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Review

Diabetes Psychiatry: The Missing Piece of the Puzzle to Prevent Complications of the Diabetes Pandemic

by
Bradley M. Brooks
1,
Ashley M. Nettles
2 and
Brandon M. Brooks
2,*
1
USA Department of Psychiatry, University of South Alabama, Mobile, AL 36609, USA
2
Surgical Service, Columbia VA Health Care System, Columbia, SC 29209, USA
*
Author to whom correspondence should be addressed.
Psychoactives 2025, 4(2), 13; https://doi.org/10.3390/psychoactives4020013
Submission received: 2 April 2025 / Revised: 7 May 2025 / Accepted: 12 May 2025 / Published: 14 May 2025
Browse Figure
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Abstract

:
Both Type 2 Diabetes Mellitus (T2DM) and depression are leading causes of disability despite T2DM being largely preventable and depression being among the most treatable mental health conditions. Diabetes and depression have a bidirectional association, with each condition worsening the development and progression of the other. Depression in patients with diabetes is linked with poor glycemic control, reduced treatment adherence, and increased risk of diabetes complications. On the other hand, chronic hyperglycemia, systemic inflammation, insulin resistance, and neuroendocrine dysregulation are involved in the pathophysiology of depression. Antidepressants are often used to treat depression in diabetic patients, but their metabolic impact is still a matter of concern. While some antidepressants like fluoxetine and escitalopram increase insulin sensitivity and improve glycemic parameters, others such as especially tricyclic antidepressants (TCAs) and certain selective serotonin reuptake inhibitors (SSRIs) have been associated with an increased risk of diabetes, weight gain, and poor cardiometabolic outcomes. Considering such complexities, the prescribing of antidepressants must be done carefully. This review underscores the need for evidence-based and patient-centric pharmacological management. Further, the inclusion of psychiatry in multidisciplinary diabetes care teams has the potential to maximize both metabolic and psychological health benefits, as well as reduce the complications of T2DM.

1. Introduction

Diabetes mellitus, a serious and increasingly prevalent global health issue, is characterized by a progressive dysregulation of carbohydrate metabolism resulting from insufficient insulin production or ineffective insulin utilization, leading to sustained hyperglycemia and subsequent complications [1]. Epidemiological data indicate a substantial global increase in diabetes prevalence, affecting an estimated 10.5% (536.6 million people) of adults aged 20–79 years in 2021, with projections indicating a rise to 12.2% (783.2 million) by 2045 [2]. The World Health Organization (WHO) reports a substantial increase from 200 million individuals living with diabetes in 1990 to 830 million in 2022, with a more rapid increase observed in low- and middle-income countries (LMICs) compared with high-income countries [3,4]. This chronic condition elevates the risk of macro- and microvascular complications as well as amputation. The two primary subtypes of diabetes are type 1 and type 2, with type 2 diabetes mellitus (T2DM) being the most common [1]. The impact of diabetes extends beyond metabolic dysfunction, significantly affecting brain insulin resistance (IR), which can impair mood and cognition and is implicated in neurodegenerative processes including amyloid-beta metabolism and tau phosphorylation [5,6]. These chronic conditions, including major depressive disorder (MDD), collectively diminish both the quality of life and life expectancy. Notably, individuals with MDD exhibit a twofold increased likelihood of developing T2DM [7,8], and depression is significantly more prevalent in individuals with both type 1 (three times higher) and type 2 diabetes (twice as high) compared to non-diabetics [7,9,10,11].
Depression, characterized by persistent sadness and a marked reduction in interest or pleasure in previously enjoyable activities [12], is a common comorbidity in patients with T2DM. A bidirectional relationship between T2DM and depression has been consistently reported, potentially arising from shared etiological factors such as hypothalamic–pituitary–adrenal (HPA) axis dysregulation, inflammation, hippocampal structural alterations, and weight gain [13,14]. A study involving 225 patients with T2DM (mean age 63.8 ± 10.7 years) found a depression prevalence rate of 32%. The co-occurrence of depression and T2DM appears to have an additive negative impact, leading to poorer treatment adherence, reduced quality of life, an elevated risk of dementia, and increased cardiovascular events. Globally, approximately 28% of individuals with T2DM experience depression of varying degrees, with 14.5% meeting the criteria for major depressive disorder [10,11].
Healthcare guidelines recommend antidepressants for moderate to severe depression, though their side effects vary. However, guidelines for depression in patients with chronic conditions remain limited and non-specific. Managing multimorbidity poses challenges in applying the existing recommendations [15].
The historical recognition of the interplay between diabetes and mental health dates back to the 17th century when Thomas Willis linked diabetes to “lasting melancholy”. While the connection has been acknowledged for centuries, it has only recently garnered significant scientific attention, with research increasingly highlighting the complex ways in which these conditions influence each other [16,17]. As comorbid depression has such a profound effect on diabetes management and outcomes, the importance of having integrated psychiatric care as part of diabetes management is increasingly being understood. Polypharmacy is common in T2DM due to the need for metabolic control and complication management. Adding antidepressants increases the risks of side effects, drug interactions, poor adherence, and reduced quality of life [15,18]. No studies have assessed antidepressant prescribing within the broader diabetic regimen. Treating depression in T2DM is crucial, however, unclear guidelines, limited long-term safety data, and polypharmacy risks complicate prescribing decisions. Understanding the prescribing trends and patient characteristics could reveal safety concerns or potential undertreatment. This review aims to explore the intricate association between diabetes mellitus and depression, the role of antidepressant medications in this population, and the imperative for a specialized approach that integrates psychiatry and diabetology to optimize patient care.

