Multiple Sources of Trauma

This chapter addresses:

1. The effects of pre-trauma psychological variables on the formation of a PTS condition
2. Comorbity of chemical dependency and psychological trauma
3. Comorbity of ACA/spousal trauma

Introduction

Literature reviews of the ETM theory for addressing multiple sources of trauma are best directed to 3 subjects: the importance of pre-trauma psychological variables, comorbity of chemical dependency and psychological trauma, consideration of ACA and spouse trauma. These 3 subjects present the preponderance of arguments against the ETM theory for addressing multiple sources of trauma, which tends to run contrary to nosotropically-influenced diagnostic and treatment planning modules.

Before beginning, an overview of our rationales for addressing these 3 subjects might be helpful. Pre-trauma psychological variables are important to the multiple sources of trauma theory because they tend to divert attention from the address of the most recent trauma; treatments begin with the current trauma and then are switched to other problems that existed before the traumatic event. The etiology is not identified and reversed because of the diversion. The literature sheds helpful light on this conflict. Comorbity of chemical dependency and psychological trauma appears to be a classic representation of the chicken-egg (Which came first?) conflict. The literature, however, shows that this appearance is deceptive; there are clear lines of fact and logic that guide professionals through this difficult issue. Lastly, after reaching the age of majority (adulthood), adult children are argued to be attracting into situations that cause additional trauma. For example, adult children are accused of attracting into marriages where the new partner batters the adult child; the battering reminds the adult child of the old days, satisfying a need to return to or in other ways continue them. The problem with this view is that it minimizes the trauma received from the battering, and the etiology resulting from the assaults may not be identified and corrected; this prospect is antithetical to ETM logic, so the conflict between the two ideas must be addressed. They are.

Pre-trauma Psychological Variables

The psychological professions have heretofore focused on pretrauma psychological variables as a prospective cause of PTSD. We believe this focus is actually a challenge to the concept of the existence of the condition. The argument turns on whether pre-trauma psychological variables ("pretrauma psychological variables infers dysfunctional pretrauma variables") exist to the extent that they are responsible for the post-traumatic stress experience. That research is considered here along with the ETM/TRT perspectives of the issue.

Conclusions by leading PTS scholars about the role of pretrauma variables in the formation of a PTS condition are mixed. Scrignar states "research does not indicate a clear-cut relationship between pretraumatic personality and the development of a PTSD" (Scrignar 1988, pg. 148). Van der Kolk states "There is a strong relationship between pre-existing personality factors and chronic PTSD symptomatology" (1987, pg. 12). Both van der Kolk and Scrignar provide reviews of the literature that support their conclusions. Herbert Hendin and Ann Pollinger Haas also address the same and similar data in their book on post-traumatic stress and its effects on Vietnam veterans (1984). We emphasize their description of the data by paraphrasing it in the next several paragraphs because we believe it best explains the contrasting views.

Hendin and Haas explain that at the beginning of the history of the treatment of trauma, the focus was on catharsis, or what Freud called "abreaction." His view was that people suffering trauma needed to pass through the emotional experience accompanying it. When the catharsis itself failed to produce the desired change, Freud shifted the focus to childhood issues, assuming therein lay the deeper cause of the stress reaction (quote Freud, International Universities Press, 1921). Immediately following World War II, two other approaches to therapy continued to explain the stress from war as having its origin in early childhood (sexual) and/or family issues (quote Saul, 1945, Litz, 1946). Saul and Litz identified linkages with childhood histories that provided a prospective cause of the stress other than the combat experience itself. In support of Saul and Litz, Brille and Beebe (1951), found that World War II veterans who became psychiatrically disabled were 6 times more likely to have suffered personality disorders prior to the service. Additional perceptions of preservice predictors of post-traumatic stress came from (quote) Hunter (1978), Yager (1976), Worthington (1978), and Heltzer (1979). A study by Heltzer in 1987 (addressed in a later paragraph) and not included in Hendin and Haas's 1984 publication, supports the idea that preservice (pre-trauma) psychological variables play a role in producing a PTSD.

In contrast, Hendin and Haas show that another group of researchers found data that countervailed the pretrauma variable idea. This data would show that the post-traumatic stress experience was a consequence only of the combat or persecution experience. These studies were not limited to combat veterans, but included the study of trauma's effects on WWII civilian casualties and concentration camp survivors. For example, Leo Eitenger found that 99% of 226 Norwegian citizens held in concentration camps experienced post-trauma disturbances for some years. "Eighty seven percent had persistent nervousness and irritability, 60% had sleep disorders and 52% had continuing nightmares" (Hendin quotes Eitenger, 1969). In Hendin's and Haas's review of Eitenger's study, the two therapists concluded that "the majority of these cases could be diagnosed as suffering from post-traumatic stress" (p. 35). In other words, virtually everyone in the sample suffered post-traumatic stress, thus ruling out the theory that the symptoms relating to the experiences of the traumas were results of earlier personality disturbances; unless, of course, it could have been determined that everyone in the town suffered personality disorders prior to their abductions.

Abram Kardiner, in his work with combat veterans (1947), reached an opposite conclusion from that expressed by Freud, Litz, Saul and Brille. Kardiner found that the stress response was due to the nature of the combat experience. In a study of civilians affected by trauma, Horowitz (1976) concluded that the symptoms are strikingly similar and that almost everyone will report the same experiences given the extent of the traumatic event. In a large study of the consequences of post-traumatic stress, Frederic Hocking (1970) reports: "There was no correlation between the symptoms and the preexisting personality or any other factors in the patient's earlier life." Hocking concluded that pre-existing personality characteristics do little more than determine how long an individual can tolerate the situation before the onset of neurotic symptoms. Thanks to Hendin and Haas for that review.

