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Can vMEMES cause Clinical Depression..?

Updated: 24 January 2019

The Gravesian approach lies at the core of Integrated SocioPsychology. The following is a plea to psychiatrists, clinical psychologists, mental health workers and those involved in research into various areas of psychopathology to examine rigorously Clare W Graves research with a view to its implications for mental health conditions.

There are literally millions of people whose suffering could be alleviated if we understood more of the psychological processes underlying it.

There are a multiplicity of reasons why the work of Clare W Graves (1970, 1971b/2002, 1978/2005) needs to be taken up much more comprehensively by the academic communities and investigated rigorously for its validity. (Which will result in a much higher profile and wider acceptance of his theory.)

One of these reasons, I propose, is the applicability to mental health of the Gravesian approach. Strangely enough, for all the many champions of Graves’ work and the Spiral Dynamics ‘build’ developed by Don Beck & Chris Cowan (1996), little has been said about the relationship between Graves’ Spiral of motivational systems (vMEMES) and psychological disorders.

Although my plea is for research into the Gravesian approach related to all forms of mental illness, in this piece I will be focusing primarily on Clinical Depression.

There are thousands of research projects to be undertaken and hundreds of books to be written to apply the arguments I will put forward not only to Depression but many other forms of psychological disorder. However, the limitations of space and time – plus, to some extent, my own expertise – mean we shall restrict ourselves primarily to Depression in this piece.

So…can vMEMES cause Clinical Depression (aka Unipolar Disorder or Major Depression)? Since vMEMES are the neurological systems which motivate us according to the life conditions we experience in both our internal and external environments, the answer per se has to be ‘No’. However, by putting together certain pieces of evidence, it is possible to see how certain vMEMES in certain conditions could dispose some of us to Depression.

Generally these days the principal approach to psychological illness – as well as many physiological illnesses – is to view such conditions as the result of a Diathesis-Stress interaction. ‘Diathesis’ is the predisposition to develop the condition. ‘Stress’ means environmental and/or behavioural factors which trigger the onset of the condition. Effectively epigenetic modification. The concept of a genetic predisposition to certain physiological illnesses such as heart disease and cancer has been accepted in the medical professions for a number of decades, with interventions being made through such domains as diet and exercise to minimise the likelihood of the environmental triggers for the onset of the illness being fired.

The Diathesis-Stress model was first applied to psychological disorders by Joseph Zubin & Bonnie Spring (1977) in attempting to understand how Schizophrenia develops. The diathesis can lie in abnormalities in brain structures and/or too high or too low levels of neurotransmitters such as dopamine, GABA, serotonin and noradrenaline. There is increasing evidence that, in many cases, the underlying cause of such abnormalities is genetic in nature. As we shall see, for women, in particular, fluctuations in hormones can have devastating effects on mood. A stress factor could be lifestyle – eg: cannabis use has become increasingly identified with the development of Schizophrenia – see the Blog: Time to turn against Cannabis! – or a specific event – eg: the sudden death of your partner/spouse.

How much the onset of a condition will be due to Diathesis and how much to Stress will depend on the particular psychological disorder and in any case will vary widely from individual case to individual case. Certainly some individuals seem to experience the onset of a condition purely from stress factors; while having a diathesis for a condition, in most cases, by no means dooms someone to develop that condition.

It is reasonable to assume that vMEMES are part of the complex Diathesis-Stress interactions. Since the crux of the Gravesian approach is the interaction between the internal coping mechanism (vMEME) and the life conditions (what’s going on) in the environment (internal or external), it fits the Diathesis-Stress frame rather well.

Biological diatheses
Major/Clinical Depression has tended to be termed either Endogenous – ie: it comes from within; so it is primarily due to the diathesis factor – or Reactive – ie: the condition is the response to stressing environmental factors. ‘Endogenous’ and ‘reactive’ are no longer used in the West as ‘either/or’ clinical categorisations . However, they they are used in discussion and analysis and are treated as poles on a continuum along which they depressed client may locate in the Diathesis-Stress interaction.