2. Materials and Methods

This review of the literature used a synthesis strategy to review the current body of knowledge on the overlap of diabetes mellitus and mental health. A thorough search was performed on electronic databases, including PubMed, Scopus, and Google Scholar, with the use of appropriate keywords like “diabetes”, “type 2 diabetes”, “type 1 diabetes”, “depression”, “mental health”, “antidepressants”, “psychiatry”, and “integrated care”. The inclusion was based on studies examining the relationship between diabetes and depression and the effect of antidepressant treatment on patients with comorbid diabetes. Articles were identified based on relevance to the question being addressed and the quality of the methodology. The data from the chosen articles were synthesized to provide an overall picture of the existing knowledge and to emphasize the necessity of specialized psychiatric treatment in diabetes.

2.1. The Bidirectional Relationship Between Diabetes and Depression

Type 2 diabetes mellitus (T2DM) and depression have a bidirectional relationship, with each causing the other’s development and severity [19]. T2DM increases depression risk due to self-management challenges, fear of complications, and physiological stress from dysglycemia. Conversely, depression hinders essential diabetes self-care, including medication adherence, diet, and exercise, leading to poor glycemic control and worsening health outcomes [19,20]. This interplay complicates treatment, underscoring the need for holistic management strategies addressing both psychological and physiological aspects.

2.2. Hypothalamic–Pituitary–Adrenal Axis Dysregulation and Brain Metabolism

Depression and T2DM are both linked to hypothalamic–pituitary–adrenal (HPA) axis dysregulation, which affects immune function and brain glucose metabolism. Preclinical studies suggest that depression is associated with increased glycolysis, reduced Krebs cycle activity, frontal hypometabolism, and limbic hypermetabolism [21,22,23]. Treatment with paroxetine has been shown to improve brain glucose metabolism in depressive patients, further demonstrating the metabolic–neurological connection [21].