We have two views about the issue of pre-existing psychological variables as causal or contributing to the development of post-traumatic stress. The first is that post-traumatic stress has been (and still is) minimized. The intrusion from the trauma itself is considerably more profound than is recognized by the first group's analysis of those who do not show symptoms of post-traumatic stress. Specifically, we believe Eitenger's findings are comparable to other groups suffering post-traumatic stress. Thus, most people who have experienced trauma are seriously affected by it. We believe further that studies describing trauma victims as unaffected by the trauma have not adequately accounted for the dissociation (next paragraph) experienced by the trauma victims. Subsequently, the studies do not account for the denial of the trauma and its symptoms. An example is Heltzer's statistical review of post-traumatic stress disorder in a catchment area survey of the general population (Heltzer, et. al. 1987). In this review, the study found that 5 of 965 men suffered post-traumatic stress disorder. Three were wounded Vietnam veterans, 1 was a non wounded Vietnam combat veteran and 1 was a beaten and mugged civilian victim. Others listed (as a part of the 965 man sample) who had experienced trauma included 12 more wounded Vietnam veterans, 28 more Vietnam combat veterans, an additional 68 beaten and mugged people, and an equal number of combat veterans from other wars.

None of this group qualified as suffering post-traumatic stress disorder. There were three interviews, one by questionnaire, one by phone, and one face to face. The statistics were gathered in conjunction with concurrent attempts to identify 40 other psychiatric disorders. As we understand, no consideration was given to denial of the trauma and its symptoms other than through the survey's methodology for acquiring the information; there was a reference to the possibility that some of the symptoms may have been "forgotten." We suggest that it is highly unlikely, if not impossible, for any beaten or mugged person, to complete the life cycle without showing symptoms of post-traumatic stress to someone. The idea that 68 such beaten and mugged people, and another 80 combat veterans, some of whom were even wounded, could be randomly found that had not produced post-traumatic stress symptoms is, for me, beyond the realm of possibility.

In support of our criticism, additional studies are finding that trauma results in dissociation rather than just an anxiety reaction as currently recognized in the DSM-III definition of PTSD. The result, according to Arthur S. Blank, a member of the committee that drew up the original post-traumatic stress diagnosis, is that "In general, the role of dissociation in PTSD has been underestimated." (Bower, 1988). Blank concludes that "the disorder is more difficult to recognize because traumatic memories and emotions are shut out of consciousness and often cannot be talked about by the survivor." Appendix A provides additional literature review (Laufer, 1985, van der Kolk, 1985, 1987) of the problems with PTSD symptom presentation.

We do not believe that the evidence shows that trauma and attendent survival responses are a consequence of pre-existing conditions except as that earlier state, existential and operational components of identity that existed prior to the trauma's occurrence, has been intruded on by the event.

Furthermore, searches for pre-existing variables that contribute or cause the PTS condition are themselves in existence only because the traumas underpinning those conditions were not resolved completely in the first place. In other words, reverse the etiology and pre-existing conditions are irrelevant.

Comorbity: Chemical Dependency and PTSD

This subsection considers chemical dependency-caused trauma. The subsection also addresses comorbity of chemical dependency, chemical dependency-caused trauma, and PTSD resulting from trauma not caused by chemical dependency.

"Chicken or Egg" in PTSD and Substance Abuse

The post-traumatic stress field generally considers drug abuse and alcoholism to be symptoms of stress caused by the underlying post-traumatic stress condition. The literature has not, as a rule, addressed the pathological chemical use experience as a cause of post-traumatic stress, but mostly as an effect (van der Kolk, 1987 quotes Lacousierre). In addition, many summaries of post-traumatic stress symptoms include alcohol and drug abuse at the top of the list. Hendin and Haas (1984) speak directly to the issue of chemical dependency disease treatment vs. post-traumatic stress treatment. As I recall from their text, their view is that the chemical dependency treatment facilities with whom they have had association are so caught up with the disease concept and getting people sober, including the application of their particular modalities, which I presume refers to the Twelve Step programs, that the chemical dependency treatment people miss the underlying post-traumatic stress condition that, in some PTS expert theory, is the cause of the pathological use. Scrignar (1988), the most prolific identifier of PTSD symptoms, on the other hand excludes substance abuse or chemical dependency as a symptom of PTSD.

Kosten and Krystal (1988) make what we believe to be the best neurobiological argument for the PTSD-causes-chemical dependency-view by showing a prospective relationship between the neurobiology of psychological trauma (also reviewed in section 2 -- this appendix) and the neurology of chemical dependency. Generally, that relationship is hypothesized to be a function of a stress (trauma) induced locus ceruleus to hypothalamic pituitary axis activity that overloads opioid receptor functionings until they become desensitized, culminating in the need for exogenous opioid or other alternative receptor binders. Ethanol, although not a receptor-binding oriented drug, has the effect of mollifying the locus ceruleus (noradrenergic) activity by anesthetizing it. Such anesthetic effects are demonstrated in studies on the relationship of noradrenaline and alcohol (quotes Lynch, M., 1983 and Brick, J., 1983). Thus, from Kosten's presentation pathological drug use becomes a biological consequence of PTS.

The most comprehensive review of PTSD and substance abuse studies has been produced by Terence M. Keane, Robert J. Gerardi, Judith A. Lyons, and Jessica Wolfe (1990 -- from now on referenced as "Keane"). Keane reviews the research on Vietnam veterans and substance abuse (Vietnam veterans are the only group of trauma victims for which there is empirical data on the relationship between trauma and substance abuse) and in the context of various substance abuse theories and political mandates for the studies. Generally, Keane finds that the studies are equivocal in determining the trauma/substance abuse relationship. Some of this equivocation is a function of methodological problems with the studies; Boscarino (1981) and others are quoted. Where Boscarino believed the data demonstrated a statistical link between combat and substance abuse, Keane demonstrates that no such conclusion could be reached based on this data. Some equivocation is a function of contradicting views. For example, Egendorf (1981) shows a prospective relationship between combat and substance abuse while Heltzer (1984) is shown by Keane to produce the opposite by representing no linkage between combat and the abuse, but showing possible linkage between the abuse and preservice factors.

