Recent Research on Blood Pressure and Aging

Here I'll point out a couple of recent research publications on the topic of blood pressure in aging. Blood pressure is a useful metric in the progression of aging, not least because it can be cheaply and reliably measured. It is also a good example of the split between primary and secondary aging, as processes from both categories lead to higher blood pressure.

Primary aging is made up of the processes we cannot avoid, and only modestly slow via lifestyle choices. It is damage that accumulates as a consequence of the normal operation of metabolism. The accumulation of cross-links in the extracellular matrix and calcification of tissues leads to a progressive stiffening of blood vessel walls, and this loss of elasticity in blood vessels appears to be enough to explain the age-related rise in blood pressure that in some people is large enough to lead to clinical hypertension. Even lesser levels of high blood pressure slowly deform and weaken important structures in the cardiovascular system, exacerbate the processes causing atherosclerosis to develop in blood vessel walls, and increase the harm done to the brain by breakages in tiny blood vessels.

Secondary aging is caused by poor lifestyle choices. Most of the truly bad choices known to negatively impact life expectancy - including lack of exercise and being overweight - raise blood pressure in addition to their other effects, and this increase in blood pressure has all of the same detrimental effects as the increase caused by the processes of primary aging. Becoming fit in the general sense, through exercise and maintaining a sane weight, tends to lower blood pressure. One of the mediating mechanisms here is the influence of visceral fat on metabolism, but there are numerous other possibilities, all with varying degrees of supporting evidence.

What is known of the role of high blood pressure in the chain of cause and consequence that leads to age-related disease and death provides many good reasons to work on reducing your own personal pace of secondary aging. In fact the medical community is starting to think that past guidelines on blood pressure goals have been, if anything, too lax. If you spend too long with high blood pressure, and even the best of presently available treatments, drugs to reduce blood pressure, while capable of reducing risk of death cannot undo the restructuring and weakening of the cardiovascular system that has already taken place.

How Low to Go for Blood Pressure?

A new study finds that at least 16.8 million Americans could potentially benefit from lowering their systolic blood pressure (SBP) to 120 mmHg, much lower than current guidelines of 140 or 150 mmHg. The scientists calculated the potential impact of preliminary results from the Systolic Blood Pressure Intervention Trial (SPRINT). The initial analysis of SPRINT showed that using antihypertensive medications to reach a lower SBP target of 120 mmHg could greatly reduce risk for heart failure, heart attack, and death, compared to a target of 140 mmHg (SBP is the top number in a blood pressure reading). It's estimated that one in three U.S. adults have high blood pressure, or hypertension, a significant health concern. "SPRINT could have broad implications. Millions of Americans whose blood pressure is under control according to current guidelines may be considered uncontrolled if new guidelines adopt the intensive target of less than 120 mmHg studied in SPRINT."

A Randomized Trial of Intensive versus Standard Blood-Pressure Control

The most appropriate targets for systolic blood pressure to reduce cardiovascular morbidity and mortality among persons without diabetes remain uncertain. We randomly assigned 9361 persons with a systolic blood pressure of 130 mm Hg or higher and an increased cardiovascular risk, but without diabetes, to a systolic blood-pressure target of less than 120 mm Hg (intensive treatment) or a target of less than 140 mm Hg (standard treatment). At 1 year, the mean systolic blood pressure was 121.4 mm Hg in the intensive-treatment group and 136.2 mm Hg in the standard-treatment group. The intervention was stopped early after a median follow-up of 3.26 years owing to a significantly lower rate of myocardial infarction, other acute coronary syndromes, stroke, heart failure, or death from cardiovascular causes in the intensive-treatment group than in the standard-treatment group (1.65% per year vs. 2.19% per year).

Blood Pressure Medication Can't Undo All Damage

Treating out-of-control blood pressure with antihypertensive medication can greatly reduce your risk for heart attack, stroke and heart failure, but the current approach to treatment can't undo all of the previous damage or restore cardiovascular disease risk to ideal levels, a new study suggests. "The best outcomes were seen in those who always had ideal levels of blood pressure and never required medications. Those who were treated with medication and achieved ideal levels were still at roughly twice the risk of those with untreated ideal levels. And, of course, people with untreated or uncontrolled high blood pressure were at even greater risk." The new findings strongly suggest that there should be an even greater effort to maintain lower blood pressure levels in younger adults to avoid increases in blood pressure over time that may eventually require medication.

Those of us following SENS rejuvenation research should be thinking at this point that all of the data above only reinforces how important it is to make inroads in repairing the damage of primary aging. In this case that means finding a way to break down the most common cross-links that contribute to loss of elasticity in human tissues, those based on glucosepane. The SENS Research Foundation is one of the few organizations funding gluosepane research with the aim of a treatment to clear these cross-links. An effective therapy here would likely provide a greater and more reliable impact on cardiovascular aging and blood pressure than any presently available treatment, since it would be removing one of the root causes of blood vessel stiffening, which is in turn a root cause of high blood pressure.


Talking about glucosepane and the recent paper in Science... SRF's 2012 annual report already said that Dr. Spiegel's lab had developed a method to make glucosepane in the lab. Are they different methods? Or simply the paper writing/reviewing took too long?

Posted by: Antonio at November 13th, 2015 2:17 AM

Hi Antonio,

A couple of things ... first, the final synthesis that was published was much simpler and required fewer obscure and/or expensive reagents, and unlike the original synthesis doesn't involve an intermediate that kept going rogue on them. Second, while the final result was very important, he and his group were also occupied with publishing the other tools that they developed along the way to study AGE and AGE chemistry in vivo and in vitro. And third, it DOES then take a while to get together a rich enough paper and run the peer-review gauntlet to get a paper published in Science, an then to just wait for it to actually get published once accepted (though this last step is brief for Science compared to many journals, especially with the advent of advance electronic publication).

Posted by: Michael at November 13th, 2015 6:14 PM

Many thanks for the reply, Michael. Now it is clear.

BTW, your first two links seem to be broken.

Posted by: Antonio at November 13th, 2015 7:30 PM

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