In the present study, we have demonstrated that the relationship between T and the inflammatory markers (CRP and FER) is not independent of BMI, which suggests that this association is conditioned by body fat (Table 3). Bivariate correlations between age and inflammatory markers, lipid profile, and androgen profile and between BMI and inflammatory markers, lipid profile, and androgen profile. Simultaneously, age and BMI correlated positively with most of the inflammatory markers (CRP, AAG, FER, and IL-6) and the lipid profile variables (TC, LDL, non-HDL, and TG) and negatively with the androgen profile parameters (T, fT, and fT/C ratio) and HDL concentration.
Relationship between anthropometric factors, hormone levels, and hsCRP in patients with and without testosterone deficiency. Therefore, future studies should incorporate a broader panel of inflammatory markers to more accurately characterize the immunometabolic alterations underlying the pathophysiology of obesity-induced testosterone deficiency. I have seen clients whose inflammatory markers normalized and testosterone improved by 100 to 200 ng/dL after addressing gut permeability with L-glutamine supplementation at 5 to 10 grams daily, elimination of inflammatory foods, and probiotic support. Simultaneously, we are aware of the limitations of our study, especially that related to the cross-sectional design of the research and the limited number of studied men, which impeded us from establishing a firm causality between the androgen status and the inflammatory markers and blood lipid profile.
Additionally, serum concentrations of hormones such as total testostero e (TT), estradiol (E2), dehydroepiandrosterone sulfate (DHEA-S), insulin (I), and sex hormone binding protein (SHBG) were assessed via ELISA using commercially available reagent kits (DRG-MedTek, Warsaw, Poland). While causality cannot be inferred from this observational study, the findings suggest a possible link between systemic inflammation and testosterone deficiency in aging men. Panels cover hormones, thyroid, metabolic markers, cholesterol, blood sugar, nutrient levels, and more. Panels test hormones, thyroid, metabolic markers, cholesterol, blood sugar, nutrient levels, and more. Your gut microbiome influences testosterone through multiple pathways including estrogen metabolism, inflammation regulation, nutrient absorption, and direct hormone signaling.
In the recent comprehensive review on the inflammatory etiology of cardiovascular diseases by Ruscica et al. (2), the role of evaluation of the pro- and anti-inflammatory profiles for appropriate guidelines and treatment of this disease was pointed out. Age-related upregulation of the inflammatory response (described as "inflamm-aging") (1) and the worsening of the blood lipid profile are of great importance because these changes are linked to atherosclerosis, enhanced cardiovascular risk, and the development of metabolic syndrome. Therefore, a low serum T concentration appears to be an independent risk factor in the development of atherosclerosis and cardiovascular diseases. This article was submitted to Translational Endocrinology, a section of the journal Frontiers in Endocrinology Testosterone is the predominant gonadal androgen in men. Federal government websites often end in .gov or .mil. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of int r st
One may speculate that a moderately higher level of physical activity affects positively both the testosterone and HDL concentrations, however, recent data have indicated that a more important risk factor for cardiovascular events is HDL cholesterol efflux capacity (63), which could be influenced by gonadal androgens (64). Taking into account that we have reported a significant positive correlation between the AAG concentration and BMI see Table 2 and "Results" in (11), one may suggest that a higher body fat stimulates AAG production by hepatocytes through the secretion of pro-inflammatory cytokines, mainly TNF-α and IL-6. The negative relationship between T concentration and fat mass has often been demonstrated (31, 32). The significant bivariate correlations between BMI and the markers of both androgen and inflammatory profiles (see Table 2) support such conclusions.
The study investigated the correlation between anthropometric factors, hormone levels, and hsCRP concentrations in patients with and without testosterone deficiency (Table 1). The relationship between anthropometric factors, and hormone levels in the group of patients with testosterone deficiency syndrome (TDS) according to hsCRP concentration. In Table 3, the relationship between anthropometric factors, and hormone levels in the group of patients with testosterone deficiency (TDS) was analyzed based on hsCRP concentration. In Table 2, the relationship between anthropometric factors, and hormone levels in the group of patients without testosterone deficiency was analyzed based on hsCRP concentration. This cross-sectional study aimed to examine the relationship between total testosterone (TT) levels, the diagnosis of testosterone deficiency syndrome (TDS), and high-sensitivity C-reactive protein (hsCRP) concentrations in aging men. The training-induced changes in the androgen concentrations, regardless of whether they are related to the direct stimulation of the HPG axis or to the effects of body fat–androgens interactions, may be of great importance because we have demonstrated that they are inversely correlated with markers of inflammation and blood lipids (Figures 1 and 2). Although we have demonstrated that physically active men tend to have higher sex hormone concentrations than do the inactive ones (see Results, Bivariate Correlations), there was a significant negative correlation between age and the androgen status, especially the fT concentration, i.e., the biologically active form of gonadal androgens (see Table 2).
Moreover, adipose tissue releases leptin, which suppresses the hypothalamic–pituitary–gonadal axis by interfering with gonadotropin signaling in Leydig cells, resulting in reduced androgen production (4). This enzymatic transformation inhibits the hypothalamic–pituitary axis, thereby diminishing testosterone synthesis (3). These associations merit further investigation in longitudinal and mechanistic studies to clarify directionality and underlying biological pathways.
Rotter I, Ciosek Ż, Syroka A and Ryl A (2025) A cross-sectional study of testosterone deficiency and inflammatory markers in older men. Moreover, the positive correlation between testosterone and physical activity level suggests that exercise training may reduce the age-related decrease in gonadal androgens, which seems to be one of the main beneficial effects (anti-inflammatory one) of physical activity in aging men. Based on the above literature data, it may be inferred that the correlation between androgens and inflammatory markers observed in this study is not accidental.

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