Locally produced anandamide also may be involved in the regulation of gastric emptying and intestinal peristalsis, two processes that are inhibited by this endocannabinoid . Thus, intestinal anandamide appears to serve as an integrative signal that concomitantly regulates food intake and gastrointestinal motility. The predominant peripheral component of feeding suppression induced by SR141716A led us to analyze whether the modulation of food intake derived from CB1 receptor stimulation/blockade may interact with that produced by the noncannabinoid anand amide analog OEA . Our results indicate that the hyperphagic effects elicited by CB1 receptor stimulation were counteracted by the administration of OEA, whereas CB1 receptor blockade potentiates the suppression of feeding evoked by OEA. Because the intestinal levels of anandamide and OEA are inversely correlated , it is tempting to speculate that both compounds act in a coordinated manner to control feeding responses through their opposing actions on sensory nerve terminals within the gut.This study found that higher ACE scores were significantly associated with a self-reported history of OD at initial assessment. The findings from this study are consistent with a larger cross-sectional study published in 2017,microgreens grow rack which showed that ACE scores were associated with previous OD in a medical inpatient setting.That study by Steinet al13 had a sample size of that was predominantly male with a White ethnicity , and approximately half of their respondents experienced 4 or more ACEs.
Their study showed that a one-point increase in ACE score was associated with a 1. increase in the expected odds of reporting a lifetime OD. The study by Stein et al coupled with our findings sug gests that these traumatic childhood experiences could also in crease the likelihood of OD in this population. These results in dicate that patients presenting with SUD and a history of OD could also benefit from trauma-informed care. Similarly, screen ings for ACEs can serve as an opportunity for referrals to men tal health treatment if needed. Our results further indicate that social and structural conditions may be just as significant in the relationship to self-reported OD as the type of substance used. Research has shown that certain populations are more susceptible to a negative impact from ACEs because of their socioeconomic and educational backgrounds.In a cross-sectional study examining the Behavioral Risk Factor Surveillance System data , those with a history of ACEs were more likely to report a lower socioeconomic status, higher rate of unemployment, and lack of high school completion.Prevention programs targeting at-risk youth can also use the ACE score to screen for highly vulnerable populations who might be at risk for early initiation of substances and potential OD. A systematic review of interventions in 2019 showed that parenting education, social service referrals, and social support for families can reduce the impact of ACEs on young children.18 Results from our study lend support for the critical need to continue address ing the impact of ACEs on substance use and ODs. As expected, we found that those with older age were more likely to report having experienced a nonfatal OD. This is consistent with the US drug OD death data, as adults aged 35 to 44 years have the highest rate of drug OD deaths from 1999 to 2019.The public health implications of these data are vast considering that OD survivors experience health challenges and higher death rates compared with the general public.
It is important to note that older patients had a longer duration of substance use history, thereby increasing the opportunity for an OD, so these analyses should be interpreted with caution. Overdose death rates during 2018–2019 increased among persons 65 years or older in the United States.In particular, rates increased among persons 65 years or older, non-Latinx Blacks, and Latinx, and in the Northeast and the West regions. In one study, individuals born between 1947 and 1964 had a no tably increased risk for OD death.Several theories have been proposed for the increase of OD history in older age. The generation of the “baby boomers” born between the years of 1946 to 1964 has been reported as having a generational mindset that was more accepting of substance use.Our finding that older age was a risk factor for OD has clinical implications for patient screening in this setting.Although the ACEs scale has been validated in previous populations, there has been limited research on the validity of the ACEs scale in people in treatment for SUD. As such, we conducted a principal component analysis to increase the validity of our analysis and findings. Results from the PCA results suggest that the original ACE scale is an appropriate tool to assess child mistreatment and household dysfunction in a population of individuals seeking treatment for substance use and mental health disorders. Almost all of the 10 items fell within 2 theoretical do mains, which provides evidence that all original ACEs are relevant in this population and should all be retained for clinical use. Notably, “physical violence toward the mother” loaded onto the “child mistreatment” component rather than the “house hold dysfunction” component. A recent study by Afi and col leagues also found evidence for a 2-factor structure, but consistent with previous studies, exposure to physical intimate-partner violence loaded onto the “household dysfunction” component. The high loading of this item in our study with “childmis treatment” suggests that perhaps witnessing physical violence to ward a mother figure in childhood may have different implications for this population.
