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Sex Addiction Stress, and Stress

Stress, Sex And Addiction: Roles Of Corticotrophin Releasing Factor, Oxytocin And Arginine- Vasopressin In Sex Addiction Stress.

Sex Addiction

Sex Addiction Stress

Stress sensitivity and sex are predictive factors for the development of neuropsychiatric conditions. it has been thought stresses are the sole cause for addiction but this isn’t true since triggers can also cause relapse to drug use. Sex Addiction Stress and stress involve similar pathways.

The development and clinical course of addiction-related disorders do appear to involve neuroadaptations within neurocircuitries that modulate stress responses and are influenced by several neuropeptides. These include corticotropin-releasing factor, the prototypic member of this class, as well as oxytocin and arginine-vasopressin that play important roles in affiliative behaviors. Interestingly, these peptides function to balance emotional behavior, with sexual dimorphism in the oxytocin/arginine-vasopressin systems, a fact that might play an important role in the differential responses of women and men to stressful stimuli and the specific sex-based prevalence of certain addictive disorders.

Stress and Sex Addiction Stress

Stress generally is defined as any stimulus that challenges physiological homeostasis—that is, which alters the balance or equilibrium of the normal physiological state of the organism.

Individuals exposed to chronic stress exhibit a higher propensity to become addicts. Stress-induced relapse is also higher in addicts. In general, there is a higher prevalence of addiction in patients diagnosed with anxiety disorders and depression. Additionally, childhood trauma is associated with increased vulnerability to addiction. Exposure to high peer deviance in childhood and adolescence is among the strongest known risk factors for drug use and drug abuse. Interestingly, a very recent study has found that individuals with increased risks of drug addiction because of parental divorce or genetic liability are more sensitive to the pathogenic effects of peer deviance.

Stress and addiction are interconnected in several ways. For example, stressful life events may predispose individuals to engage in addictive behavior or relapse.

Sex Addiction Stress

Epidemiological studies have observed significant sex- specific differences among patients suffering from addiction and other neuropsychiatric disorders. The onset, severity, clinical course, and treatment response of anxiety disorders also differ significantly in women compared to men. Importantly, the sex bias in neuropsychiatric disorders, including post- traumatic stress disorder (PTSD), remains even after adjusting for the type of trauma, pre-existing psychiatric disorders, and sex differences in reporting. Several studies have found increased prevalence of depression in women. Similar sex differences exist for addictive disorders. For example, more adult males abuse addictive drugs than females across most drug classes, including alcohol, psychostimulants, and narcotics. However, women develop addiction more quickly. There are also critical differences in the way that illicit substances affect the two sexes.

Men and women also show different propensities to relapse, and are differentially affected by triggers for relapse to drug taking, putting women at greater risk for repeated relapses despite the higher prevalence of drug abuse in men. Interestingly, once the addiction cycle resumes, women show longer periods of drug use before their next quit attempt.

The sex differences may also be a result of hormonal and neural differences between men and women in relationship to their response to the addictive behavior.

Corticotropin-releasing factor and  Sex addiction Stress.

CRF is a 41-amino acid-containing neuropeptide. CRF orchestrates the stress response by acting at the level of the pituitary to initiate the HPA axis response to stress, as well as centrally to modulate limbic and brain monoamine systems that are important in autonomic and behavioral components of the stress response. CRF causes its effects by stimulation of corticotropin-releasing factor 1 receptor (CRF1R) and CRF2R, and displays an 18-fold greater affinity for CRF1R than CRF2R.

