Why it takes so long to break down the regulation of the major homeostatic mechanisms

First off: an admission. It may be possible that BP is always appropriate, except in hypertensive crisis. Why? Because of so many push-pull mechanisms used to balance it.

But more likely, it does not take a long time, as a level two physical health exam would show.

But the short answer to the question is that there are so many push-pull regulatory systems to keep us in balance. When one effector gets unbalanced, say by nutrient deficiency, another corrects it back into balance. Consider BP: there are major effectors in the baroreceptors, the pituitary/hypothalamus, the thyroid, the adrenals, the kidneys, and of course the moment by moment effects of mental states, conscious and unconscious, mediated by the autonomic nervous system. How difficult it is to throw such a multiply balanced system off! How messed up must one be to throw it out of balance at a relatively young age!

One way to unbalance a key regulatory system is to have a spontaneously “irreversible” event. A tumor growing in the adrenals can constitutively overproduce aldosterone. The normal feedback that rebalances any hyperaldosteronism is a reduction in the rate of production of the hormone. The growing tumor blocks that avenue. Consequently, without removing the tumor, there is no rebalancing of this event. Long-lived high BP is the expected result. Another “irreversible” event – stiffening of the arteries reduces the stretching per unit BP. The CNS ends up “permanently” resetting the BP to a higher level in response to an incorrect reading of the true arterial pressure in the aorta and/or carotids. The set point has changed. The other regulatory systems will equilibrate the BP to the new set point.

Of course neither tumors nor artery stiffenings are completely “irreversible,” and “irreversibility” is always “irreversible with present technology.”

Nutrients are subject to competitive grabbing, with the most important systems getting first dibs. This means that the least important systems may begin to show deficiencies quickly. These least important systems inevitably include sub-systems of important regulatory systems and sub-systems of less important regulatory systems, which relay information to the more important systems.

However, these nutrient deficiencies are compensated for by drawing on stores, by making substitutions, and by making major changes in gene expression patterns. When a nutrient is deficient, the body makes two major adaptations, requiring de novo gene expression changes:  both the efficiency of absorption of a deficient nutrient is increased and the extent of its excretion is decreased. As always, there is a catch-22. Both of these systems are powered by other nutrients. Consequently, the ability to deal with deficiency in any nutrient is dependent on other nutrients not being deficient. How likely is that?

In addition, where applicable, alternative pathways are activated to shore up the adverse consequences of chronic deficiencies. Is this what is happening as the walls of arteries are thickened? Is it, at least in part, a protective mechanism, executed in response to deficiencies, which created weak spots in vessel walls, as Pauling suggested?

Back to multiple, compensatory difficulties: For example, consider blood pressure regulation again. If someone has a pressure of roughly 120/80, we call him normal. However, all may not be well. A person may have a “normal” BP because he has two or more compensatory problems. For example, mild hypothyroidism coupled with mild hyperaldosteronism [not due to a tumor] or hypercortisolism [also not due to a tumor]. These are things that could be revealed with a detailed level two physical health examination. Molecularly, when long-term nutritional deficiencies have weakened less important subsystems, which feed information, in the form of molecules or nerve impulses, to each of these important systems, things are thrown off a bit, but the major homeostatic systems are still in balance.

However, it may also be true that sometimes the break down in regulation is only apparent. For example, older people whose SBP approximates [Age/2] + 100 are often diagnosed as having high BP, when common sense says they do not – that is the presumptively natural increase in SBP with age. In fact, how often such individuals feel light-headed -a symptom of their pressures being too low- when doctors treat their BP to bring it down to the one-size-fits-all “normal” level of about 120/80.

Note: is the increase in BP with age normal? These authors dispute that, using the “primitive” Yanomamo people as an example. Mancilha-Carvalho JJ, de Oliveira R, Esposito RJ. Blood pressure and electrolyte excretion in the Yanomamo Indians, an isolated population. J Hum Hypertens 1989; 3: 309–314.

So the increase of BP with age may not be normal – however, when treating a patient with 140/90 to bring him down to 120/80, who then complains of light-headedness, perhaps the error is just the “one size fits all” model, when appropriate BP is “personal and specific.”


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