If they had access to these memories of themselves, they would inform their conscious ego that they were in a dire, life-threatening situation, information that is too catastrophic to accept. Over time, these memories of themselves in relationship to their rejecting parent coalesce and form internal representations. The process of dissociation of memories of the self and of the parent is called "splitting of the ego" or simply "splitting", because part of the childs original conscious ego (or self) is "split off" from the rest of their normal view of themselves and hidden in their unconscious. Similarly, the memories of that part of the angry, enraged and irritated parent are split off from the "normal" aspects of the parent and held in the unconscious as well. The memories of the angry parent are appropriately called the "Rejecting Object" in Fairbairns model. "Object" is an awkward term used in psychoanalytic theory to designate a person outside the self. So both the terrified memory of themselves and the abusive aspect of the parent (the object) are split off from the conscious self and they become "part selves" and "part objects", The terrified part of the self (called the "Antilibidinal Ego" in Fairbairns model) and the terrorizing part of the object are cut off from consciousness and are no longer associated with the conscious representation of either the self or the object. This affords the child a (false) sense of security that prevents them from feeling anxious about their fate from moment to moment.
However, there is ongoing debate over the active mechanisms, including whether the main cause is the direct toxic effect of alcohol itself or whether the disease is a result of alcoholism-related malnutrition. A 2019 metastudy found that the relationship between ethanol toxicity and neuropathy remained unproven. Effects due to nutritional deficiency
Frequently alcoholics have disrupted social links in their lives and have an irregular lifestyle. This may cause an alcoholic to change their eating habits including more missed meals and a poor dietary balance. Alcoholism may also result in loss of appetite, alcoholic gastritis, and vomiting, which decrease food intake. Alcohol abuse damages the lining of the gastrointestinal system and reduces absorption of nutrients that are taken in. The combination of all of them may result in a nutritional deficiency that is linked to the development of alcoholic polyneuropathy.There is evidence that providing individuals with adequate vitamins improves symptoms despite continued alcohol intake, indicating that vitamin deficiency may be a major factor in the development and progression of alcoholic polyneuropathy. In experimental models of alcoholic polyneuropathy utilizing rats and monkeys no convincing evidence was found that proper nutritional intake along with alcohol results in polyneuropathy. In most cases, individuals with alcoholic polyneuropathy have some degree of nutritional deficiency. Alcohol, a carbohydrate, increases the metabolic demand for thiamine (vitamin B1) because of its role in the metabolism of glucose. Thiamine levels are usually low in alcoholics due to their decreased nutritional intake.