Physiological responses to stress involve the release of CRF from the paraventricular nucleus (PVN) of the hypothalamus, followed by stimulation of ACTH release from the anterior pituitary. ACTH, in turn, stimulates the secretion of cortisol/corticosterone from the adrenal glands. In addition, CRF has an extensive extrahypothalamic influence across the corticostriatal-limbic regions, and plays a critical role in modulating subjective and behavioral stress responses. Central catecholamines, particularly noradrenaline and dopamine, are involved in modulating brain motivational pathways that are important in regulating distress, exerting cognitive and behavioral control, and tempering behavioral and cognitive responses critical for adaptation and homeostasis. The hypothalamic and extrahypothalamic CRF pathways and central catecholamines target brain motivational path- ways to critically affect adaptive and homeostatic processes. CRF dysregulation has been linked to the pathophysiology of mood and anxiety disorders. During stress, release of limbic CRF can modulate monoamine systems that have been implicated in mood and cognition. Although activation of both the HPA axis and central monoaminergic systems by CRF during acute stress is adaptive, the inappropriate or persistent activation of these systems can have adverse consequences leading to psychopathology.

Oxytocin and arginine-vasopressin in Sex addiction Stress

Sex addiction and stress

Sex addiction Stress and stress

Cells originating in the PVN have specific pathways that efficiently deliver OXY to other structures in the brain including the amygdala, BNST, septum, hippocampus, and NAc. OXY released by peripheral organs or by the posterior pituitary does not readily cross the blood–brain barrier, with only 1–2% crossing. In disparity, the local expression of OXY receptors is highly variable and explains differences in social attachment within and between species. OXY exerts anxiolytic and anti- depressive effects in various models.

OXY, in collaboration with hormone dopamine, is vital for pairing and bonding in prairie voles. When OXY is infused into the VTA, it increases dopaminergic activity in the NAc, and stimulation of oxytocinergic projections within the VTA increases extracellular DA within the NAc while concurrently inducing penile erection. OXY-induced dopaminergic release within the meso- limbic DA system may impact the attribution of incentive salience to a variety of social stimuli and ultimately influence an organism’s drive towards such objects thus causing addiction.

Sex Addiction Stress is a menace that should be fought by all means that is why we at Integrative Addiction Institute are committed to availing help to addicts and offering training to Health care providers in Integrative Addiction. Call on Dr. Dalal Akoury (MD) today for assistance.

Stress And Sex Addiction Stress: Roles Of Corticotrophin Releasing Factor, Oxytocin And Arginine- Vasopressin In Sex Addiction.


Beta-Endorphins (Β-Ε) Levels and Alcoholism

The Effects Of Low Intensity Exercise On Beta-Endorphins (Β-Ε) Levels And Urge For Alcohol In Alcoholic Patients.

What are Beta-endorphins?

beta endorphinBeta-endorphins, or B-endorphins, are substances created by the pituitary gland. They specifically function as neurotransmitters, or conductors of messages between nerve cells. These substances are found around both the central nervous system and the peripheral nervous system. The Beta-endorphins is classified as a peptide since it contains 31 amino acids linked together. The beta-endorphins circulate around the brain, spinal cord, and secondary nerve systems in the body. Two glands, the pituitary gland and the hypothalamus, have a particular prevalence of the substance. The pituitary gland is responsible for releasing this endorphin into the blood, where it then travels to the central nervous system in the first legs of its journey. The beta-endorphins are agonists. They therefore connect to a cell and kick-starts a response. Beta-endorphins targets portions of a cell called opiate receptors in particular. The substance can reach these receptors in bodily tissue via a process called diffusion.

Beta-endorphins and alcohol

When alcohol is consumed at below risk levels it is known to be very rewarding health wise, it improves the quality of life but when a person begins taking alcohol in higher levels then there are problems that he will definitely have to suffer as a result of the severe effects of alcohol consumption. There are myriads of alcohol disorders needless to mention many accidents occur when people are drunken making alcohol a lead cause of accidental deaths.