2.3. Inflammation, Insulin Resistance, and Neurotransmitter Dysfunction

T2DM is characterized by chronic low-grade inflammation and triggered by oxidative stress and proinflammatory cytokines. This inflammatory state contributes to atherosclerosis, obesity, osteoarthritis, and neuropsychiatric disorders [24,25]. Additionally, IR and pancreatic β-cell dysfunction drive hyperglycemia and further systemic inflammation [26,27]. Chronic inflammation in T2DM is linked to cognitive impairment, slowed processing speed, and depressive symptoms [19].
Moreover, brain IR disrupts neurogenesis, synaptic plasticity, and the reward system, all of which are associated with depression [28]. A post-mortem study revealed a link between dopaminergic gene expression and insulin signaling in mentally ill patients, reinforcing the role of brain insulin dysfunction in depressive behavior [29]. Dysregulated serotonin signaling in T2DM further contributes to depression, as impaired insulin and glucose metabolism affect serotonergic neurons. Given this relationship, antidiabetic drugs may have antidepressant effects, while serotonergic antidepressants could impact glucose homeostasis, emphasizing the complex metabolic–psychiatric connection [30].

2.4. Obesity, High BMI, and Depression Risk

A higher BMI (>30 kg/m2) increases depression and suicidality risk [31,32]. Individuals with comorbid depression and obesity have worse clinical outcomes and reduced antidepressant response [31,32]. T2DM is twice as likely to lead to depression, especially in women and those with uncontrolled diabetes. A cross-sectional study of 142 hospitalized T2DM patients found that 70 (49.2%) had depression [33]. Another study showed that one in three women and one in five men with T2DM and obesity experienced depressive symptoms [34,35].

2.5. Depression and T2DM Progression: Impact on Complications and Severity

Depression exacerbates T2DM complications, increasing the risk of both macrovascular and microvascular issues. A systematic review linked depression to a higher likelihood of complications in T2DM patients [36]. A population-based study of 38,537 T2DM patients with depression found higher rates of complications and mortality compared with 155,148 T2DM patients without depression [37]. Microvascular complications, including neuropathy, nephropathy, and retinopathy, are more common in T2DM patients with depression [38]. Furthermore, psychological stress and depression contribute to poor glycemic control and inadequate diabetes management [39]. Depression in T2DM is twice as common as in non-diabetics, rising from 29% to 53% with insulin therapy and worsening with disease progression [40]. Painful neuropathy is a key predictor of worsening depressive symptoms, and hyperglycemia-induced neurochemical imbalances may trigger depression, particularly in T2DM patients with peripheral neuropathy [41,42].

2.6. Dyslipidemia and Serotonin Dysregulation in T2DM-Related Depression

T2DM-induced dyslipidemia exacerbates depression by increasing inflammation and reducing the brain serotonin (5HT) levels. High LDL, triglycerides, and LDL/HDL ratios correlate with depressive episodes [43,44]. Dyslipidemia severity strongly predicts depression intensity, and depression itself heightens obesity and cardiovascular risks [45]. Hyperglycemia further worsens depressive symptoms via oxidative stress, neuroinflammation, and the inhibition of glial-derived neurotrophic factor (GDNF) [46,47]. The pathophysiology of depression in T2DM involves reduced tryptophan hydroxylase-2 activity, impairing serotonin synthesis [48]. 5HT receptors are dysregulated in T2DM, reducing antidepressant efficacy [49,50,51]. However, in depressed patients and diabetic mice, 5HT receptor upregulation in the frontal cortex may compensate for serotonin deficits; additionally, dysregulated insulin signaling increases leptin activity, impairing serotonin function, further linking T2DM to depression [49,50,51].

3. Antidepressants and Diabetes Mellitus

Depression in diabetic patients requires a comprehensive approach including pharmacological and psychological treatments, regular screening, follow-ups, and medication adherence. Guideline-based treatments include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), and atypical antidepressants [52]. Some studies have reported a risk of developing diabetes while others, like a UK cohort, found no significant difference in T2DM risk among various SSRIs in youth [53]. Table 1 illustrates the broad classification of these antidepressants. A careful risk-benefit assessment is crucial, particularly for pediatric patients; SSRIs and SNRIs remain the preferred choice for the short-term treatment of comorbid depression and diabetes due to their efficacy and safety [54,55].

