My mother died recently, indirectly as a consequence of a second, very severe stroke which destroyed 80% of her brain function, left her in a coma for months and then more or less totally paralysed from the neck down.
She had been diagnosed with high blood pressure (HBP) since her first stroke some 20 years ago – and despite the medications, in the end it was a burden she just could not overcome when her chronic HBP ruptured an aneurysm in the brain.
Her death was noted as “cardiac failure due to old age” (she was 86), but this terse statement is symptomatic of an outdated system that prefers simple categorisation of the causes of death rather than active investigation of the facts for use in later analysis.
So although HBP may be the underlying cause, deaths are reported in murky categories such as heart failure, stroke, kidney failure or even “old age” – and each of these categories may have other causative factors such as infections or genetics.
Taken as a whole, HBP may well be the biggest single killer in many countries – but due to the way deaths are reported, we just don’t know for sure.
* How blood pressure is measured
Many of you would know that blood pressure is measured as an expression of the systolic over the diastolic blood pressures (systolic pressure is when the heart beats and diastolic is when the heart relaxes).
What you might not know is that blood pressure is measured using a sphygmomanometer – and the recommended reading is around 135/85 (the number measurements are in mmHg or millimetres of mercury, due to the first reliable device invented by Riva-Rocci which was based on using a short column of mercury).
To be a little more precise, what is being measured by a sphygmomanometer is the pressure of blood on your blood vessel walls in response to your heart beat.
This is a significant statement because it means that, unless there is some disease or genetic disorder involved, HBP (also known as hypertension) is almost certainly a consequence of one’s lifestyle.
And unfortunately, for many people, HBP is often also a one-way switch – once developed, it is a condition not easy to reverse. Let me explain.
We start with a simple example which can profoundly affect HBP: sodium chloride, or food salt. This is a compound crucial for life as the nervous system relies on sodium as a core electrolyte for managing the transmission of nerve signals – and 38.76% of salt is sodium.
Our taste buds are each collections of several taste cells and the entire taste bud is often primed by the taste cell for saltiness opening its ion channel when detecting sodium chloride.
Sodium chloride, or salt, can profoundly affect blood pressure. Photo: AFP/Istock
This is one reason why we are often very fond of salty food because salt causes our taste buds to react more to other tastes – a classic example is pepper: pepper in hot water is pretty tasteless until salt is added, upon which the pungency of pepper is “released”.
Also, our lips have only taste cells for salt which explains why we lick our lips when expecting a delicious dinner.
The human fondness of salt is probably linked to the fact that salt was normally heavily restricted from our Palaeolithic ancestors’ diets, despite that fact that sodium is so critical for survival – in fact, in the 6th century, the Moors valued salt as much as gold.
It is only in the last century that salt became the ubiquitous low-cost commodity that we now know – but, like sugar, we still have not lost our sensitivity or proclivity for it. This means that it is a cheap additive which food producers can add to processed foods to make them tastier – and these days, most of the salt ingested by the general population comes from restaurants and processed food items.
How salt induces HBP is somewhat complex as it probably has several answers, but one usual explanation is that ingested sodium gets into the blood where it raises osmotic pressure (and reduces the water potential of blood).
This means that more water will get absorbed from the body into the blood circulatory system (a process called water retention) and this additional volume of fluid will increase blood pressure.
The kidneys will attempt to remove the excess sodium but it would take some time for the water retention effect to wear off.
Compounding the problem is another factor: arteries leading to the kidneys may get narrowed by persistent HBP, causing the kidneys to become less effective. This in turn leads to more sodium remaining in the blood, leading to more water retention and higher blood pressures.
However, I have to admit that although the above explanation sounds plausible, it is also somewhat theoretical and derived originally from experiments on rats which were fed the equivalent of 60 times the amount of salt humans would normally ingest.
What is less contentious is a study called DASH-Sodium conducted between 1997 and 1999 on over 400 individuals – if you’re curious, the acronym DASH stands for Dietary Approaches to Stop Hypertension.
Among the results of the DASH-Sodium study was the conclusion that “reducing sodium intakes to the lower level resulted in significantly lower systolic blood pressure in all sex, race, and hypertension status subgroups with the exception of non-black participants without hypertension”.
Even more compelling evidence is Finland – since the late 1970s, the country had instigated public health initiatives to reduce salt intake.
An analysis done in 2002 found that salt consumption was down 40% since the effort began, diastolic blood pressure for the population had decreased by 10 mmHg and deaths from strokes and coronary heart disease had decreased by over 75%.
All this is likely to be due solely to salt reduction as other health risk factors such as obesity and consumption of alcohol had actually increased in the country during the same period.