Keane does establish, however, an absolute relationship existing between heavy substance abuse problems and those veterans seeking treatment in VA inpatient facilities. That is, between 63 to 80 percent of presentments (Sierles, 1983, Keane, 1983, and Keane pg. 43) at VA facilities are suffering substantial substance abuse problems. Keane recommends that to fully understand what he calls this "chicken and egg" (pg. 44) and prospectively "dual disorder patient" controversy, studies need to be made of non or social chemical use PTSD sufferers as it "clearly is impossible to study PTSD when it is accompanied by substance abuse."

Edgar Nace (1988) is more specific about the relationship of PTSD and substance abuse when considered from a remedial perspective. Nace points out that both chemical dependency (quote Galanter, M., 1982, and Moore, R., 1972) and PTSD (Blank, A., 1985) are not as a rule diagnosed by the psychiatric profession. Nace includes a number of other references, statistics, and prospective rationales supporting the idea underlying this failure by the treatment community (pg. 10).

In support of the ETM approach to identifying both issues, Nace presents assessment criteria that closely parallels the ETM model. Moreover, because of the proclivity to deny both variables as problem issues, the assessment process is continued into and through the treatment experience. Nace is also unequivocal that the substance abuse needs to be addressed first, via abstinence and possibly a more confrontive therapy, and the PTSD addressed later with "a carefully timed titration of affect" pg. 24. Nace does not in this article, however, identify psychological trauma, that is, the 4 psychological trauma patterns described in the TRT and ETM models, as a specific consequence of the pathological chemical use.

The "Skewed" Effect

In his book A Natural History of Alcoholism, (1982) George Vaillant followed the lives of over 600 people for 45 years (he did not conduct the data accumulation himself, but appraised the data from studies begun before he became involved with the project). Vaillant's idea prior to beginning the interpretations of the data was that psychological variables would be found that predicted alcoholism. He reported that he was "surprised" to find that no such predicting variables existed (ABC interview, 1987). One of his conclusions was that attempts to determine true psychological traits as opposed to those appearing after the onset of the alcoholism is like looking into a pool of water and attempting to detect the true location and size of a fish that is swimming below the surface. The nature of the light's reflections in the water skewed the actual location and size of the fish and make true identification of location and size impossible.

We believe the "skewed" perspective by Vaillant is one of the best bodies of research supporting the TRT four patterns theory as it is extrapolated to people affected by psychological trauma caused by chemical dependency. That is, the information supports the idea that pre-pathological chemical use psychological personality traits and variables are different than post-pathological use traits and variables, which we hypothesize to be the first and third psychological trauma patterns; respectively, the first pattern evolves from toxic thoughts and behaviors that contradict existential identity (pre-trauma personality traits and variables) and the third pattern evolves from survival responses that contradict existential identity. Moreover, the finding that pre-trauma, pre-pathological chemical use, variables are no more identifiable (abnormal) in this population than in non pathological chemical users (controls), gives evidence that there is something (values, beliefs, images and reality) to contradict during the onslaught of the pathological chemical use.

Biology of Alcohol Use as a Cause of the
Four Psychological Trauma Patterns
(Cause of Dissociation)

If there is substance to Vaillant's findings (described in the preceding paragraph) and our proposal that the pathological use provides its own intervention upon the pre-use psychology and that the pathological use culminates in contradictions to existential identity and the subsequent development of defenses, that is, survival responses (the third psychological trauma pattern), then there must be an explanation for how intrabiological influences bring about the original (from the pathological use) prospective psychological changes, and a body of evidence that supports the explanation. In fact, we have found a number of comprehensive works that offer substantial insights into different aspects (and specifics) of the biology of chemical dependency and its influences on neuropsychology and behavior. They include: The Molecular Pathology of Alcoholism (1991) by Palmer, "Biochemical Basis of Alcoholism: Statements and Hypotheses of Present Research" (1985) by Topel, The International Handbook of Addiction Behavior (1991) by Glass, "Hepatic Encephalopathy Coexistent with Alcoholism" (1991) by Tarter, Arria, and Van Thiel, "Neurohormonal Basis of Alcoholism" (1990), S. Parvez, H. Ollat, I Nevo, Y. Burov, and H. Parvez, and "Ethanol and Neuromodulator Interactions: A Cascade Model of Reward" (1990) by Blume and Kozlowski).

Referring to these and other works, this section will review:

1. The effects of alcohol use induced physical/molecular trauma upon brain functionings with an eye toward the influence of the damage on thought and behavior.
2. The effects of alcoholism induced physical/molecular trauma to liver functioning on neurological processes and subsequent thought and behavior.
3. "Alcohol" is the most used drug and the one having the most far reaching effects. For purposes of saving space, we explain through our overview method alcohol's influences -- referencing where to find the other drug effects like opioids/cocaine, which have similar and dissimilar biological influences, and which are pronounced in their own right.

Biological Effects of Alcohol Use-Caused Trauma
on Neuropsychology -- Outcome on Thought and Behavior

Psychological trauma resulting from the direct interaction of chemical use on brain physiology is a function of physical trauma upon and subsequent exogenously induced change to neuronal structure and functioning, the net effect of which is dissociation of the psychology that provides ongoing management for the organism.

For purposes of simplification, Littleton (1991) provides a restricted explanation for some of the molecular factors underlying intoxication, tolerance, and dependence. Through focus on these 3 processes, dissociative neuropsychological effects spawned by the biological processes are apparent.

Littleton, accompanied by disclaimers about his attempt to simplify these issues, explains that alcohol has both anxiolytic and anesthetic effects on the central nervous system. Anxiolytic is thought to be a positive reinforcer during the initial level of intoxication and the anesthetic effect is less positively reinforcive; numbing and incapacitation occur to the degree that there is loss of control. These two effects are then described as components of intoxication, the molecular basis of which (Littleton's explanation) is the subject of the next 2 paragraphs.