3.1. Positive Impacts: Enhancing Metabolic Health with Antidepressants

3.1.1. Glycemic Control: General Improvements Across Studies

Research indicates that antidepressant medication may have a positive influence on glycemic control. A pre-post study by Rohde and colleagues demonstrated lower HbA1c levels following the commencement of antidepressant therapy [56]. Additionally, Brieler and colleagues found that antidepressant medication therapy during the acute phase was linked to achieving glycemic control within 36 months [57]. Supporting these findings, meta-analyses have shown a mean decrease in HbA1c with antidepressant medication compared with the placebo, and overall improvements in glycemic control with pharmacological treatment for depression, as observed by [58,59]. A recent study found that duloxetine significantly reduced the HbA1c levels compared with gabapentin and pregabalin, with no notable difference between gabapentin and pregabalin [60].

3.1.2. Glycemic Control: Targeted Benefits from Specific Antidepressants

Studies have highlighted that escitalopram specifically exhibits a positive impact on glucose regulation in diabetic patients [61]. Fluoxetine enhances glycemic control in T2DM patients [62]. Milnacipran and mirtazapine improve glucose control, the latter by enhancing pancreatic β-cell function [63,64,65,66,67]. Agomelatine, bupropion, and duloxetine benefit glycemic control and weight management [68,69,70,71]. Sertraline effectively regulates blood glucose and HbA1c in T2DM patients [72,73]. SSRIs enhanced insulin secretion via 5HT regulation in pancreatic β cells [74,75]. Since 5HT supports β-cell proliferation and glucose homeostasis [76,77,78], SSRIs may aid T2DM management through this pathway. Antidepressant-induced dopamine modulation may boost insulin secretion, as dopamine in pancreatic β cells plays a role in regulating insulin release and maintenance [79].

3.1.3. Insulin Regulation: Fine-Tuning Sensitivity and Secretion

Paroxetine improves insulin sensitivity [80]. Fluoxetine improves insulin sensitivity and secretion independently of weight loss [62,81] and enhances neuroendocrine responses to hypoglycemia [82,83]. However, it is important to note that increased norepinephrine (NE) inhibits insulin release and reduces sensitivity. Thus, the effects of antidepressants on T2DM depend on their specific mechanisms.

3.1.4. Cardiometabolic Health: Broad Protective Effects

Beyond glycemic control, antidepressants may also offer benefits concerning cardiometabolic risk factors. Rohde and colleagues proposed that prescribing antidepressants may have a modest protective effect on cholesterol levels [84]. Regular use of antidepressants, especially SSRIs and tricyclic/tetracyclic antidepressants, was associated with a lower risk of macrovascular complications and all-cause mortality [85]. It was also linked to a reduced risk of myocardial infarction in older diabetic patients and correlated with decreased cardiovascular morbidity and mortality in women [86,87]. On the other hand, long-term antidepressant use may lower mortality in T2DM patients [88].

3.1.5. Cardiometabolic Health: Drug-Specific Actions for Cardiovascular Wellness

Fluoxetine enhances the lipid profiles in T2DM patients [62], while citalopram shows neutral or beneficial effects on T2DM risk [89,90], possibly by regulating the HPA axis and reducing inflammation [91,92]. Nefazodone reduces weight [93], while agomelatine, bupropion, and duloxetine benefit weight management [68,69,71]. Antidepressants generally do not increase the T2DM risk. A retrospective study of 60,516 subjects also found no increased T2DM risk with antidepressants [94]. It is also crucial to recognize that dopamine receptor blockade by antipsychotics can interfere with metabolism [95]. Antidepressants are commonly prescribed for depression as well as other medical conditions such as painful peripheral neuropathy, chronic pain syndrome, and fibromyalgia [96,97]. While depression may confound the T2DM risk in individuals using antidepressants, treating depression has been shown to enhance glucose regulation and lower glycated hemoglobin levels [98].