So regardless of the uncertain ways in which sodium chloride affect blood pressure, we have some pretty convincing evidence that it does have a significant impact on HBP.
Much as it pains me to admit it, I have come across several studies which indicate reducing the consumption of alcohol has a significant impact on reducing HBP.
There may also be some additional linkages concerning the quantity of alcohol and the consumption pattern (infrequent, regular or excessive) – but regardless, apart from the initial tiny, positive effect of some arterial dilation after a small quantity of alcohol, continued drinking appears to be always associated with at least some aspects of HBP.
Several studies indicate that reducing the consumption of alcohol has a significant impact on reducing HBP. Photo: Bloomberg
This is a little surprising as the expected physiological response to alcohol is normally the dilation of arterial vessels which should reduce blood pressure.
However, it may be that the effort of removing alcohol from the blood, especially enzymatic processes such as the catalysation of ethanol into the more toxic acetaldehyde before final scrubbing via yet other enzymes, can provoke some inflammatory responses which lead to HBP.
If you are curious how alcohol is processed by the body, there is an earlier article about the Alcohol Dehydrogenase (ADH) and Aldehyde Dehydrogenase (ALDH) enzymes at Star2.com (goo.gl/t1fP7E).
This does cause me to sometimes regard my wine racks with a little ruefulness – but on a positive note, it does provide a valid reason (if I choose to use it) to not offer wines to friends as it would be impolite to damage their health.
To be sensible, although Finland indicates that salt may be a more significant risk factor for HBP, I am definitely not discounting alcohol as a risk factor either.
A recent paper suggests that sugar may play a significant role in HBP, especially for people who have developed some resistance to insulin – this would cover quite a large proportion of the population in the developed world.
In bodies with high insulin levels, it appears that sugars, in particular fructose, via a complex interaction, can affect the Renin-Angiotensin-Aldosterone System (RAAS) in the kidneys, causing the over-production of an octapeptide (a polypeptide that consists of eight amino acids) called angiotensin II.
The role of angiotensin II is primarily as a vasoactive peptide which causes small blood vessels (known as arterioles) to constrict, thereby increasing blood pressure.
A recent study claims that the impact of sugar on blood pressure is more significant than the impact of salt. Photo: AFP/Istock
The US paper, published in July 2016, claims that the impact of sugar on blood pressure is more significant than the impact of salt.
It also curiously suggests that a diet high in salt may help improve the uptake of glucose in bodies with insulin resistance by provoking an increase in the GLUT-1 and GLUT-4 proteins (GLUT stands for GLUcose Transporters) – these proteins help to scrub glucose from blood.
This theory may or may not be a valid addition to the existing advice that consumption of sugar leads to HBP due to its effect on obesity – a lot will depend on new research.
Over-consumption of high-calorie foods of any kind generally leads to obesity – and obesity is strongly linked with HBP.
The principal reason is obvious – a higher body mass needs more blood vessels to service more (fat) tissue, resulting in the heart having to pump harder to cover the increased areas of the body.
Additionally, there may be a vicious circle effect as fat-based substances are likely to clog up the arteries, especially when they are damaged by HBP – and this constriction of the blood vessels in turn requires the heart to pump even harder.
* Don’t forget stress
Stress is one of the more significant internal causes of HBP. A body under stress will be over-producing hormones such as adrenaline and cortisol – adrenaline directly causes an increase in the heart rate and blood pressure as it primes the body for physical action, while cortisol increases blood sugar and prevents cells from losing sodium, again in anticipation of some demanding exigency.
Prolonged exposure to stress can cause a body to become desensitised to insulin due to long periods of high glucose levels – and the increased heart rate and blood pressure may eventually damage arterial walls.
Damaged arterial walls are usually plugged by a fat-based plaque known as atheroma and if this is not checked, it will lead directly to arteriosclerosis and further HBP.
* Other factors
Some other factors which cause HBP are kidney disease (which affect the body’s ability to remove excess water from blood), pregnancy (for obvious reasons), and deleterious compounds such as cigarette smoke, environmental pollutants, trans-fats, cooking by-products, recreational drugs, et cetera (due to their ability to damage organs and affect the heart rate, hormone production, and other body functions).
Highly significant too would be genetics where lifestyle changes would not be effective in reducing HBP.
Another factor is also the lack of exercise – this may be because exercise helps the body to reduce fat and improve muscle tone and not doing enough exercise is a contributory cause of obesity and poor blood circulation.
There will be some notes about the options for managing risk factors leading to HBP and some odd facts in the next section.