Page 65 - JCBP-2-4

Journal of Clinical and
Basic Psychosomatics Schizophrenia and metabolism

loss, dietary recommendations such as limiting saturated exert their effects through interactions with receptors such
fatty acid intake, and pharmacological approaches as dopamine, serotonin, acetylcholine, and histamine
29
involving antioxidants, melatonin, and probiotics/ receptors in the hypothalamus, culminating in heightened
prebiotics, which was selected targeted treatment based sympathetic nerve stimulation, elevated glucagon levels,
30
on individual differences. and increased liver gluconeogenesis levels. Concomitant
31
Cluster 2 spotlighted “The positive and negative changes in insulin secretion, dyslipidemia, fat deposition in
18
syndrome scale (PANSS) for schizophrenia” as the most the liver and adipose tissue, and insulin resistance emerged
frequently cited article. This reference, a requisite source as compounding factor underlying MS. 31
for numerous SZ-related articles, delved into the positive In delving into research trends, our citation burst
and negative symptoms experienced by SZ patients, also analysis elucidates the evolutionary trajectory of this
notable in this cluster was research concerning “Risk of discipline. The surge in high citation rates from 2004 to
metabolic syndrome and its components in people with early 2012 underscores that “atypical antipsychotic drugs”
schizophrenia.” This meta-analysis highlighted that were a central research focus during this period. At that
26
elderly individuals, those taking AAPS such as olanzapine time, MS was deemed a severe side effect of second-
and clozapine, and patients with severe mental illness generation antipsychotic drugs such as “olanzapine,”
constituted high-risk factors for SZ patients with MS. “clozapine,” and “risperidone” in critically ill patients
33
Notably, this meta-analysis represented the first large- These studies all reflected that AAPS was a dominant cause
scale endeavor to explore MS and its risk factors, revealing and research hotpot of MS recently.
that antipsychotic drugs significantly contribute to the
risk. Similar to the study in Cluster 2, Cluster 3 extended In keyword co-occurrence analysis Cluster 3,
our understanding of the relationship between second- “cognition,” “inflammation,” “depression,” and
generation antipsychotic drugs and MS. With this cluster, “association” are more frequent keywords. Research
“Effectiveness of antipsychotic drugs in patients with chronic elucidates significant positive associations between
schizophrenia” emphasized the duration of treatment genetically predicted depression and the risk of MS, waist
22
34
cessation for weight gain and MS, notably longer in the circumference, hypertension, and triglycerides. This
olanzapine group compared to quetiapine or risperidone cluster also explores the intricate connections among
groups. In addition, “Second generation (atypical) MS, cognitive function, and inflammation. Additional
antipsychotics and metabolic effects: a comprehensive quality investigations reveal that MS in middle-aged individuals
29
review” underscores the treatment-specific risk associated grappling with depression may potentiate atherosclerosis
35
with clozapine and olanzapine, revealing the highest risk of through inflammatory mechanisms. A meta-analysis
clinically significant weight gain, while the risks associated involving 27 studies and 10,174 patients with SZ showed
with other drugs remain relatively low. These insights have that SZ patients with MS or obesity or diabetes have
28
significantly contributed to the evolving understanding significantly greater overall cognitive deficits. The
of the impact of antipsychotic medications on metabolic current research suggests that cognitive impairments
health in SZ patients. In keyword co-occurrence analysis, associated with MS risk factors are most likely related
Cluster 2 also shined a spotlight on keywords such as to metabolic changes, which are associated with
“atypical antipsychotic,” “weight gain,” and “olanzapine.” microvascular and macrovascular processes believed to
Nowadays, the relationship between MS and SZ is complex cause brain structural abnormalities and subsequently
28
and multifactorial, and the current mainstream view was cognitive impairment. In addition, insulin resistance
that the use of AAPS played a major role. In addition to the mediates inter-organ communication between adipose
31
side effects of medication, other factors such as unhealthy tissue and the brain through extracellular vesicles derived
lifestyle, reduced physical activity, smoking, improper diet, from adipose tissue and their cargo microRNAs, leading
36
and genetic predisposition could also contribute to MS. to cognitive impairment. Hypertension is a major risk
31
Notably, olanzapine, a second-generation antipsychotic factor for both major and minor stroke events, and its
drug, was recognized for its propensity to induce weight most severe form can lead to severe cognitive impairment
37
gain and further contribute to the development of MS. and vascular dementia. Keyword co-occurrence analysis
6
Research revealed that SZ patients enduring long-term Cluster 4 delves into “drug-naïve patients,” “diabetes,”
olanzapine use (≥48 weeks) experience an average weight and “insulin resistance.” Investigations underscore the
gain of 5.6 kg. The current research underscored the coexistence of MS, diabetes, and insulin resistance
32
significant impact of AAPS on various organs, including in drug-naïve patients. 38,39 Notably, research by Chen
the brain, liver, and pancreas, as well as their influence on et al. underscores the frequent occurrence of impaired
the equilibrium of glucose and lipids in tissues. These drugs glucose tolerance in first-episode drug-naïve SZ patients,

Volume 2 Issue 4 (2024) 9 doi: 10.36922/jcbp.4238