3.2. Negative Impacts: Potential Risks Associated with Antidepressant Use in Diabetic Patients

3.2.1. Increased Risk of Type 2 Diabetes

Extended use of antidepressants, especially TCAs and SSRIs, has been associated with a higher risk of developing T2DM [99]. A case–control study of 165,958 depressed patients demonstrated that using antidepressants for more than two years notably raised the risk of T2DM [100]. These findings have been supported by other studies reporting an increased risk [101]. Furthermore, one French longitudinal cohort study that followed about 64,000 women over 6 years presented an elevated risk of T2DM with SSRI, imipramine-type, and mixed antidepressants versus non-users [102]. SSRI use has also been found to be linked with long-term use and abdominal obesity, hypercholesterolemia, and risk of T2DM in a cross-sectional study of 25,315 individuals [103]. Long-term SSRI use has also been proposed by studies to slightly elevate the T2DM risk in adults [99,104]. A recent study found that antidepressant use was the primary contributor to increased T2DM risk in MDD patients [105].

3.2.2. Adverse Effects on Glucose Regulation and Insulin Sensitivity

Some antidepressants can impair glucose homeostasis and insulin sensitivity, with noradrenergic drugs like desipramine linked to hyperglycemia [104]. TCAs further impair glucose regulation by inhibiting norepinephrine reuptake, stimulating glycogenolysis and gluconeogenesis and blocking the M3 and α-1AD receptors, thereby reducing insulin secretion and causing hyperglycemia [106]. In vitro, sertraline and paroxetine have been shown to inhibit IRS-1 and insulin signaling via JNK and MAPK activation, worsening insulin resistance (IR). A study on 23 non-T2DM depressed patients showed maprotiline caused more weight gain and insulin resistance than fluoxetine [107,108], and nortriptyline worsened glucose control in T2DM patients [109]. Sertraline has also been shown to induce pancreatic β-cell damage and apoptosis [110], and SSRIs contribute to T2DM risk by dysregulating the HPA axis and promoting IR [111]. A cohort study linked antidepressant use to higher odds of glucose-lowering drug prescriptions, implying potential disruption of glucose regulation [84]. In contrast, serotonergic antidepressants like fluoxetine may enhance insulin sensitivity but can also induce symptomatic hypoglycemia [112,113].

3.2.3. Metabolic Side Effects and Cardiovascular Risks

Prescription of antidepressants for diabetic patients is crucial to avoid metabolic side effects like weight gain, dyslipidemia, and increased cardiovascular and cerebrovascular risks [114]. TCAs are associated with weight gain and cardiotoxicity [115]. Weight gain is a key factor, particularly with TCAs, though SSRIs generally reduce weight, except for paroxetine, which promotes weight gain [116,117]. Vascular issues can worsen depression, with olanzapine and quetiapine causing metabolic side effects, while brexpiprazole has a minimal impact on weight [118,119]. Long-term duloxetine use slightly increased the metabolic markers but without clinical significance [120].

3.2.4. Other Adverse Effects

A study found higher microvascular complications in antidepressant users, while benzodiazepines showed no diabetic benefits [85]. Furthermore, antidepressant use did not affect the peripheral artery disease risk [87]. A Scottish study found increased prescriptions of antidepressants and antipsychotics in T2DM patients from 2004 to 2021, likely due to prolonged drug use and the broader application of SNRIs like duloxetine for diabetic neuropathy-related pain [121].