Alcohol consumption has been reported to influence the activity of the endogenous opioid system. Reports indicate that acute exposure to ethanol leads to an enhanced release of brain Beta-endorphins (β-E) which through its interaction with μ and δ receptors mediates, at least in part, neurobehavioral effects such as reinforcement and acquisition of ethanol drinking behavior. Specifically, ethanol intake has been shown to increase β-E release by the pituitary and hypothalamus, an action that is mediated by the increase of corticotropin releasing hormone in a dose dependent manner. Furthermore, some reports indicate a biphasic effect of ethanol on hypothalamic Beta-endorphins release. However, the ethanol-induced increase of Beta-endorphins release is fast and transient, lasting about 15-20 minutes before normalizing again. Besides its effects on pituitary and hypothalamic Beta-endorphins, ethanol administration enhances Beta-endorphins release in the nucleus accumbens. This is a brain region important for the processes of reward and reinforcement. Therefore, the activation of μ and δ receptors by the increase in Beta-Endorphins levels due to ethanol intake may be pivotal in reinforcing properties of alcohol intake. On the other hand, chronic exposure to ethanol may cause adaptive responses of neuronal systems linked to negative reinforcement. Decreased Beta-endorphins production following chronic ethanol exposure may be responsible for some of the feelings of discomfort and the presence of negative reinforcement. Reports indicate that chronic ethanol abuse results in lower concentration of Beta-endorphins in the cerebrospinal fluid and plasma of male and female alcoholics. Therefore, chronic ethanol abuse might result in a central opioid deficiency. That deficiency might be related to decreased synthesis and release of Beta-endorphins in the hypothalamus and pituitary as well as lower density and activity of the opioid receptors.

A group of scientists conducted a research study to find out the effects of low intensity exercise on Beta-endorphins (β-E) levels and urge for alcohol in alcoholic patients. These researchers were Athanasios Z Jamurtas, Nikos Zourbanos, Kalliopi Georgakouli, Panagiotis Georgoulias, Eirini Manthou, Ioannis G Fatouros, Marios Goudas, Yiannis Koutedakis and Yannis Theodorakis.

This study used nine chronic alcoholic patients of whom 8 were males and 1 was female. These participants who were undergoing alcohol detoxification were recruited from a psychiatric hospital in Greece and 9 healthy controls volunteered to participate. Patients were diagnosed as being alcohol dependent according to the DSM-IV and the Alcohol Use Disorders Identification Test (AUDIT). AUDIT consists of 10 questions scored individually from 0 = never to 4 = 4 or more times per week. A total score of > 8 is an indication of alcohol abuse, a score of > 15 indicates serious abuse/addiction whilst a score between 8 and 10 is an indication of being at risk. Cronbach’s alpha coefficient was .73. Alcoholic patients were young and the medical exam revealed no presence of cardiovascular or metabolic disease in the participants. However, five patients were receiving antidepressant medicine, five were receiving anticonvulsant medicine and seven of them were receiving Thiamine, Pyridoxine, and Cyanocobalamine (three times a day) and folic acid (5 mg a day).

The findings of the study

beta endorphinsAll patients had a history of addiction of 10 years or more. All subjects were able to complete a 30-minute workout and the mean relative exercise heart rate was 61.1 + 4.9 % and 62.2 + 3.5% of their maximum heart rate for the alcoholic patients and healthy controls, respectively. Beta-Endorphins levels were significantly lower (p<0.001) in alcoholic patients whereas exercise resulted in significant increases (p<0.001, Cohen’s D: 3.31) only in the alcoholic group. Lactic acid at baseline was not significantly different between groups and increased significantly (p<0.001) after exercise in both groups. Analysis for CBC parameters revealed a significant time effect for red blood cells, hemoglobin and hematocrit. None of the remaining parameters was significantly different between groups nor was changed due to exercise. Pearson correlation analysis revealed non-significant relationships between Beta-endorphins and urge for alcohol (r = 0.23, p = 0.58). Finally, results on the Beta-Endorphins test revealed no significant changes in scores for alcohol urge in alcoholic patients (pre: 2.3 + 1.17; post: 1.87 + 1.17).

Finally, we at AWAREmed Health and Wellness Resource Center are committed to availing help to addicts by availing some of the most integrative approaches to healing an addict. Be it issues with Beta-Endorphins or general addiction treatment needs, we are here to help. We advocate for natural healing to all kinds of addiction. Call on Dr. Dalal Akoury (MD) at Myrtle Beach, South Carolina for help.

The Effects Of Low Intensity Exercise On Beta-Endorphins (Β-Ε) Levels And Urge For Alcohol In Alcoholic Patients.