Organisational structure
The organisational structure embraces every cell in the body unless a tissue has been put beyond control by, for instance, fibrosis. Otherwise, no matrix can operate independently: that is the integral part of their definition. In traditional medicine, the organs are so named because they are seen as the operating centres for metabolic organisation; in modern medicine, the organs constitute the vital means for life to continue. So much is common sense: ancient observation is supported by modern understanding of the incessant need of every tissue for oxygenation. Here the heart and lungs play a primary role and provide a stable and constant environment for metabolic management to proceed. Failure of oxygen supply, as everybody knows, becomes critical within minutes. The hourly needs are maintained by the liver and kidney, and the at least daily need for fluid management and excretion provided by the skin and kidney.
It is to the longer term organisational structures (though still constrained by circadian rhythms) that medicinal plants contribute their most penetrative and lasting effects. These structures are primarily neuroendocrine, though they must necessarily depend in turn upon the presiding catalytic matrix without which oxygenation itself would be impossible. These neuroendocrine structures dominate the characteristic responses of an individual. This output and outlook—the behaviour of life—is primarily congregated in the hypothalamus. So it is in intrauterine life and this output is relayed to the developing foetus by the pituitary which is itself a bridge between ectoderm and mesoderm. With the later extrauterine development, when the calcification of the skeleton nears completion, the thalamic mind (see later in this section) matures and starts to inform the emerging self–consciousness. The latter comes to dominate or even constitute our lives while, so far as processing power is concerned, the obverse is actually the case: our thalamic self is that on which who we think we are actually sits.
The mobilising behavioural structures are interactive with each other and with their analogues in the peripheral tissues. These are aminergic networks in the central nervous system: based upon dopamine, adrenaline, noradrenaline, histamine and their interactions in turn with diffuse cholinergic networks. It makes little sense to try to extricate the disposition of the Autonomic Nervous System of an individual from these aminergic and cholinergic fields. Serotonin is another central amine that is crucial to the regulation of resource command, and secondarily of mood. Though crucial to central regulation, it is quantitatively more expressed in peripheral tissues, notably the retina, blood and small intestine. The precursor tryptophan needs the B–vitamins and an adequate dietary source. Dietary supply of the other amino acids, especially tyrosine and histidine needs also to be considered. Besides these biogenic amines, there are numerous peptides and amino acids with profound regulatory effects upon mood, behaviour, digestion and thought.
There are hypothalamic hormones or factors which are released in pulsatile fashion58 and at least some of them have been shown to be entrained by the cells of the SCN in the hypothalamus, the final locus of circadian patterning. These factors regulate pituitary function in their four axes (two catabolic, two anabolic). Thus, Corticotrophic–Releasing–Factor (CRF) wakes up the adrenal axis which has a permissive effect upon its target organ and thus secondarily upon other organs and tissues. Gonadotrophin–Releasing–Hormone (GN–RH) initiates the release of FSH & LH. The Somatotrophic axis is more complex as it involves mammatrophes and somatotrophes as well as inhibitory hormones in the pituitary. Growth–Hormone–Releasing–Hormone (GH–RH) has that self-styled effect but is modified by Somatomedin. TRH stimulates TSH which in turn initiates the eventual discharge of the thyroid hormones from the gland but also stimulates and mobilises Prolactin. As is well known, this latter hormone is in reciprocal tonic inhibition with an inhibiting factor, mostly Dopamine. Yet there are different Dopamine networks and at least six different receptors for this hormone–transmitter, so it is important not to use plants to modify either Prolactin or Dopamine indiscriminately.
The probable configuration of all four axes must be viewed in each patient with respect not only to their target endocrine organs but also the exocrine products of the pancreas, liver, small intestine and the fat deposits themselves. Of course, the current state means very little without reference to historical, developmental and initial states.
An important modifier of the current hormonal state of the patient, with all its symptomatology, is the relative dominance of each of the two posterior pituitary hormones, namely oxytocin and anti–diuretic–hormone (ADH), that I like to call the intensifiers. These are both nano-peptides with the same amino acid (cysteine) at positions 1 and 6 joined by a disulphide bridge and which differ only at positions 3 and 8. They are secreted by nerve endings. Oxytocin amplifies pleasure and pain: as an intensifier of experience you might expect it to be associated with responsiveness and emotivity. Like the amines, it is widely distributed and is also found in neurones that project to other parts of the brain and spinal cord. Its peripheral activity is gonadic in both sexes as well, notably in the nipple and areola; its function in sex, childbirth and the ejection of milk is well documented.
While doubtless there is some congruence between these two intensifiers, the secretion of ADH is more phasic: the discovery of ADH receptors in the Supra Chiasmatic Nuclei emphasises the connections of the circadian pulse to renal function, phasing of micturition and the maintenance of a constant internal milieu. Thus ADH (vasopressin in the US and sometimes AVP for arginine vasopressin) has more to do with maintenance of osmolality and cardiovascular status than with responsiveness, although the polyuria with small volume (that may show up in someone whose reactivity is controlled and dampened internally) may owe much to an ADH as strong as their oxytocin. When it comes to the micturition habits of our patients, we cannot think of ADH in isolation but have also to consider the kidney, renin/angiotensin and the bearing of ACTH on aldosterone. According to Duraffourd's model of the horizontal pulse through the pituitary gland itself, ADH relaunches ACTH on its next round of hormonal golf.59 Strongly corroborative of this idea is the fact that corticotrophin–releasing–factor (CRF) and ADH are both released from the median eminence (within the hypophyseal portal system connecting the hypothalamus with the pituitary) and act together to release ACTH.
Put more briefly and simply, these two hormones reflect the two opposite requirements of circadian life: to react to random events for reasons of survival and to ignore them for reasons of conservation of energy and homeostasis. My own hunch based upon what I hope is an educated guess, is that while ADH is bound by the normal negative feedback system, oxytocin is more coupled with unusual events which makes it more autonomous: by acting upon tissue that has been primed by the steroid hormones of the gonadic axis, oxytocin is capable of switching for short bursts to positive feedback, ever–tightening the loop, until it pops. Such a switch is known to occur in the prelude to ovulation. Oxytocin is of course essential to the normal delivery of a child at the end of pregnancy and is probably associated with orgasm in both sexes and post–coital sperm transport through the womb and fallopian tubes. While these amines are clearly implicated in human behaviour, the complexity of the interrelations between them should deter us from falling into a facile hormonal behaviourism. The following table (which is reproduced from a paper by Christian Duraffourd) highlights some critical relationships between the hypothalamus and the periphery.
The clinical significance of these hormones will not be lost on herbalists as a good number of medicinal plants are oxytocic while others are anti–oxytocic. While very few influence ADH directly, there are those that inhibit mineralocorticoid activity and diminish hypothalamic stimulation of the pituitary. It is well known that many plants are oestrogenic