3.3. Antidepressants and Diabetic Foot Complications

Antidepressants are beneficial for neuropathic pain relief in the treatment of diabetic peripheral neuropathy (DPN) but may increase the risk of diabetic foot ulcers (DFUs) and amputation, particularly with TCAs and SSRIs at high doses [122]. Duloxetine, an FDA-approved SNRI, demonstrates greater efficacy than the placebo in treating patients with DPN [123]. However, antidepressant treatment, especially in naïve patients, is linked to increased DFU incidence, which aggravates with cumulative dosage [122]. Furthermore, painful neuropathy is a key predictor of worsening depressive symptoms, however, interestingly, the use of antidepressants among T2DM patients lowered prolonged opioid use following forefoot amputation (Figure 1) [124]. Figure 1 demonstrates how depression can impact diabetic foot complications, showing that depression is associated with poor dietary choices and lack of self-care [35,124,125] Given that both emotional distress and pain are complex, the inclusion of psychiatrists and other mental health clinicians as members within multidisciplinary limb preservation teams is key to improving DFU care as well as care following complications of DFUs such as amputation [124,126,127].

4. Discussion: The Role of Psychiatrists in Antidepressant Management of the Diabetic Patient

Given the complex and at times delicate interaction between the treatment of diabetes and comorbid depression, including pharmacological interventions such as antidepressants, the need for psychiatric input is key in providing customized care for patients. While antidepressants may improve mood and possibly glycemic control in some diabetic patients, their potential risks cannot be overlooked. The latest studies have pointed to the higher risk of developing T2DM through prolonged antidepressant therapy, especially with TCAs and certain SSRIs as well as to their negative effects on glucose metabolism and cardiometabolic disorders.
In this regard, psychiatrists have advanced knowledge and expertise important for dealing with these complexities. Their work is not limited to diagnosing and treating depression; they play a critical role in performing a proper risk–benefit analysis for every patient with diabetes who might need antidepressant treatment. This evaluation includes considering the patient’s unique diabetes care, possible drug interactions with current diabetes drugs, and unique metabolic profiles to inform the use of antidepressants with minimal metabolic side effects. For instance, certain SSRIs, such as fluoxetine and escitalopram, exhibit a relatively favorable metabolic profile in specific patient populations. In contrast, paroxetine has been linked to weight gain. TCAs, as a class, are generally associated with greater adverse effects on glycemic regulation. Furthermore, consultation-liaison psychiatrists also provide regular checks on glucose levels, weight, and cardiometabolic parameters with psychological support for enhancing medication adherence and diabetes self-management. The American Diabetes Association (ADA) itself promotes incorporating mental health care into standard diabetes care, validating the need for psychiatrists and other mental health clinicians in multidisciplinary diabetes care teams.

5. Conclusions

This review underscores the complex, bidirectional interaction between depression and diabetes, highlighting how each condition exacerbates the other, thereby complicating treatment and negatively impacting the clinical outcomes. Managing these conditions in isolation has been proven to be less effective than adopting an integrated approach that simultaneously addresses both metabolic and mental health dimensions. The implementation of collaborative care models, involving endocrinologists, dietitians, pharmacists, psychiatrists, podiatrists, and primary care providers, is essential for optimizing patient outcomes. Although considerable research has been conducted, there are still gaps in understanding the causal mechanisms connecting diabetes and depression. Future research should prioritize large-scale, long-term study designs to clarify these pathways, identify modifiable risk factors, and explore new treatment options. Additionally, the metabolic effects of antidepressants warrant further investigation to refine treatment strategies and minimize risks in diabetic populations. The role of emerging technologies, including digital health tools and telemedicine, should be explored to enhance care accessibility and cost-effectiveness. With the increasing incidence of diabetes and depression, the emergence of “diabetes psychiatry” within the subspeciality of consultation-liaison psychiatry could optimize patient care, minimize complications, and improve the overall well-being of individuals.

