation of blood vessels. Control of blood pressure is considered highly important in modern medicine, and raised blood pressure is one of the most important factors determining risk of cardiovascular disease and mortality.

Given the justifiable focus on high blood pressure and its consequences, it is interesting to note that there is evidence for blood pressure in the population at large to peak and then drop in later life. As the paper here notes, the simple hypotheses for this phenomenon, such as that people with high blood pressure tend to die at a greater rate before reaching older ages, don't in fact explain enough of the phenomenon. My first guess at a mechanism was weight loss in later life due to frailty and pre-clinical levels of age-related disease, but that also doesn't seem to be enough to explain all of the effect.

A second guess might involve the effects of age-related muscle loss, sarcopenia, on the strength of the heart. This is something that doesn't appear to be all that well studied in older individuals without heart disease, and isn't commented on in the paper here. Unfortunately it isn't a straightforward relationship, given all of the ongoing changes in the cardiovascular system; older patients with either healthy hearts or hearts weakened by heart failure can exhibit higher blood pressure, lower blood pressure, or anything in between depending on their specific circumstances.

Blood Pressure Begins to Decline 14 Years Before Death, Study Says

Researchers looked at the electronic medical records of 46,634 British citizens who had died at age 60 or older. The large sample size included people who were healthy as well as those who had conditions such as heart disease or dementia. They found blood pressure declines were steepest in patients with dementia, heart failure, late-in-life weight loss, and those who had high blood pressure to begin with. But long-term declines also occurred without the presence of any of these diagnoses.

Doctors have long known that in the average person, blood pressure rises from childhood to middle age. But normal blood pressure in the elderly has been less certain. Some studies have indicated that blood pressure might drop in older patients and treatment for hypertension has been hypothesized as explaining late-life lower blood pressures. But this study found blood pressure declines were also present in those without hypertension diagnoses or anti-hypertension medication prescriptions. Further, the evidence was clear that the declines were not due simply to the early deaths of people with high blood pressure.

Blood Pressure Trajectories in the 20 Years Before Death

Both systolic blood pressure (SBP) and diastolic blood pressure (DBP) follow progressive upward trajectories from childhood to middle age, but blood pressure (BP) trends at older ages are unclear. Several studies reported flattening of the upward trend or a decrease in BP at advanced ages, although a few have reported continued BP increases. Blood pressure decreases in older age have been associated with poorer health, onset of dementia, and excess mortality. Hypothesized explanations for BP decreases in later life include (1) advancing age; (2) increasing end-of-life disease, especially heart failure, suggesting a link to the years before death rather than to age; (3) more intensive use of antihypertensive medications; or (4) that excess mortality of hypertensive individuals leaves healthy survivors with lower BP. Data to test these hypotheses are currently limited.

Observing individuals with multiple repeated BP measures over time could help clarify the causes underlying trends. If increasing end-of-life disease explains BP changes, then similar downward BP trajectories should not be observed in age- and sex-matched controls who die much later. In this study, we used the Clinical Practice Research Datalink (CPRD) to estimate clinically measured SBP and DBP trajectories for 20 years prior to death, for individuals dying at 60 years and older. Second, we compared the linear SBP trends for years 10 to 3 years before death in patients who died and age- and sex-matched controls who survived at least 9 years. These approaches aimed to separate age from end-of-life associations, and avoid healthy survivor biases.

Twenty years before death, estimated mean SBPs increased with increasing age at death (60-69 years, 139.5 mm Hg; ≥90 years, 150.0 mm Hg). All age-at-death groups initially experienced increasing SBP, reaching peak values and then declining with proximity to death. Peak SBPs occurred 14 years before death in those dying aged 60 to 69 years (mean peak SBP, 146.3 mm Hg) to 18 years before death for those dying aged at least 90 years (mean peak SBP, 150.8 mm Hg). Overall, 64.0% of individuals experienced SBP decrease of more than 10 mm Hg following the peak.

Antihypertensive medication was prescribed to 85.1% of patients for at least 1 year during the analysis period: mean SBP changed by -20.8 mm Hg from peak to year of death in those treated vs -11.2 mm Hg in those not treated. Peak SBP occurred at a mean of 15 years before death in the treated vs 14 years in those not treated. Adjustment for antihypertensive treatment made little difference to the main model results. Smoking status, alcohol consumption, and levels of physical activity measured in the 20 years prior to death had little association with SBP decreases. Weight loss (the difference between the maximum weight during the first 10 years of follow-up and weight in the final year) findings showed that patients losing at least 20 kg experienced a bigger absolute SBP decrease (mean, -24.87 mm Hg) compared with those who did not lose weight.

More work is needed to elucidate the specific mechanisms involved in late-life BP dynamics. Such studies may also be useful in addressing ways of optimizing the clinical care of older patients who experience decreasing BP. Also, downward BP trajectories before death have the potential to introduce reverse causation or "reverse epidemiology" effects in risk analyses, yielding misleading associations between BP and outcomes in older patients.