Anxiolytic effects occur as a function of ethanol's influence on the electrical component of the charge; most specifically, ethanol affects GABAergic neuronal processes -- the principal CNS neuronal structures responsible for inhibitory activity. GABA neurotransmitters bind on GABA receptors and then open Cl- ion channels that allow the Cl- ions to cross the membrane. Cl- ions inhibit the neuron's movement toward the action potential, which inhibition provides for a reduction in the prospects for action potentials to be transmitted along the membrane -- excitability is reduced. When alcohol enters the area around the GABA synapse, it interferes with the GABA (A) receptor functions, resulting in the continued opening of the Cl- channels and an increase in the amount of Cl- ions to flow across the membrane, increasing the likehood of inhibition of the neuron. The net effect is reduction in neuronal excitability; the neuron inhibited by the affected GABA receptors results in fewer action potentials -- the anxiolytic component of intoxication.

The anesthetic component of intoxication is explained by Littleton as being a function of alcohol's molecular interaction with the process that carries the charge through the synapse. Alcohol reduces the flow of Ca2+ ions, apparently pre synaptically, which reduction reduces neurotransmitter release. Because reductions in neurotransmitter passage across the synaptic gap will have an effect on membrane depolarization, which is required for the action potential to be released, the Ca2+ ion interference has synaptic transmission and electrical charge conductance influences: apparently to mean fewer transmitter releases results in fewer bindings and more Cl- ions flowing across the receiving neuron's membrane (that carries the charge; the excitatory neuron is inhibited. Thus, intoxication is a function of the strengthening of the inhibitory effect of GABAergic activity (anxiolytic) and a reduction of synaptic transmission of neurotransmitters (anesthetic), the locus of such reduction being a proportionate reduction in Ca2+ ion availability to the pre-synaptic membrane.

According to Littleton, the development of tolerance and dependence to alcohol is a consequence of neuronal structural and functional adaptation to the ethanol's influences on GABA and Ca2+ activities; those influences being the molecular substrate of intoxication that was just described in the immediate previous paragraphs. This adaptation is both decremental and oppositional.

Decremental adaptation is described by Littleton as resulting from the neuron's changing of itself to prevent the alcohol's entry into the membrane and synaptic areas. Thus, such prevention can lead to increasing tolerance without dependence.

Oppositional adaptation, however, leads to both increasing tolerance and dependence. That is, while comingled with alcohol, the neuron adapts during withdrawal by developing itself as the opposite of its state while functioning in interaction with the alcohol molecule. In this opposite neuronal adaptation, GABA loses its effectiveness when binding with GABA receptors and the number of Ca2+ channels increase, producing the opposite neuronal activity that occurs during intoxication. Respectively, the adapted molecular state effects a reduction in Cl- ions otherwise used to inhibit the action potential (to produce the anxiolytic component of intoxication) and an increase in Ca2+ release, causing an increase in the prospects for neuro transmission of the charges (the opposite of the anesthetic effect occurring during toxicity). This physical change then produces hyperexcitability after the drug is eliminated from the CNS, which excitability is again assuaged through alcohol's reincorporation into the functional and structural neuronal activity.

Dependence then increases with a corresponding increase in Ca2+ channels and decreasing effectiveness of GABA on GABAergic receptors. A "vicious circle" ensues, according to Littleton, where the neuronal adaptation to toxicity requires greater toxicity to offset the increasing adaptation -- cell functional and structural alteration. Ca2+ channel capacity in the neuron's membrane is hypothecated to be a function of genetic determination -- the capacity to produce more or less channels is determined by the particular genetic structure. The greater that capacity the more pronounced the cycle.

The behavioral correlates to this cyclical molecular process include

1. the highs and disordered thoughts and behaviors occurring during intoxication (= anxiolytic and anesthetic effects) which is underpinned molecularly by the Cl- increases and Ca2+ decreases
2. the production of withdrawal symptoms as the drug is eliminated from the neuron(s) and the increased number of Ca2+ channels produced during the intoxication as offsets to it begin to flow Ca2+ ions.

The GABAergic failure results in closed Cl- channels -- a reduction in Cl- to provide its inhibitory effects. The results are neuronal hyperexcitability and behavioral hyperexcitability.

In a very comprehensive review of the various CNS factors related to alcohol consumption, "Neurohormonal Basis of Alcoholism" (1990) by S. Parvez, H. Ollat, I Nevo, Y. Burov, and H. Parvez (from now on referenced as "Parvez") shows the comprehensive effects of alcohol consumption on the totality of CNS process. Because of the completeness of these effects, there should be no doubt for anyone reading Parvez about the alterations, incurred as a result of the use, to the substrate of existential identity -- virtually every neuronal system related to the formation and maintenance of that identity is affected.

To begin, Parvez shows (pg. 154) that the key ingredients to memory retention, among other things to include the capacity for autophosphorilization of second messenger activity like cAMP and Tyrosine, respectively, the accelerating components of LTP and the messengers themselves, without which there would be no long term potentiation (existential identity substrate), are inhibited by alcohol. Moreover, the inhibitory effects on all neuronal protein phosphorilization influence the elemental functions of cell process required to sustain psychological function; alcohol reduces neurotransmitter release and membrane activity required for processing of charges though ion channels and so forth -- the basic elements required to produce neuron excitability.

In addition to the effects of alcohol at the level of the cell and synapse, where neuronal charge, LTP, and memory storage occur, a wider picture is presented through Parvez's consideration of alcohol's effects on the basic neurotransmitter systems. For example, alcohol is shown to affect the noradrenergic, dopaminergic, serotonergic, and GABAergic transmission systems. Some of these effects, which occur based on genetic differences influencing the various systems, are described by Parvez.

• Noradrenergic systems are stimulated during intoxication, but retarded after prolonged use (Pgs 161 - 162).
• Like the noradrenergic system, the dopaminergic system also is overworked during intoxication; the result is the depletion of the system's capacities to function properly during withdrawal. The reapplication of alcohol replaces the altered dysfunction (pg 165).
• Serotonergic activity is stimulated in the beginning of the alcohol consumption and depleted over a longer period involving chronic use (pg 168).
• In support of Littleton (described earlier), Parvez also shows that ethanol influenced GABAergic activity stimulates Cl- (increasing inhibitory effects on the neuron) during the short run, but depresses GABAergic capacity to function over the long run -- more alcohol is needed, which when withdrawn unmasks the GABAergic deficits brought on by the use. Examples include: "personality and behavioral disorders, anxiety, mood disorders, and psychotic manifestations, etc."