The concordance rates for Major Depression tend consistently to show a strong genetic component in the illness. For example, M G Allen’s widely-respected 1976 study found mean concordance rates of monozygotic (from the same egg; 100% the same genes) twins suffering from Major Depression to be 40% while the rate for dizygotic (from 2 separate eggs; 50% the same genes) twins was only  11%. Thus, the theory states, the more genes in common with somebody with Depression, the more likely you are to develop the illness yourself. Nonetheless, Major Depression still tends to have the lowest concordance rates of the serious mental illnesses. Allen found Depression’s rather ugly cousin, Bipolar Disorder, to have a monozygotic twin concordance rate of 72%. Thus, if one identical twin develops Bipolar, according to Allen, there’s a statistical probability of 72% the other will develop it. With Major Depression, the other twin becoming similarly depressed is more of a significant possibility than an outright probability – down to 40%.

So the Diathesis effect in Major Depression is important – particularly for those who suffer from purely Endogenous Depression! – but the ability to cope with the stressing factors is perhaps more important in the majority of cases. That ability to cope results from a mix of endogenous, motivational and learned factors.

There is undoubtedly a genetic element in many instances of Depression. Recent research by Alexander Neumeister, Dennis Charney & Wayne Drevets (2004) from the US National Institutes of Mental Health suggests that tryptophan depletion unmasks an inborn trait – the essential amino acid tryptophan being the chemical precursor for the generation of serotonin. Lowered serotonin levels, which have been associated with Major Depression for many years, affect emotion-regulating circuitry involving the anterior cingulate cortex, thalamus, hypothalamus, ventral striatum and orbitofrontal cortex. Essentially this means that some people are unable to extract enough tryptophan from what they digest to form sufficient serotonin to keep these neural networks functioning effectively. Since monoamine oxidase (MAO) enzymes at the synapse break down serotonin, there is a need to build up new supplies regularly of this neurotransmitter. People who have difficulty naturally in processing tryptophan, therefore, are at a major disadvantage. Alan Ogilvie et al (1996) found a significant number of depressives had a shorter SERT gene, meaning their ability to manufacture serotonin transporter proteins was more limited, thus hindering their ability to increase serotonin levels. John Mann et al (1996) confirm impaired serotonergic transmission in people with Depression.

Keeping with the notion that MAOs break down serotonin, there is, unfortunately for a number of women, a gender bias in the way Depression often works. The levels of the hormone oestregen decrease (as progesterone increases) as a part of the menstrual cycle. High levels of oestregen help inhibit this breakdown or ‘reuptake’ of serotonin. (Monoamine oxidase inhibitors (MAOIs), such as Rivvol, and serotonin specific reuptake inhibitors (SSRIs), like Prozac, are used as anti-depressant drugs because they have the same effect.) When oestregen levels drop in the approach to menses, MAOs are less inhibited in their breakdown of serotonin – and this is thought to be a key contributing factor to PreMenstrual Syndrome (PMS) and the depressed mood of many women 2-3 days before and after the commencement of their periods.

Lowered oestregen levels and, thereby, lowered serotonin levels may well be a principal contributing factor as to why twice as many women as men are diagnosed with Depression in the Western world. It may also help explain why more women are ‘chocoholics’ with a preference for milk chocolate. Tryptophan is abundant in milk; and milk is used plentifully in the production of milk chocolate. Effectively: eat milk chocolate and boost your serotonin levels!

While approximately 75% of women experience some degree of PMS on a regular basis, by no means do all of them experience depressive symptoms to the levels required for a DSM diagnosis of Depression. So there must be other factors involved – biological, behavioural or environmental.

There may, in fact, be a double whammy for women when it comes to serotonin as there is some evidence female brains are less effective at manufacturing serotonin anyway.  According to Mirko Diksic & Sadahiko Nishizawa (reported in Ellen Leibeluft, 1998), male brains are up to 52% better at synthesising serotonin.

However, the role of serotonin, a neuromodulator for dopamine and noradrenaline levels, in Depression is far from being clear cut. John Mann, Victoria Arango & Mark Underwood (1990) have associated lower levels of serotonin with aggression as well as Depression – see Biological Factors in Crime.  – in which case, serotonin cannot be the sole causal factor. In any case, Patricia Teuting, Stephen Koslow & Robert HIrschfield (1981) were just the first set of a slew of researchers to find lowered levels of noradrenaline as well as low serotonin in depressives. Pedro Delgado (2000) has even questioned whether low levels of neurotransmitter are a cause of Depression or whether, in fact, Depression reduces neurotransmitter levels.