Comments

Hi there ! Just a 2 cent,

I'm curious too, this is puzzling. I am guessing this must be the body is compensating - in the younger years there is a rise in BP, until later in the elderly age, it is incompatible for continuous survival; thus it is loss of cardio vascular homeostasis. The body sort of responds by lowering BP progressively; it is either a compensation (responding to failing homeostasis) and/or a consequence (the damage to the blood vessel) means the heart is slowing or is damaged/tired itself; the blood vessels cannot take much more pressure loading and anyway, at that age (or let's say at that 'late point' before Soon-Death, the strength of 'blood pressure' is weaker thus the flow is not as strong, this means that BP drops. The actual damage and 'exhaustion' of the heart (since it pumped SO much More in the years previously (because of High BP, it had to pump harder to get the blood through; this accelerated heart aging/exhaustion along with the endovascular network being damaged by high BP/hypertension)).

Thus, a 'consequence' of that early state of long-term High BP, is that the body is now insufficient (a few years before death), thus low BP
OR
it is Only a compensatory metabolistic 'change' as an 'last-ditch' answer for 'last stage' survival, the metabolism (its speed) slows down, so does BP. Metabolism dysfunction is oftenly seen in elderly whom display slowed metabolism (people with excess weight have slowed metabolism or metabolistic disorders), yet in this study they say the people lost lots of weight while the people whom did not die (or as quuickly) kept their weight.

This means that Keeping your weight is crucial - and we must Differentiate/Nuance this, it doesn'T mean becoming Obese but just keeping what you have (because otherwise, if morbidly obese it is assured you will suffer metabolistic disorder at some point. Centenarians are not skinny nor obese, they are 'normal/average' BMI for their heigth and keep it that way). Thus the study, is really about people keeping their 'Sane' weight/BMI and elderly people (very old ones approaching 80-90 or people who lose weight suddenly for no reason (often have a deadly silent disease, I went through this and lost 40 lbs because of atherosclerosis in the space of 2 weeks without changing anything (Diet/exercice...etc, I was dying. THe body uses all the fat stores it has a extra glycogen3energy to try to 'combat'/compensate the deadly damage. It's why you look ghastly and can start becoming a skeleton))))). One of the reason, is that 'just enough weight' protects you by adiponectin in subcutaneous fats adipocytes whom can protect you from over fragility/frailty by being extra energy source for burning besides glucose (often when you become anorexic near skeleton like), thus this goes along with sarcopenia, frailty, precipitous large loss of weight (for no reason), metabolistic changes - and thus, BP loss and death later on.

It is thus a combination of compensation and consequence that brings you reduced BP close-to-before death. Another point that demonstrates this, is that centenarians have kept 'Adequate' BP their whole life - yet quite a few centenarians have High BP, thus this demonstrates that the body must Absolutely - Maintain - a certain 'Window' of BP - neither too low neither too high. Too high and it is Hypertension / accelerated epigenetic aging of the vascular system - and thus you die young (and you will most likely experience a drop in BP a decade before your death as this study shows. IT almost seems an illusion to make you think you are going better because your BP has lowered but it's a lie, it's just a 'coasting last ditch' effort before you die/a compensation or a consequence that you had high BP all your life and now you are entering the last 'survival' phase (low BP) before death). While, it also the same if you experience low BP all your life, that's dangerous too (comatose/hypocardia/brain dead (no glucose/no O2)/akin to hypoglycemia/hypothermia/your heart could stop it's just not beating altogether and/or the pressure is too weak in the blood vessel thus the O2 throughput is so low it's just as bad. Also the osmotic pressure will be changed inthe blood vessel, it can'T work for vascular system/incompatible with human lifespan (in other animals yes, not in human's peculair vascular system).

I think this can explain in part this weird reverse BP effect.

Just a 2 cent.

Posted by: CANanonymity at December 6th, 2017 10:09 PM

PS:

''Antihypertensive medication was prescribed to 85.1% of patients for at least 1 year during the analysis period: mean SBP changed by -20.8 mm Hg from peak to year of death in those treated vs -11.2 mm Hg in those not treated. Peak SBP occurred at a mean of 15 years before death in the treated vs 14 years in those not treated. Adjustment for antihypertensive treatment made little difference to the main model results''

This terrifies me because you would think antihypertensive would have done Something (I mean -20.8 mm Hg is very substantial)...nothing besides slightly cutting some slack on the vascular system/which might have helped the person's health slightly - this means, that it is faster Epigenetic Aging in the making. And antihypertensive do not revert that (or even slow it at all), hypertension is accelerated epigenetic aging of vascular system. It shows you how finnicky the vascular system is.

This also demonstrates how SENS has to rise above a Everest Mountain for this type of diseaes, senescent cells are behind this of course but it's more that this, it's epigenetic aging and replicative senescence acceleration right there (endothelial cells exeperience rapid telomere loss in such BP changes, and why hypertension or hypotension or atherosclerosis or ischemia or CVDs all add up to faster epigenetic aging of vascular system)).

I think the single strongest element that improves such disease, is the vasodilation/vasoconstriction in the blood vessel, which is in tandem with BP. CGRP (Calcitonin gene related peptide) release is oftenly low or delayed in people with high BP and CVDs. As such, they suffer from microtears and microdamage in microvessels from excessive constriction.
Stress also grealy increases constriction, so does extreme temperature change. Low BP is often an excess of vasodilation and a lacking of vasoconstriction. It is such a 'finite' balance and why you would see no results from antihypertensives in patients with a history of high BP.

Posted by: CANanonymity at December 6th, 2017 10:48 PM

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