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Like you, I experienced true forgiveness. I felt the forgiveness of Jesus. I believed His blood had more power than my sin in which I was choosing to participate. I felt cleansed and this would last for days or weeks until I acted out in the sin again; then wham-o!
The guilt and shame came back and I would be forgiven again. I think you get the picture. Most of you lived the same movie: act out in your addiction patterns sin , ask for forgiveness, and do it all over again. This pattern is all too familiar for most of us. Why wasn't I getting free? Why wasn't God helping me? Why was I falling again and again? Well, quite simply, I was using the wrong principle to get the result I truly needed.
My desire for alcohol and drugs left me at my salvation commitment at 19 years of age, though I first accepted Christ as a youth in a Salvation Army camp thank God for the Salvation Army! I struggled with my sexual addiction.
A Christ-centred 12 Step Recovery Program
I was in seminary, working on my master's degree, preparing to go into full-time ministry. I had a roommate in my dorm who was slightly different from me; a really awesome and gracious man of God. One day, I genuinely felt the Lord tell me to let my roommate know every time I sinned in a sexual way. I was not excited about this at all, but my deal with God was to do percent of what he told me to do, so I told my roommate what the Lord told me to do, and he was OK with it.
Not even a week later, I needed the courage to tell my roommate I had fallen. I never felt so humiliated in my entire life. He graciously forgave me. About a week or so later, I fell again and felt really humiliated when I told my roommate. However, something wonderful happened after that second time. I genuinely did not want to do the behavior anymore.
The desire to act waned greatly. I had a few more slips, but they were many weeks apart. After I married, I always told my wife when I slipped. A few months into our marriage, being totally honest broke my addiction. I began living in real recovery.
I have not participated in ungodly sexual behavior or pornography in decades. Occasionally, I even take a polygraph to verify my recovery. I got free and stayed free, and God has used me to help others get free and stay free. The prayer of a righteous person is powerful and effective. This means "if" I confess, I can be healed or made free. If I don't confess, I am guaranteed to stay sick, or in my case, addicted. I was utilizing the principle of confessing my faults acts or behavior to another Christian of the same gender, so recovery and healing came to my life and stayed.
Check back for biblical principle two and three. Doug Weiss, Ph.
The dark side of emotion: the addiction perspective
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Do not post, directly or through links, viruses, misleading, malicious or off-topic content. Again, NPY does not act in isolation to reduce stress during alcohol withdrawal. There is evidence that two other neurotransmitter systems, nociceptin and endocannabinoids, may have effects to buffer the activation of brain stress systems. Nociceptin also known as orphanin FQ is a amino-acid polypeptide that is the endogenous ligand for the nociceptin opioid NOP receptor formerly referred to as opioid receptor-like-1; Meunier et al.
The neuroanatomical distribution of nociception containing neurons is high in the extended amygdala, cortex, and midbrain. Nociceptin generally attenuates stress-like responses and has a broad anxiolytic-like profile in animals Ciccocioppo et al. Nociceptin and synthetic NOP receptor agonists also blocked alcohol consumption in a genetically selected line of rats that is known to be hypersensitive to stressors, decreased reinstatement of drug-seeking behavior Economidou et al.
Substantial evidence implicates endocannabinoids in the regulation of affective states. Biphasic effects of cannabinoid agonists on anxiety-like behavior have been observed in rats and mice Viveros et al.
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The elevation of interstitial endocannabinoid levels through the inhibition of endocannabinoid clearance mechanisms produces anxiolytic-like effects in various animal models of anxiety, particularly under stressful or aversive conditions, and a reduction of CB 1 receptor signaling produces anxiogenic-like behavioral effects Serano and Parsons, Additionally, the disruption of CB 1 receptor signaling impairs the extinction of aversive memories, which may have similarities to deficits associated with stress pathophysiology, such as posttraumatic stress disorder Serano and Parsons, Several studies indicate that endocannabinoid production is increased in response to stress Patel et al.
Equally compelling for the current thesis, there is some evidence that drug-seeking behavior can be blocked by endocannabinoid clearance inhibition Scherma et al. Thus, dysregulated endocannabinoid function may also contribute to the negative affective disturbances associated with drug dependence and protracted withdrawal, which can again be part of the establishment of negative emotional states that drive drug seeking in dependence. As with the other stress buffers discussed above, one could speculate that endocannabinoids play a protective role in preventing drug dependence by buffering the stress activation associated with withdrawal.
We hypothesize that these brain stress neurotransmitters that are known to be activated during the development of excessive drug taking comprise a between-system opponent process, and this activation is manifest when the drug in removed, producing anxiety, hyperkatifeia, and irritability symptoms associated with acute and protracted abstinence. In addition, there is evidence of CRF immunoreactivity in the ventral tegmental area, and a CRF 1 receptor antagonist injected directly into the ventral tegmental area blocked the social stress-induced escalation of cocaine self-administration Boyson et al.
Thus, we argue that anti-reward circuits are recruited as between-system neuroadaptations Koob and Bloom, during the development of addiction and produce aversive or stress-like states Nestler, ; Koob, ; Aston-Jones et al. A critical problem in drug addiction is chronic relapse, in which addicted individuals return to compulsive drug taking long after acute withdrawal. The hypothesized allostatic, dysregulated reward and sensitized stress state produces the motivational symptoms of acute withdrawal and protracted abstinence and provides the basis by which drug priming, drug cues, and acute stressors acquire even more power to elicit drug-seeking behavior Vendruscolo et al.
Thus, the combination of decreases in reward system function and recruitment of anti-reward systems provides a powerful source of negative reinforcement that contributes to compulsive drug-seeking behavior and addiction. A compelling argument can be made that the neuroplasticity that charges the CRF stress system may indeed begin much earlier that previously thought via stress actions in the PFC.
The overall conceptual theme argued here is that drug addiction represents an excessive and prolonged engagement of homeostatic brain regulatory mechanisms that regulate the response of the body to rewards and stressors. The dysregulation of the incentive salience systems may begin with the first administration of drug Ungless et al. This cascade of overactivation of the stress axis represents more than simply a transient homeostatic dysregulation; it also represents the dynamic homeostatic dysregulation termed allostasis see above.
How to Break the Anxiety Cycle and Overcome Worry
Repeated challenges, such as with drugs of abuse, lead to attempts of the brain stress systems at the molecular, cellular, and neurocircuitry level to maintain stability but at a cost. For the drug addiction framework elaborated here, the residual decrease in the brain reward systems and activation of the brain stress systems to produce the consequent negative emotional state is termed an allostatic state. This state represents a combination of recruitment of anti-reward systems and consequent chronic decreased function of reward circuits, both of which lead to the compulsive drug seeking and loss of control over intake.
Where the ventral striatum and extended amygdala project to convey emotional valence, how frontal cortex dysregulations in the cognitive domain linked to impairments in executive function contribute to the dysregulation of the extended amygdala, and how individuals differ at the molecular-genetic level of analysis to convey loading on these circuits remain challenges for future research.
The argument that opponent processes play a role in the negative emotional state of drug withdrawal has been extended in parallel to the domain of pain with the hypothesis that repeated administration of opioid medications can produce a hyperalgesic state that can ultimately perpetuate or exaggerate the original pain state being treated.