Returning to brain structure, the great Anglo-German psychologist Hans J Eysenck (1967) certainly saw parts of the brain as determining natural temperament. On his Dimensions of Temperament model, people high in Introversion (due to overstimulation of the cortex by the ascending reticular activating system) and high in Neuroticism (as a result of a very reactive amygdala) will be Melancholic personalities. Such people will tend to easily become anxious, moody pessimistic and unhappy. Clearly a natural diathesis!

While it is far from being unambiguous just how biological factors influence Depression, obviously there are people with the endogenous potential to become depressed; and it would appear women are more at risk. Thankfully most people will need some form of stress factor for Depression to take hold.

But what have these biological diatheses got to do with the Gravesian approach? you may ask. One way to answer that is by using the 4Q/8L  framework Don Beck (2000b, 2002b) developed from the All Quadrants/All Levels concepts (1996) of Ken Wilber .

The Upper Quadrants in this schematic represent ‘I’. The Lower Quadrants represent the external world – including ‘We’ – in which ‘I’ operates. The Upper Right represents the functioning of the biological mechanisms which manifest themselves as what we call ‘mind’ in the Upper Left. Thus, the vMEMES of the Upper Left, which enable us to cope with the external world of the Lower Quadrants, are dependent on the effective functioning of the biological mechanisms of the Upper Left.

So biological malfunctioning – preferences, even – in the Upper Right will affect our ability to develop coping systems (vMEMES) in the Upper Left. And that could make us very vulnerable indeed!

4Q/8L immediately demonstrates how complex the Diathesis-Stress relationship is – the Upper Right impacting upon the Upper Left’s ability to cope with life – the Lower Quadrants. Robert Dilts’ Neurological Levels (1990) construct provides us with a model for how changes at the levels of Identity and Values & Beliefs should drive changes in Skills & Knowledge and Behaviour as the Environment (internal and/or external) changes – life conditions. If change in the life conditions requires a vMEMETIC shift in response and the individual cannot make that shift because of biological restrictions/preferences in the Upper Right Quadrant, almost by definition they will be unable to cope with their life conditions.

Not being able to cope causes stress and anxiety and, if prolonged, can lead to Depression.

A frequent cry of the ‘Depressed’ is: “I can’t cope!”

Cognitive diatheses
So, having established that biologically-determined diatheses can influence both our vulnerability to psychological disorders such as Depression and the capacity to develop vMEMES as coping mechanisms, is it possible for there to be cognitive diatheses?

The answer is – unfortunately, in one sense at least – a resounding ‘Yes’.

Numerous studies over the years have established a link between negative thinking and Depression. For example, back in 1992 Susan Nolen-Hoeksma, Joan Girgus & Martin E P Seligman found that a negative attributional style in older children predicted the development of depressive symptoms in response to stressful life events. Laura Alloy & Lyn Abramson (1999) also found that students with negative thoughts were more at risk of Depression. The link between negative thinking and Depression was demonstrated by Rachel Grazioli & Deborah Terry (2000) in a study in which they assessed the cognitive vulnerability of 65 women in the third trimester of pregnancy and compared that assessment with which of the women suffered Post-natal Depression. Those with high levels of negative thinking were more likely to suffer Post-natal Depression.

However, a meta-analysis by Zindel Segal & Rick Ingrams (1999) of studies into cognitive vulnerability found no significant differences between those who were depressed and those who had recovered from Depression. Again this indicates the difficulty in trying to ascertain specific causal factors.

With regard to locus of control and situational/dispositional attributions, it seems that having an external locus for success and an internal locus for failure predisposes people to having a vulnerability to Depression. J H Yost & Giff Weary (1996) compared 58 depressed and 57 non-depressed university students on a standard correspondent inference task. The depressed students  had much less of a tendency to make internal attributions. This, Yost & Weary suggest, is because depressed persons are significantly more likely to use an external reference meta-programme in which they see their choices as dictated by others or by circumstances.. Correspondingly, Terri Wall & Jeffrey Hayes (2000) assessed  Depression and attributional style in 160 clients of a university counselling service. They found that the depressed clients tended to make internal attributions for anything that went wrong in their own lives. As ‘cool’ self-sacrifice vMEMES tend to drive external referencing and attribute internal failure to conform or obey for problems, clearly these systems have a part to play in depressive negative thinking.

