https://www.sciencedirect.com/science/article/pii/S0753332224002130

TLDR; Benzos are more effective than SSRIs, have better long term tolerability, dont cause Alzheimer and, instead of being demonized, a tailored approach for each individual should be made by the doc instead of -"no benzos, take this SSRI".

The only danger is for the idiots blacking out and abusing them.

For the lazy fella I'm citing some quotes.

Neuroinflammatory protection

The administration of BZDs demonstrated effective inhibition of neuroinflammatory signaling in RSD mice, leading to the reversal of anxiety-like and depressive-like behaviors. This effect was achieved through the enhancement of GABAergic activity in the brain [79]. Numerous prior investigations have demonstrated that diazepam possesses significant immunomodulatory properties. Falcón et al. discovered that [119] diazepam can attenuate persistent inflammatory immune responses and hinder the effective presentation of antigens. Furthermore, when diazepam was administered to mice with Experimental autoimmune encephalomyelitis (EAE), a decrease in clinical manifestations was observed, and it protected against axonal injury and demyelination.

These medications can exert their effects by inhibiting cytokine secretion, altering cell expansion, impacting immune cell migration, and modifying cellular phagocytic movemen

Effectiveness in GAD and depression

BZDs have been observed to exhibit a rapid reduction in symptoms of anxiety among patients, demonstrating acute efficacy in clinical settings. The Lancet published a network meta-analysis in 2019. The findings indicated that BZDs monotherapy demonstrated efficacy in treating GAD compared to placebo, and exhibited greater effectiveness than certain antidepressants, including Citalopram, Imipramine, Maprotiline, Vilazodone and Vortioxetine.

Freire et al [131]. examined the long-term outcomes of patients with panic disorder following clinical remission. They observed that individuals who received clonazepam treatment exhibited a lower relapse rate than those randomly assigned to paroxetine.

Cortisol inhibition

It is worth mentioning that diazepam, another classical BZD, can reduce plasma corticosterone and ACTH levels in vivo.

Nonetheless, the effectiveness of diazepam in lowering cortisol diminishes as the body develops resistance to its effects after continuous usage over three weeks [74], [75]. In addition, diazepam was observed to modulate the regulatory effects of the cannabinoid system on neuroendocrine function.

When combined with an endogenous cannabinoid reuptake inhibitor, diazepam significantly reduced plasma corticosterone levels compared to those treated solely with cannabinoid compounds (lol yeah weed helps)

Insomnia

BZDs, a class of GABAergic hypnotic drugs, have been observed to facilitate sleep through a variety of ways potentially. They have the ability to enhance the transmission of GABAergic in subcortical regions that regulate the brain networks between the thalamus and cortex, hence exerting an impact on delta activity [103].

No universal agreement exists on the pharmacological intervention that demonstrates optimal effectiveness or a favorable balance between risks and benefits [94]. Four pharmaceutical therapy options for insomnia exist that regulatory agencies have approved by the FDA. The initial pharmacological strategy for addressing insomnia is the administration of sedative-hypnotic medications that target the GABA system, which are known as BZRAs, encompass BZDs (e.g., estazolam and lorazepam) and Z-drugs (e.g., zopiclone, zaleplon, and zolpidem).

(Personal opinion) I think doctors opting to prescribe antipsychs instead of benzos or z-drugs are just lunatic, considering side effect profile and efficiency of said classes.

Anxiety and depression

BZDs have been observed to exhibit a rapid reduction in symptoms of anxiety among patients, demonstrating acute efficacy in clinical settings. The Lancet published a network meta-analysis in 2019. The findings indicated that BZDs monotherapy demonstrated efficacy in treating GAD compared to placebo, and exhibited greater effectiveness than certain antidepressants, including Citalopram, Imipramine, Maprotiline, Vilazodone and Vortioxetine.

Freire et al [131]. examined the long-term outcomes of patients with panic disorder following clinical remission. They observed that individuals who received clonazepam treatment exhibited a lower relapse rate than those randomly assigned to paroxetine.

Tibrewal et al [133]. contended that an exaggerated perception of the likelihood of dependence could lead clinicians to exhibit bias against drug administration. The development of tolerance to the anxiolytic effects of BZDs does not occur. The efficacy of long-term BZDs treatment remains consistent over time.

Do they really cause Alzheimer?

A rigorous and comprehensive evaluation of drug data and outcomes in a prospective cohort study conducted in the United States involving non-demented older adults revealed no association between BZDs use and cognitive decline [149]. Subsequently, the findings were validated through an extensive cohort study conducted in Denmark focused on patients diagnosed with affective disorders.

Conclussion

BZDs, as representatives of GABAergic medications, have been utilized in clinical practice for numerous decades, serving as crucial treatments for conditions including generalized anxiety disorder, panic attacks, social phobia, insomnia, and various other disorders. This article thoroughly reviews the effects of BZD use on six interrelated domains, emphasizing the pressing need for a comprehensive evaluation, focusing on the necessity for additional clinical studies, especially concerning the long-term utilization of BZDs. In the context of effective treatments, when adverse events occur, they should serve as prompts for comprehensive patient assessment and follow-up rather than leading to the blanket avoidance of BZDs. Comparisons between BZDs and antidepressants are essential to identify suitable treatments for specific patients, considering patient preferences. In the future, the aim is to better tailor treatments to individual patient profiles, ultimately advancing the personalization of clinical practice.