Effects of Alcohol on Liver Functioning and
Subsequent Effects of Hepatic Trauma on
Neuropsychology

Aside from the direct effects of alcohol on neurophysiology, that is, as a source of trauma, there are indirect neurological effects that result from alcohol's influences on liver functioning -- alcoholic liver damage leads to alcoholic brain damage. Like the neurophysiology of alcoholism, liver (hepatic) issues are also complex. For a thorough explanation of alcohol/alcoholism and the liver, we reference in Palmer's The Molecular Pathology of Alcoholism, 1991; "Alcohol and the Liver," C. Lieber, (1991) and "Alcohol and Aldehyde Dehydrogenases," Jornval, H., Persson, B., Krook, M., and Hempel, J., (1991). See also "Vulnerability to Alcoholic Liver Disease," Arria, A., Tarter, R., Van Thiel, D., (1990), and "Genetic polymorphism of the alcohol metabolizing enzymes as a basis for alcoholic liver disease," Grant, D., (1983).

An overview of Lieber's (1991) introductory explanation (pgs 60-62) of alcohol's metabolism and subsequent pathological effects on the liver follow. About 90% of ethanol is oxidized by the liver. The other 10% is processed through other organs like the lungs and kidneys. Depending on the amount of alcohol and the kinds of metabolism provided by the liver, including hepatic dysfunctions, the 90% figure will or will not be achieved. Circuitously, failure to oxidize alcohol properly culminates in liver pathology and liver pathology increases the likelihood of the failure to metabolize.

There are several pathways or means through which the liver metabolizes alcohol, but only one of import for this summary -- alcohol dehydrogenase or ADH, an enzymic "system" that mediates ethanol metabolism. I emphasize "system" because an important feature of ADH is that it is comprised of many like, but at the same time slightly different, components. These differing components are more important when considering the genetic aspects of alcoholism, thus we will return to these differences in the section on genetics. In the mean time, the central role of alcohol dehydrogenase is its enzymic function of oxidation of ethanol; hydrogen is "transferred from the substrate to the cofactor nicotinamide adenine dinucleotide (NAD), converting it to the reduced form, NADH." During this chemical process, the system becomes overloaded with NADH -- there is not adequate removal (of NADH) capacity. Acetaldehyde is produced, which is then converted by aldehyde dehydrogenase to acetate. These reactions in the liver produce overabundances of reducing agents which overages then adversely influence the ability to continue the otherwise homeostatic metabolic process; in the interim, myriad liver metabolic disorders are initiated. In layman's terms, the chemical reactions in the liver are not adequate to process the alcohol through the body and they (the reactions) become in and of themselves contributors to additional failed attempts to process the drug -- neurotoxins are produced and remain in the blood to effect neurological functioning. The subsequent disorder in which we are most interested because of its linkage to neuropsychological change is hepatic encephalopathy.

In "Hepatic Encephalopathy Coexistent with Alcoholism," (1991) Tarter, Arria, and Van Thiel (from now on "Tarter") describe the process through which liver pathogenesis causes neurological damage with attendant thought and behavioral changes (symptoms). Importantly, the locus of the neurological change is continued even after abstinence and until the liver pathology is reversed. This hepatic/brain combination for pathology is such that liver transplants are shown to reverse the encephalopathy. The following is a summary of pertinent segments of Tarter's explanation of hepatic encephalopathy (pgs 206 - 220).

Chronic alcoholic hepatic encephalopathy is underlied by cirrhosis and is called portal systemic encephalopathy (PSE), which name describes its cause II a portal shunt, or alteration, that sends the blood around the portal side (where the portal artery is located) of the liver and in the process prevents it from removing neurotoxins from the blood. Where PSE's most acute effects occur in later stages of the disorder, some of the effects begin with the onset of cirrhosis, which on the average occurs during the person's most productive years (third to fifth decades). Thus, when we write in this section about PSE's acute effects incurred in the latter stages of cirrhosis, those effects have their beginning at a much earlier time in the alcoholism/liver pathology -- the effects are assumed to be graded (explained by Tarter in a later chart).

Tarter (by quoting Zieve, L., 1979) describes the etiology of PSE:

1. Decreased brain glucose and oxygen consumption.
2. Increased ammonia levels in the blood, brain, spinal fluid and muscles.
3. Increased glutamine levels in the brain, spinal fluid and muscles.
4. Increased short chain fatty acid levels in the blood and possibly in the brain.
5. Decreased normal neurotransmitter levels in the brain.
6. Increased false neurotransmitter levels in the brain, blood, urine and muscles.
7. Increased mercaptans in the blood, brain, breath and urine.
8. Altered amino acid ratios.
9. Decreased affinity for hemoglobin for oxygen.
10. Increased concentrations of neurotransmitter metabolites in both the brain and spinal fluid.

Early stage behavioral symptoms of PSE mimic some "functional psychiatric disturbances" (pg 208). They include: "euphoria, depression, mental slowing, inappropriate affect and behavioral and sleep disorders" and "hysteria." In addition, Tarter quotes Bernthal, P., (1987) by printing his (and Tarter's) chart depicting the graded (4 stages) presentation of PSE's effects on 6 factors, and then offers various methods for screening for the differences between similar symptoms for some psychiatric disorders and PSE caused encephalopathy. You can find Tarters chart summary in Tarter, 91, pg 210.

Importantly, Tarter demonstrates that PSE induced cognitive impairment can be reflected in testing prior to other symptom manifestations. Other tables in this article describe the PSE/cognitive relationship including emphasizing reversibility of the impairment through time, and especially reversing the impairments through liver transplants (Table IV, pg 218).

