By using a fixed-effects model, each of these suppositions was tested. This empirical approach also has the advantage of adjusting for the effects of unobserved characteristics, thus moving closer to a causal representation.The results showed clearly that the hypothesis presuming that increases in marijuana use lead to more symptoms of depression is tenable. There was no support for the other hypotheses, however. Depressive symptoms did not affect subsequent marijuana use, nor are these two outcomes part of a reciprocal loop.This supports previous research demonstrating that marijuana use increases the risk of depressive symptoms among young people. Furthermore,the findings fail to support the self-medication hypothesis that proposes that marijuana use is a coping mechanism in the presence of depression or that it serves to alleviate symptoms .

Whereas some youth may self-medicate with illicit substances when depressed, the analysis suggested that this is not common enough to support a general self-medication hypothesis.Of course, this is simply one study and, even though it provided clear evidence in support of one hypothesis, replication is necessary to confirm the presumed causal association between marijuana use and subsequent depressive symptoms. Moreover, since the mechanisms that underlie the potential causal effects of marijuana use are not known at present, future studies should consider a broader range of explanatory variables, including those that gauge neurophysiological,neurochemical, genetic, and family history factors that place youth at risk of substance abuse and depressive symptomatology. In addition, the FWHS used in the analysis did not collect the sample in a random manner, so there are threats to external validity that should be considered. The FWHS was also not anethnically or geographically diverse sample, thus the results have limited utility for considering the broader population of young people in the U.S. or elsewhere. The increased incidence of complications related to natural and synthetic cannabinoids has drawn great interest. In this recent time frame direct pulmonary toxicity caused by SC has also increased.

Our patient developed ARDS and DAH as defined by the Berlin criteria. Since our patient had bilateral ground glass opacities and bilateral air bronchograms that could not be explained by another condition, our patient conformed to the diagnosis of ARDS and DAH . These opacities were not caused by cardiogenic pulmonary edema since the echocardiogram was normal. The patient had significant impairment of gas exchange. Medical history revealed the only risk factor for the development of ARDS and DAH in this patient was SC inhalation that night and late morning prior to admission.Initial blood gases following endotracheal intubation revealed profound hypoventilation despite high level of pulmonary compliance. During endotracheal intubation, pink, frothy sputum emanated from the trachea. Although PEEP and pressure support settings of mechanical ventilation were high, this patient was unable to ventilate and maintain oxygenation adequately. Therefore, it was determined that this patient should be placed on VV-ECMO which was done within one hour following endotracheal intubation.

Endotracheal intubation was not associated with aspiration. The patient made an uneventful recovery, improving both clinically and radiographically.Few case reports of diffuse lung injury caused by SC requiring mechanical ventilation have been found.Many reports have focused on the depressive effects of SC on respiratory drive.In these patients chestx-rays were unremarkable because the effect of SC was on the central nervous system’s control of respiratory drive rather than the lung parenchyma itself.Since 2019, few reports of SC associated diffuse lung injury requiring mechanical ventilation have been described. Of these, only one utilized ECMO as a form of life-saving bridge therapy . Review of the other cases demonstrates similar bilateral alveolar infiltrates, one in which was noted to be secondary to diffuse alveolar hemorr hage. There has only been one reported case of SC inhaled by water pipe method . Our patient used a water pipe similar to the bucket method as described in Yamanoglu, et al. ,2018 . It has been proposed that a higher concentration of the heterogenous toxic metabolites from SC may cause a more direct injury to the lungs with this method of inhalation. In fact, synthetic marijuana potency relative to THC can be up to 660 times greater. In this particular case, a similar bloody and pink,frothy aspirate suggests acute lung injury not caused by other entities .This patient remained on ECMO for four days in our care with gradual clinical improvement. She was then transferred to an academic center where, after three more days, was decannulated and then self-extubated the next day. The patient was discharged one week later and made an uneventful recovery.