Author Contributions

Conceptualization, B.M.B. (Bradley M. Brooks), B.M.B. (Brandon M. Brooks), and A.M.N.; Methodology, B.M.B. (Bradley M. Brooks), B.M.B. (Brandon M. Brooks), and A.M.N.; Investigation, B.M.B. (Bradley M. Brooks), B.M.B. (Brandon M. Brooks), and A.M.N.; Data curation, B.M.B. (Bradley M. Brooks), B.M.B. (Brandon M. Brooks), and A.M.N.; Writing—original draft preparation, B.M.B. (Bradley M. Brooks), B.M.B. (Brandon M. Brooks), and A.M.N.; Writing—review and editing, B.M.B. (Bradley M. Brooks), B.M.B. (Brandon M. Brooks), and A.M.N. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Not applicable.

Acknowledgments

This material is the result of work supported with the resources and use of facilities at the Dorn Veterans Affairs Medical Center in Columbia, SC.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
T2DMType 2 diabetes mellitus
SSRIsSelective serotonin reuptake inhibitors
TCAsTricyclic antidepressants
SNRIs Serotonin-norepinephrine reuptake inhibitors
MAOIsMonoamine oxidase inhibitors

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Figure 1. The Diabetic foot–pain–depression cycle. Source: Brooks et al. [124], reprinted with permission.
Figure 1. The Diabetic foot–pain–depression cycle. Source: Brooks et al. [124], reprinted with permission.
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Table 1. Various antidepressant classes and their potential impact on diabetes mellitus.
Table 1. Various antidepressant classes and their potential impact on diabetes mellitus.
Antidepressant Drug Class Effect(s)/Potential Impact on Diabetes Mellitus and its Complications
SSRIs: Selective serotonin reuptake inhibitorsInhibition of insulin release secondary to pancreatic cell dysfunction; dysregulation of the HPA axis and development of insulin resistance; weight changes (gain or loss); weak anticoagulants (may increase the risk of bleeding with the potential to reduce vascular inflammation and improve endothelial function).
TCAs: Tricyclic antidepressantsWeight gain and insulin resistance.
SNRIs: Serotonin-norepinephrine reuptake inhibitors Weight changes (gain or loss). Potential for neuropathic pain relief in the treatment of diabetic peripheral neuropathy (DPN).
MAOIs: Monoamine oxidase
inhibitors		Weight gain; hydrazine-type MAOIs have been observed to decrease the fasting blood glucose and improve glucose tolerance in diabetic patients.
NDRIs: Norepinephrine-dopamine reuptake inhibitorsAssociated with a potential risk of type 2 diabetes, especially with long-term use and in higher doses.
NMDA-RAs: N-methyl-D-aspartate receptor antagonistsEnhanced glucose tolerance; some research suggests that NMDA-RAs can help protect or even regenerate pancreatic islet cells.
NRIs: Norepinephrine reuptake inhibitorsPotentially worsening glycemic control in some cases and improving it in others.
5-HT2 antagonistsWeight gain is rare.
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Brooks, B.M.; Nettles, A.M.; Brooks, B.M. Diabetes Psychiatry: The Missing Piece of the Puzzle to Prevent Complications of the Diabetes Pandemic. Psychoactives 2025, 4, 13. https://doi.org/10.3390/psychoactives4020013

AMA Style

Brooks BM, Nettles AM, Brooks BM. Diabetes Psychiatry: The Missing Piece of the Puzzle to Prevent Complications of the Diabetes Pandemic. Psychoactives. 2025; 4(2):13. https://doi.org/10.3390/psychoactives4020013

Chicago/Turabian Style

Brooks, Bradley M., Ashley M. Nettles, and Brandon M. Brooks. 2025. "Diabetes Psychiatry: The Missing Piece of the Puzzle to Prevent Complications of the Diabetes Pandemic" Psychoactives 4, no. 2: 13. https://doi.org/10.3390/psychoactives4020013

APA Style

Brooks, B. M., Nettles, A. M., & Brooks, B. M. (2025). Diabetes Psychiatry: The Missing Piece of the Puzzle to Prevent Complications of the Diabetes Pandemic. Psychoactives, 4(2), 13. https://doi.org/10.3390/psychoactives4020013

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