Before closing this description of alcohol-effected liver influences on CNS functioning, Parvez shows (pgs 154 - 155) that during the liver's metabolism of alcohol through the ADH (alcohol dehydrogenase) enzymic pathway, acetaldehyde is produced that condenses with catecholamines forming tetrahydroisoquinolines or "TIQs." This substance "binds with neuronal membranes" and has other CNS effects including "inducing neuronal lesions in catecholaminergic and serotonergic systems." Other hepatic influences on neuronal functions and systems are described in the same section.

Genetics

This section addresses 3 questions related to genetics. They are:

1. What is the known role of genetics in the biology of drug use-caused psychological trauma?
2. What is the prospective role of genetics in the same issue?
3. What is the relevance of the first 2 questions and their answers to the proposition that biological alterations to liver and neural functionings and structures cause an individual affected by chemical dependency to also be affected by psychological trauma resulting from the direct use?

The third question is answered first because it goes to the heart of the relevancy of this section.

Question (3)

Genetic information provides a non personality-or non psychological-related etiological element of the multifactorial process involving pathological use, which as previously described leads to biological damage that continues the use and the advent of additional damage, including interruptions to the psychological management system. This information argues that pathological use can be initiated or not from within a cell -- a genetic code is giving biological commands that influence the biologies' responses to the use instead of the commands coming from a system of cognitive logic imparted by society for the purposes of maintaining social control (admonitions to use drugs responsibly) and then adapted by the individual. In that regard, if the genetic etiology is true, or eventually proven so, then it will eventually require changes in social management theory and application, as it would be incongruous to keep telling people to use drugs responsibly should it be found that such advice is not possible to follow.

Because such didactic advice giving approaches represent the current and predominant social management method, the method itself controls the perception of the use: people have to be responsible for it because there is no other way to manage everyone who uses drugs. It follows under this method that if we see people as responsible for the use, such application of responsibility is inseparable from the correlate that they have also chosen the use -- they are to blame for it. If such blame is assigned, it is necessary to find a reason, which the psychological causal theory provides. That is, there is something that the individual is doing, thinking, or feeling as result of those activities and thoughts, either consciously or unconsciously, that requires pathological use. Subsequently, it is impossible to simultaneously see the effects of the use as an interruption to the psychological system of management because the ascendent view is that the system is getting what it really wants and needs. In contrast, the genetic view that the use is a consequence of the non psychological-related biological activity makes obvious the psychological trauma resulting from the use because the pathological drug use is seen as an obvious intrusion -- the use is imposing upon the psychological system of management the opposite of what it wants or needs. In other words, the availability and selection of the particular social management method (social assignment of responsibility for the use) has been the determing factor as to whether the psychological trauma resulting from the chemical use will be identified and addressed, regardless of the truth of its existence or not. Heretofore, this culture's adapted management methods have assured that such trauma will not be identified or addressed -- resulting in controversy stemming from genetic facts about the subject and consideration of additional and related facts. The relevance of the questions pertaining to the facts surrounding genetic data related to chemical dependency and their individual/social effects are that the questions and answers directly impact society's and its leadership's, including its clinical leadership's, abilities to consider not only the fact that psychological trauma results from the chemical use, but that the current social methods used to manage related issues are prospectively incorrect ones.

Question (1)

With regards to question (1) (What is the known role of genetics in the biology of drug use-caused psychological trauma?), there are two kinds of answers: cellular findings of fact and empirical/statistical data related to heritage of pathological chemical use. The former are considered first; the latter are considered later.

Currently, the literature reports 4 genetic factors influencing pathological chemical use; two are liver and 2 are neuronal. Three of the 4 are related to alcohol metabolism and the other is related to other substance (cocaine) abuse. We address the liver first and neuronal second.

The two liver influences are functions of a reverse effect; that is, the genes prevent certain people from being able to metabolize alcohol easily. The basis of this prevention lies in the hepatic productions of aldehyde dehydrogenase (ALDH). A mutant form of this hepatic-based enzyme results in over production of acetaldehyde during the metabolism of alcohol. The overages then initiate autonomous system activity -- faster heart rate and respiration, the "flushing" effect, which tends to make alcohol consumption too difficult. The genes that produce the ALDH mutant responsible for this processing are codified and unequivocal in their location and effect. This "flushing" effect influences about half the oriental world population, approximately 500 million people, and various and lesser percentages of other races. You may find discussions and explanations related to the hepatic genetic influences in the following articles: "Molecular Genetics of alcohol metabolizing enzymes," 1991, by Akira Yoshida; "Alcohol and Aldehyde Dehydrogenases" by Jornvall, Persson, Krook and Hempel (1991); "Genetic Factors in Alcoholism" by Cook and Gurling (1991); "The Role of Alcohol Metabolizing Enzymes in Alcohol Sensitivity, Alcohol Drinking Habits, and Incidence of Alcoholism in Orientals" by Agarwal and Goedde (1991); from The Molecular Pathology of Alcoholism by Palmer (1991); and "Genetic Aspects of Alcohol Abuse" by Adityanjee and Murray from International Handbook of Addiction Behavior by Glass (1991).

The neuronal genetic influence is reported in "Genetic Predisposition in Alcoholism: Association of the D2 Dopamine Receptor TaqI B1 RFLP With Severe Alcoholics" (not the study argued about prior to this publication period -- 1993) by Blume, Noble, Sheridan, Montgomery, Ritchie, Ozkaragoz, Fitch, Wood, Finley and Sadlack. This influence is shown to be related to the presence of an "allele of the D2 dopamine receptor gene with severe alcoholism" (pg 59). Blume states (59) the importance of dopamine in alcohol CNS processing: "The dopaminergic circuitry in the mesolimbic/mesocortical pathway has been asserted as being important for behavioral reward and reinforcement (quote Koob, 1988 and Wise, 1989)." Also from Blume: "Alcohol's ability to stimulate dopamine release in the brain points to a possible connection between the reinforcing effects of this substance and dopaminergic circuit." Uhl in "Substance abuse vulnerability and D2 receptor genes" (1993) shows the other association between substance abuse behaviors and the "restriction length polymorphism (RFLP) markers TAQI A1 and B1 at the dopamine D2 receptor (DRD2) gene locus in caucasions" (pg 83).