Future studies should attempt to replicate and better understand these findings in different samples. There are several strengths for this study. To our knowledge, this is the first study that has examined the relationship between ACE scores and a self-reported history of OD among patients engaging in an addiction and mental health outpatient recovery and treatment program. This is important because our population was actively seeking and receiving care in an outpatient setting, which makes them distinct from many previous studies that were conducted on the general population. The advantage to having a more narrow study population is the ability to apply these findings to other outpatient dual-diagnosis treatment facilities for the improved screening of past and potential ODs. Similarly, no study, to our knowledge, has tested the reliability and validity of the ACEs scale in a population of individuals being treated for substance use and mental health disorders in an outpatient setting. There are some limitations in this study. Primarily, the interpretation of OD risk in older adults is limited by a wide CI, which is in part due to a small number of older adults . In addition, the assessment of ACEs was completed retrospectively, and there is evidence from previous meta-analyses showing that retrospective assessment of ACEs overemphasizes actual adverse experiences during childhood.The concise 10 question scale used for scoring ACEs may have missed exposure to adverse experiences during childhood, which are not captured by the questionnaire. Generalizability is limited because of the convenience sample of patients selected and the brevity of the questionnaires. The sample was obtained from a single outpatient dual-diagnosis clinic,ebb and flow flood table so almost all patients had a current or history of substance use, which limits generalizability. No in formation was collected regarding ages of exposure to ACEs or OD. The circumstances surrounding ODs were not ascertained . Information on sex failed to distinguish gender identities outside of male/female, which could limit the understanding of the prevalence of ACEs and self-reported OD in other populations. The questionnaire did not assess the participants’ prenatal history that could have been helpful in determining whether the prenatal developmental period could have influenced adult health and behavioral outcomes .Finally, these data were collected from baseline questionnaires, which are all self-report. The information contained within these questionnaires about mental health symptoms was not validated diagnoses, which precluded them from being used for analyses.The substantial body of evidence supporting familial influences on the development of alcohol use disorders , both genetic and environmental, lacks a correspondingly large literature regarding familial influences on remission from AUDs. Studies that have included family history of AUD as a predictor of remission in AUD-affected individuals have yielded few significant results, regardless of how remission was defined.
In anational population-based investigation, family history of AUD was associated with non-abstinent remission crosssectionally but not longitudinally, and had no association with abstinent remission. In a male sample ascertained at birth and followed throughout 40 years, paternal AUD predicted higher risk for developing an AUD but had no association with the likelihood of abstinent or non-abstinent remission. Family history of AUD was not associated with remission, defined as absence of AUD symptoms without regard to alcohol consumption, in population-based data or in a Native American sample. The lack of evidence for familial influences on remission from AUDs contrasts sharply with evidence that the heritability for the development of AUDs is 50–60%, and suggests that a phenotype derived from symptoms that characterize the development of an AUD may be insufficient to test familial influences on remission from that disorder. Some factors influencing remission may overlap with those influencing the development of AUDs but others might be distinct, and may even diverge from the dimension of liability underlying AUDs. Substance use disorders are often conceptualized as lying on an externalizing dimension which is characterized by impulsive and antisocial behavior and which has substantial evidence for familial transmission. Many questions used to tap behavioral symptoms of AUDs, such as whether alcohol was used in physically hazardous situations or social and interpersonal problems stemming from alcohol use, are at the same time addressing externalizing behaviors consistent with this conceptualization. Externalizing disorders are associated with poorer substance abuse treatment outcomes in clinical samples but, among abstinent individuals with histories of alcohol dependence, externalizing traits do not necessarily inhibit the ability to remit. For example, abstinent men and women recruited from a variety of sources had more life-time antisocial personality disorder symptoms and scored higher on trait measures of antisocial disposition than did non-alcoholic controls, but did not differ from controls on six of seven current ASPD symptoms, suggesting that antisocial behaviors were reduced and abstinence maintained despite an underlying antisocial disposition. Therefore, attempts to predict abstinent remission in a family member using life-time AUD in another family member, a phenotype based in large part on externalizing behaviors which might not be observed in abstinent individuals, may not provide an optimal test of familial influences on remission and may account for the null findings to date. In contrast, some of the most consistent correlates of both abstinent and non-abstinent remission are social connections such as marriage, friendship and religious or self-help group attendance. Traits that might enhance these connections, such as social cognition, might also be associated with the ability to remit. Heritable characteristics that are related to social cognition, such as prosocial behavior and social responsiveness, may represent a dimension that underlies remission in the same way that an externalizing dimension underlies AUDs, but that diverges from the externalizing domain. However, before heritable characteristics that might be associated with remission can be identified, a remission phenotype that displays a familial association, and therefore suggests some underlying genetic or familial environmental mechanisms, is needed. To our knowledge, just one previous study on remission has defined remission in both the target subject and the family member. That study used a population-based twin sample to examine the genetic and environmental contributions to the likelihood of remission, defined as absence of symptoms regardless of drinking status. Familial influences accounted for 11% of the variance associated with remission in females and 37% in males which decreased the likelihood of remission. In the current study we used data from a high-risk family study, the Collaborative Study on the Genetics of Alcoholism , which has a high prevalence of life time AUD in the relatives of probands and thus provides enough AUD-affected, and thus potentially remitted, proband-relative pairs to model persistent AUD, non-abstinent remission, and abstinent remission in both subjects. Greater AUD severity was associated with decreased likelihood of non-abstinent remission and increased likelihood of abstinent remission in population based data and in previous work in COGA , consistent with other studies that found abstinent individuals had more severe AUD histories than non abstinent individuals. Because AUD severity might influence familial associations of remission in a way similar to its association with familial transmission of AUD, we categorized remission as abstinent and non-abstinent.