Substance use disorders (SUDs) are widely prevalent in many countries, with the highest rates observed in nicotine and alcohol use, followed by opioid and cannabis use disorders. Within the field of SUDs, nutrition has become an increasingly important area of focus in both epidemiology and public health, as malnutrition is frequently observed among individuals affected by these disorders. Research indicates that people with SUDs are more likely to experience malnutrition than the general population; however, this issue remains an often-overlooked consequence that can impact disease progression and recovery outcomes. SUDs disrupt brain metabolism, leading to changes in brain function and disturbances in glucose, protein, and lipid metabolism. Evidence shows that individuals with certain SUDs often suffer from poor nutritional status, marked by high sugar consumption and insufficient intake of key micronutrients like iron, as well as vitamins D, C, A, and B—likely due to prioritizing drug use over adequate food intake. Importantly, diet can alter the metabolism and effects of drugs, potentially amplifying or diminishing their impact. While nutrition should play a central role in SUD treatment and rehabilitation, current research—both in animal models and human studies—on the role and benefits of specific nutrients in this context remains limited. This literature review aims to synthesize the available findings on the impact of malnutrition in human and murine models of SUDs, with the goal of identifying which nutrients may provide the most support for treatment and recovery.

Rheumatoid arthritis (RA) is a multifactorial autoimmune disease in which hypovitaminosis D by calcidiol quantification has been associated with disease severity. However, other vitamin D molecules could be implicated in RA pathophysiology and its comorbidities such as cardiovascular disease (CVD), which impacts the severity and mortality of RA patients. This study aimed to assess the relationship between calcidiol, calcitriol, its hydroxylation efficiency ratio, and the soluble vitamin D receptor (sVDR) and clinical and CVD risk variables to propose potential vitamin D molecule biomarkers for RA. A cross-sectional study of females was conducted on 154 RA patients and 201 healthy subjects (HS). Calcidiol, calcitriol, and the sVDR were measured in blood serum, and vitamin D hydroxylation efficiency was estimated using the calcitriol/calcidiol ratio score. CVD risk was calculated by the high-sensitivity C-reactive protein (hs-CRP) cutoff values. Disease activity was evaluated with the Disease Activity Score for 28 standard joints (DAS28-CRP). Results: The hydroxylation efficiency ratio and calcitriol serum levels were higher in RA patients with hypovitaminosis D (p < 0.001). Moreover, RA patients had a higher probability of a high hydroxylation efficiency ratio (OR = 2.02; p = 0.02), calcitriol serum levels (OR = 2.95; p < 0.001), and sVDR serum levels (OR = 5.57; p < 0.001) than HS. This same pattern was also observed in RA patients with high CVD risk using CRP serum levels; they showed a higher hydroxylation efficiency ratio (OR = 4.51; p = 0.04) and higher calcitriol levels (OR = 5.6; p < 0.01). Calcitriol correlates positively with the sVDR (r = 0.21, p = 0.03), CRP (r = 0.28, p < 0.001), and cardiometabolic indexes (p < 0.001) also showed discrimination capacity for CVD risk in RA patients with CRP ≥ 3 mg/L (AUC = 0.72, p < 0.01). In conclusion, hypovitaminosis D in RA patients was characterized by a pattern of a higher hydroxylation efficiency ratio and higher calcitriol and sVDR serum levels. Notably, higher calcitriol serum levels and a higher vitamin D hydroxylation efficiency ratio were associated with higher CVD risk in RA patients.