Reviews of familial alcoholism abound in the literature (none are better than Cook's and Gurling's, 1991, and from which we quote here) and pretty much agree that the twin adoption studies, that is, Cadoret and Gath, 1978; Cadoret, 1980, 1985, 1987; Goodwin, 1973, 1974, 1977, and Bohman, 1978 support the genetic propensity for alcoholism and that violence (sociopathology) in the accompanyment of alcoholism has a genetic predisposition (Cloninger). The adoption studies are apparently most valuable because they are able to measure children who were adopted at birth into non alcoholic (parental) environments and which children still become alcoholic despite the lack of environmental influences. Importantly, all of these studies can be questioned in terms of certain statistical/methodological processes employed. However, the consensus by most reviewers is that the Goodwin and Cloninger studies hold-up despite the scrutiny. Importantly, most of these kinds of studies where the families histories have been the focus are now being addressed with the new capacities available through gene technology similar to that reported by Blume, Noble and Uhr (1993).

Question (2)

I raised question 2 (What is the prospective role of genetics in the same issue?) because, in studying the current information, I found and had it emphasized to me that the findings so far are only the very beginning of this investigative process. For example, known genetic influences on the aldehyde dehydrogenase alleles has been discovered from the in-depth scrutiny of only 1 and partially 2 of 5 different isoenzymes of the aldehyde dehydrogenase enzymic system. In addition to this, there are 5 more isoenzymic components of the hepatic alcohol metabolizing enzymic system alcohol dehydrogenase, for which none of the 5 structures have been (at the time of these reviews) mapped. This is just the hepatic considerations. The neuronal ones for the vast and complex neural actions are nothing less than comparable to space exploration, and these voyages are just beginning also, at least this is the commentary provided by the majority of the reviewers I have read and that are noted in this subsection. Moreover, the technology is changing so fast that these new pictures are becoming available almost faster than reviewers of the investigations can keep up.

Genetic Studies Review and Update May 2008

For an update of biogenetic issues as a cause of Alcoholism, see: Po-Hsiu Kuo, Gursharan Kalsi, Carol A. Prescott, Colin A. Hodgkinson, David Goldman, Edwin J. van den Oord, Jeffry Alexander, Cizhong Jiang, Patrick F. Sullivan, Diana G. Patterson, Dermot Walsh, Kenneth S. Kendler, and Brien P. Riley: Association of ADH and ALDH Genes With Alcohol Dependence in the Irish Affected Sib Pair Study of Alcohol Dependence (IASPSAD) in Alcoholism: Clinical and Experimental Research; May 2008.

Conclusion: Chemical Dependency

There is overwhelming evidence of the changes in the molecular foundations of existential identity as well as indisputable evidence that the changes have occurred to the degree that they rarely resemble that pre-use, pre-trauma, identity. Moreover, these changes can occur absent the influence of a simultaneously occurring stress response. That is, although environmental factors that cause stress can contribute to the alcohol's effects on neuronal system functioning, the damage can occur just from the use itself and without the stress factor, and in the process then create its own stress factors.

Multiple Codependency: Spouse/ACA

The application of the ETM multiple sources of trauma theory, principles, and guidelines to multiple codependency ("codependency" is the current usage) experiences provides for the sharpest examples of conflict existing between the ETM approach and other programs. This subsection addresses those conflicts by focusing on non alcoholic spouses of chemically dependent people; the non alcoholic spouses are also adult children of alcoholics. The question to be answered in this section is: What is the evidence and rationale for addressing the trauma resulting from the later relationship before addressing the earlier trauma.

The predominant theories that challenge the multiple sources approach are technically called disturbed personality and decompensation hypotheses, psychic determinism, and addictive (or compulsive -) behavior disorder. These models define the locus of the spouse's problem as the early childhood intrapsychic makeup of the spouse (the spouse's problem originated during early childhood); recently, some theoreticians are suggesting the spouse's problems are genetic. The decompensation hypothesis has taken this intellect a step further; it posits that the alcoholic drinks excessively for the purpose of mirroring the spouse's degenerating condition. Because these models also, as a rule, project the spouse into the relationship with the alcoholic because of the earlier childhood problems, that is, the spouse is believed to have attracted into the marriage because of the earlier problems, we consolidate these technical descriptions into one convenient term: the attraction theory.

Now, with the advent of the ACA (adult child of an alcoholic parent) movement begun in the early 1980's, the attraction theory has been accorded more usage; ACA's who marry chemically dependent people are perceived as attracting into those relationships to meet early childhood needs that are pathological, apparently because of the alcoholism's influences on parenting. The ACA wants to relive the alcoholic childhood by marrying an alcoholic.

Methodologically, the overt intent of the attraction theory is to provide an interpretation of personal behavior that helps spouses to realize the flaw, that they are attracting into bad relationships to meet earlier and degenerate childhood needs, then help the spouse to address the childhood issues and begin to take responsibility for their decisions; the spouse begins to strengthen cognitive controls. The spouse is then supposed to make new and more constructive choices that bring about less degenerative or destructive relationships.

This idea, when compared to ETM theory, is considered from first, the issue of the therapeutic purpose of the attraction theory as compared to the ETM program's purpose, Second, the differences between ETM and attraction are considered from the perspective of some of the factual information that has historically been related to the attraction theory.

In the first perspective, consideration of the methodological purpose of the attraction theory as compared to the purpose of TRT, there is no need in TRT to provide or strengthen cognitive controls to spouses of alcoholics for the purpose of helping them to choose better paths as the attraction theory provides such assistance. The resolution of the trauma through TRT results in rational and cognitive oriented controls automatically being returned to, or incorporated into, decisionmaking processes as existential identity is reconstituted and operational identity is restored: etiology is reversed. Moreover, strengthening of cognitive controls before the trauma has been completely resolved, can result in the inadvertent strengthening of those defenses that help to keep the trauma retained in the subconscious, thus diminishing the prospects for reversal of the etiology resulting from the trauma experienced as a spouse.

