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.
For instance, Fernandes et al. (24) reported that individuals who maintained regular physical activity were less likely to exhibit elevated hsCRP levels. Analysis of correlation between anthropometric and hormonal indicators and hsCRp value. Within this analysis, the group’s characteristics were deli eated, showcasing m dian alues, means, and standard deviations, as well as minimum and maximum values.
The reduced physical activity might, in turn, further compromise systemic T availability and contribute to the unfavorable changes in the inflammation and blood lipid profile. Therefore, it can be postulated that a low-to-moderate training load leads to an increase in the T concentration (20, 54), a moderate-to-heavy training load does not change it (26), and a heavy-to-maximal training load leads to a decrease in its concentration (55). The data regarding the effect of exercise training on gonadal androgens in aging males are, however, inconsistent (52, 53). However, Sartorius et al. (51) reported that, in aged men characterized by "very good or excellent" health, serum sex steroids are not reduced. It seems that the role of AAG in inflammatory progression needs to be further investigated, also in view of the recent data that demonstrated the importance of IL-6 and IL-6R (interleukin-6 receptor) in cardiovascular diseases (46, 47). It should also be mentioned that AAG was demonstrated to maintain metabolic homeostasis and to suppress inflammatory processes (44), similar to the functions of IL-6 and CRP that may also be elevated in the absence of an inflammatory state and exert anti-inflammatory effects, as recently reviewed by Del Giudice and Gangestad (45). This effect may occur through a testosterone-induced decrease of the expression of Toll-like receptor 4 (TLR4), which is known to stimulate different signaling pathways such as the NF-κB pathway (39).
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.
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.
Their results did not reveal any significant association between endogenous testosterone and systemic inflammation markers, including hsCRP. These findings suggest a close interplay between reduced testosterone levels and intensified pro-inflammatory activity in older males (28). This relationship between hsCRP levels and anthropometric parameters such as body weight and abdominal circumference has been widely documented. These results underscore the widespread prevalence of testosterone deficiency in older men when considering biochemical markers. Research involving over 2,000 men in the United States indicated that nearly 39% of men aged over 45 exhibit biochemical indicators of testosterone deficiency (22). The study also conducted an analysis examining the correlation between anthropometric and hormonal indicators and the hsCRP value (Table 4).
It is important to note that age-related hormonal changes in men may also be influenced by modifiable lifestyle factors. Additionally, no information was gathered regarding the specific motivation behind participants’ decisions to take part in the study. Furthermore, the study did not collect detailed, controlled data on socio-economic status, diet, or lifestyle factors, which prevented adjustment for potential confounders. In contrast, Zhao et al. (2015) conducted a study of 289 younger and 4212 older Chinese participants using a separate-sample Mendelian randomization approach to mitigate reverse causation. However, as these are observational studies, they should be interpreted cautiously due to the possibility of residual confounding and the absence of randomized allocation, which limits the ability to draw causal conclusions. Supporting this, Kaplan et al. also reported an inverse association between serum testosterone and high-sensitivity C-reactive protein (hsCRP) in elderly men (29). Additionally, hsCRP showed an inverse relationship with HDL cholesterol in the overall sample and among those with overweight or obesity, but not in individuals of normal weight.
We based this conclusion on the observation of the significant correlation between the markers of androgen profile and the AAG concentration in the multiple regression analysis including age and BMI as relevant and independent potential confounders (see Table 3). In this multiple regression analysis, there were significant inverse correlations (or clear tendency for it) between all the androgen profile variables and the age- and lipid profile-adjusted CRP, AAG, and FER concentrations. However, findings by Grandys et al. (2021) indicated that the relationship between testosterone and inflammation markers such as CRP and ferritin (FER) was influenced by body mass index and not independent of it (20). Relationship between anthropometric factors, and hormone levels in the group of patients without testosterone deficiency according to hsCRP concentration.

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