From the work of Lynn Abramson, Martin E P Seligman & John Teasedale

From the work of Lynn Abramson, Martin E P Seligman & John Teasedale – graphic copyright © 2001 Psychology Press Ltd

That fits with the negative version of the Cognitive Triad – developed by Aaron T Beck et al (1979) from the work of Lyn Abramson, Martin E P Seligman & John Teasdale (1978) – which depicts thinking patterns that create a cognitive diathesis for  Depression. All that’s needed is the stress trigger.

For a number of years now those who study Neuro-Linguistic Programming (NLP) have looked at the effects of  unhealthy or limiting beliefs about yourself have in contributing to anxiety and Depression by reducing your self-efficacy. This is Albert Bandura’s (1977) term for belief in one’s ability to acquire and use (the neurological level of) Skills & Knowledge – which leads us back to coping or not and the potential for Depression that not being able to cope can create.

The Meta-States model (1995) of L Michael Hall has been particularly informative in understanding how individuals – and sometimes groups! – interpret sensory information through the filters of our Values & Beliefs and the memories which support them, creating a cognitive bias. Meaning is applied to sensory input; but then that meaning is itself interpreted to produce a new level of meaning (or meta-state) which is then interpreted again to produce yet another level of meaning – a further meta-state – and so on.

It needs to be stated here that, in meta-stating on sensory input, that input can come from within as well as without. So, for example, a meta-stating pattern might be triggered by a look someone gives you or it could be triggered by feelings of queasiness in your stomach.

NLPers now take this as a substantial step in explaining how we develop healthy and unhealthy beliefs (schemas). However, it also ties in to Fergus Craik & Robert Lockhart’s Levels of Processing Theory (1972) which states that the more meaning we apply to something, the stronger the memory of it. The stronger a memory, the more it will influence us. So we end up with meta-stating patterns that influence meta-stating patterns that influence meta-stating patterns..and so on. Once we have a depressive schema, it will tend to drive us towards Depression.

Working through the Cognitive Triad that we can start to see how vMEMES will influence the creation of meta-states.

  • Internal/External: do I attribute the cause of events to myself or others? This is critical. We need to ask the question: which vMEMES attribute success to me or to others and which attribute failure to me or to others and in what circumstances? For instance, RED credits itself with success as evidence of its powerfulness but blames others when things go wrong. BLUE credits success with having external expectations to comply with – ‘doing the right thing’ – and things going wrong with internal failure to comply with those external expectations.
  • Timeless/Timebound: is the situation permanent or does it have a time limitation on it? vMEMES may influence here. For example, PURPLE tends to look back to the past from the present, RED has little or no sense of time, while BLUE and beyond tend to have a future focus.
  • Global/Specific: does the state apply to a wide range of situations or to one specific instance? Again vMEMES may influence. For example, BLUE tends to be concerned with little details whereas GREEN is very much about bigger picture views.

If we accept the proposition that we go through the Cognitive Triad at each level of meta-stating, then the dominant vMEME(S) will influence – especially in terms of whether we attribute success to ourselves or to others and whether we attribute failure to ourselves or to others.

Aaron T Beck (1967) identified that people with depressive schemas attribute failure to themselves and success to external factors,. He asserts that this is due to a ‘negative self-schema’. This is a set of beliefs and expectations about self that are essentially self-blaming and pessimistic and are likely to have been acquired in childhood through  traumatic events and/or negative treatment. Originally a psychoanalyst before he became a cognitive psychiatrist, Beck gives examples such as:-

  • the death of a parent or sibling
  • parental rejection, criticism, overprotection, neglect or abuse
  • being bullied at school or excluded from a peer group

Such experiences would seem most likely to disrupt the PURPLE vMEME’s need for acceptance and safety-in-belonging

It’s also important that Beck states people with depressive schemas tend to view situations as Timeless and Global.

Overall then, it would seem vMEMES, especially on the sacrifice-self/conformity side of the Spiral which look to others for success, can indeed, through their attributional style, contribute to Depression.

Continue…

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