Worse, the attraction theory's premise that the spouse chose the abusive relationship to meet internal psychological needs initiated out of childhood trauma, infers that the spouse wanted to experience the denigrating process occurring within the marriage. When TRT has been applied under the guidelines provided by the ETM approach, the identification of the specifics of the trauma-causing events usually carries with it an explanation, to include a specific description of the entry into the relationship. These specifics, followed by the trauma's resolution, provide a different picture (from the attraction theorists) of spousal entries into relationships with alcoholics. The conclusions reached by both patient and therapist about the entry (the conclusions are reached after the etiology has begun to be reversed) were that:

• the perpetrator was adept at hiding the propensity to assault -- there was no choice about something that was not seen.
• the idea that anyone could identify perpetrators of assault before the onset of chemical dependency (a primary and frequent underpinning of the perpetrator's pathological condition) is a fantasy constructed as a consequence of distorted hindsight (as Vaillant explained, such distortions of alcoholic post pathological use personality was a product of a skewed representation of the original personage) and a simultaneous lack of understanding by anyone making such a determination of how chemical dependency and associated violence are developed and harbored within both intrapsychic and interpsychic elements of personal psychology.
• No one stated to the spouse at the beginning of the relationship that it would likely provide her or him with psychological or physical disfigurement, and a similar psychological and physical damage to her or his future children. The spouse in turn did not state that this was the choice.
• With regards to the second perspective, the issue of the facts, research data related to the attraction theory is historically clear cut. Paolino and McCrady (1977) discovered in an exhaustive review of the literature on spouses of alcoholics that not only does empirical research refute the attraction theory (quote Ballard, 1959, Corder, 1964, Lanyon, 1970, 1973, Rae and Drewery, 1972, Mitchel, 1959, and Kogan, 1963), but the literature also indicates there is no empirical data that support's the attraction theory at all (Paolino and McCrady, 1977). Moreover, considerable research supports the opposing view that cultural (i.e., religious, economic, and social) rather than psychological factors provide the greatest influence on who becomes involved with whom (quote Orford, 1975). And finally, the Stress Theory (Joan Jackson, 1954) stating that non-alcoholic spouses of alcoholics are no different than anyone else would be who lived in an alcoholic relationship is supported by a number of empirical studies (quote Jackson, Kogan, 1965a, 1965b, Haberman, 1964, Bailey, Haberman and Alksne, 1962, Bailey, 1967, Paolino, McGrady and Kogan, 1977). In this landmark review of the research on the alcoholic marriage (The Alcoholic Marriage: Alternative Perspectives), Drs. Paolino and McCrady concluded that "the research of Haberman (1964), Bailey et al, (1962), Kogan and Jackson (1965b) Bailey (1967) and Paolino et al, (1977), strongly invalidates the decompensation (disturbed personality) hypothesis and supports the general concepts of the stress theory." (1977, pg. 77).

There are several additional considerations of fact left unaddressed by the attraction theory. Those considerations include no explanations for:

• relationships beginning before the 1600-1700's, probably because prior to that period relationships were, as a rule, customarily assigned to meet family or social political needs. The attraction theorists presumably believe co-dependency per the disturbed personality and decompensation concepts to be phenomenons of only the 19th and 20th centuries.
• those abused children who as adults married into stabilized relationships.
• why childhood abuse is recognized as true and legitimate experiences of trauma and spousal abuse is considered as less such an experience -- the abuse was secretly desired, so there could be no true or legitimate experience of trauma.

In addition, the fact that some ACA's have married chemically dependent people does not prove that ACA's are somehow drawn to such marriages abnormally. Given the frequency of chemical dependency in our society, a considerable number of such marriages of ACA's to chemically dependent people can be expected simply by chance. Our discovery through the treatment of multigenerational alcoholism with complete (see appendix E, section 4b) families (60 to 70 year old chemically dependent people with participating children ages 30 to 50) was that children from alcoholic homes are no more likely to marry chemically dependent people than are people without such back-grounds. Approximately 70% of those children had married non chemically dependent people. We found additional information by looking at ACA's from another perspective. When the adult child presented alone and without the complete family of origin, that person almost always was faced with other more current chemical dependency related issues. Either the person was married to an actively using chemically dependent person (60%) and had not yet discovered this to be true, or the adult child was chemically dependent him or herself (50%) and was yet unaware of this additional problem (10% overlap). We seldom met the ACA in this group who married into a stabilized system or who was not chemically dependent, as we observed in the multigenerational group. Our conclusion was that, generally, ACA's with current chemical dependency issues represent the predominant population of ACA's seeking assistance. Those not faced with current chemical dependency issues are, generally, not looking for help. In other words the ACA group at this beginning stage of its movement (this paragraph was originally written in 1987) is comprised of individuals who can identify childhood issues as factors, but not as readily identify current chemical dependency problems as primary concerns. Thus, we believe the samples from which the attraction theorist have drawn their conclusions, that is ACA's seeking assistance, are skewed and substantially distort those conclusions.

Obviously, however, a considerable problem remains: children from alcoholic homes have approximately one chance in three of being assaulted twice by the trauma resulting from chemical dependency. Within this context, we believe that the chief value of the attraction theory as used by some professionals is that it motivates ACA's to address their childhood experiences resulting from chemical dependency. However, this value is considerably offset by the theory's telling the twice-victimized spouse that he or she unconsciously chose the second relationship to meet "sick" needs. We believe that this sad and incorrect view perpetuates the trauma that has resulted from the spousal experience of alcoholism by supporting the spouse's survival view that if the experience was planned or contrived (unconsciously) then it was something that was wanted all along; if it was "wanted" then there could be no trauma to identify and resolve. In this scenario, the use of the attraction perspective becomes a means of denying the internal damage resulting from the most recently occurring trauma -- trauma resulting from the spousal relationship.

Conclusion

The reader is likely to not be surprised to find that I end this section by concluding that the ETM approach to the treatment of multiple sources of trauma is well supported by my review of the literature.

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Jesse Collins