As a reminder, like all the other Filters discussed (i.e. the instincts, behavioral preferences, default ways of interpreting our environment and the way we interact with it, etc.), the Engagement Formation Personality Spectrum Ensemble, is not at all likely to be understood as a trait solely via the expression of one gene. Rather, multiple genes, in concert with multiple other filters are likely necessary to understand completely the Engagement Formation Ensemble. It is the result of an ensemble of components - their presence and their expressions. Including the environment itself.

Specifically, increasing evidence suggests that varied susceptibilities to bipolar mood disorders are genetically heterogeneous. ConserveLiberty suggests that such findings would be expected for bipolar mood disorders (or more generally engagement formation).

Recurrence risk data are also consistent with monogenic inheritance of bipolar tendencies in a proportion of people with various identified types of bipolar disorders, but with different alleles for different families.

Which is exactly what a "system composed of an ensemble of parts" means.

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As would be expected for the mechanism of action generating something as complex as behavior, perception, and mood, many components are required for the assembled system. Just like something as complex as the engine of a car. The individual contributions of each of the components of the Engagement Formation Ensemble are apparently small. When genetic variations occur that alone would significantly alter the functioning of the Ensemble, often these mutations can be compensated for by other components that are around. In addition, the role of environment appears to play an even larger role with the expression of "Mood" than other of the Ensembles dealt with earlier (e.g. Reality Discernment, Habit Formation.)

Thus, except for a very few gene products, it has been difficult to identify many of the actual players in the "Formation of Engagement and Withdrawal".

In addition, it is quite evident that people are generally endowed with a "Mood Range Profile" that appears somewhat consistent over intermediate periods (1-5 years) although these profiles often evolve over longer periods, and eventually become somewhat constant after late adolescence / early adulthood. All of us who are old enough have observed this with almost everyone we know. It is as if we are born with "default behavioral instincts," and each of us seem a little bit different from everyone else. Some slightly so. Others dramatically so.

It appears it is only a small percentage of us who experience changes in our "Mood Range Profile" that are more dramatic than what is observed as "usual" among the others we know. Or, that the "Mood Range Profile" becomes "noisy", with dramatic ups and downs over unusually shorter spans of time. These may not be picked up as "unusually obvious or different from normal" when they are happening in youth, since we all are aware that youth go through expected "Mood Range Profile" changes as a consequence of maturation, and especially as a consequence of the developmental changes going on during adolescence. However, if these "high magnitude" and/or "high frequency" changes continue on into adulthood, and present with clinically significant impact, we then find that many of these remaining individuals are diagnosed with "depression", "hypomania", or bipolar disorders.

Instincts - Urges that "come naturally", with no learning required after birth in order for them to emerge naturally when the time is right.

Of course, other behaviors are learned. Do individuals have cognitive, biological machinery that identifies which learned behaviors should be embraced and maintained? And, to what degree are we able to modulate behaviors or mood dispositions which have an instinctual foundation?

Learned behaviors - those not implemented through genetic programming as natural instincts (present or latently present from birth or before)

It is therefore important for anyone wanting to:

• maintain an enhanced ability for adaptive decision making and action taking, and
• avoid moods that may be both difficult to execute productively and unhealthy (or lethal)

... to understand how Engagement Formation occurs, and to avoid moods with behaviors that are otherwise not desired.

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A few identified genetic components impacting Engagement have been identified, and thus are candidates as part of the Engagement Formation Personality Spectrum Ensemble. Selected links to representative research on these and others will be added in subsequent versions of this chapter:

• Ca_v1.2 - Calcium channel, voltage-dependent, L type, alpha 1C subunit (CACNA1C) - in humans is encoded by the CACNA1C gene. This gene encodes an alpha-1 subunit of a voltage-dependent calcium channel. Calcium channels mediate the influx of calcium ions into the cell upon membrane polarization.
  
• TENM4 - Teneurin transmembrane protein 4 (ODZ4) - Expressed by a subset of neurons as well as at sites of pattern formation and morphogenesis. ODZ4 appears to play a central role in the regulation of neuronal and synaptic connectivity.
  
  
• Neurocan - Neurocan core protein (NCAN) - in humans is encoded by the NCAN gene. It is thought to be involved in the modulation of cell adhesion and migration, and is a significant component of the extracellular matrix. It was found that NCAN genotype was strongly associated with manic symptoms in humans but not with depressive symptoms. In mice, the absence of functional Neurocan resulted in a variety of manic-like behaviors, which could be normalized by administering lithium.
  
  
• Genetics of bipolar disorder, The Application of Clinical Genetics, 2014 Feb 12; 7: 33-42; Berit Kerner

→ The Section above was last updated 30 Dec 2016 13:00 PST ←

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