I found a few studies about sex hormone binding globulin in men that may be of interest to people in this thread.
This one links high triglycerides with lower SHBG (it makes sense since insulin resistance increases triglycerides. Increased insulin is linked with decreased SHBG)
Atherosclerosis
Volume 133, Issue 2, September 1997, Pages 235–244
Relationships between endogenous steroid hormone, sex hormone-binding globulin and lipoprotein levels in men: contribution of visceral obesity, insulin levels and other metabolic variables
Abstract
Excess visceral adipose tissue (AT) and hyperinsulinemia are important correlates of an altered lipoprotein profile. It has also been reported that testosterone, adrenal C[SUB]19[/SUB] steroids and sex hormone-binding globulin (SHBG) concentrations are associated with plasma lipoprotein levels. The aim of the present study was to investigate the relative contributions of endogenous steroid hormone and SHBG levels, of visceral AT accumulation measured by computed tomography, and of fasting insulin and free fatty acid (FFA) concentrations to the variation of plasma lipoprotein levels in men. For this purpose, plasma concentrations of testosterone, dehydroepiandrosterone (DHEA), androstene-3
β,17
β-diol (Δ[SUP]5[/SUP]-DIOL), androstenedione (Δ[SUP]4[/SUP]-DIONE), estrone and estradiol, as well as SHBG levels were determined in a sample of 76 men covering a wide range of body fatness values. Higher testosterone levels were associated with a more favorable lipoprotein profile as it showed significant correlations with triglyceride (TG), total cholesterol and LDL-cholesterol (LDL-C) concentrations (
r=−0.25, −0.25 and −0.27, respectively;
P<0.05). Higher plasma adrenal C[SUB]19[/SUB] steroid levels were also associated with a favorable lipoprotein profile as DHEA, Δ[SUP]4[/SUP]-DIONE and Δ[SUP]5[/SUP]-DIOL levels were negatively correlated with total cholesterol (
r=−0.24, −0.33 and −0.24, respectively;
P<0.05) and LDL-C (
r=−0.23, −0.31 and −0.28, respectively;
P<0.05). SHBG levels were negatively correlated with TG concentrations (
r=−0.33;
P<0.005) whereas
Δ[SUP]5[/SUP]-DIOL, testosterone and SHBG were negatively correlated with apolipoprotein B levels (−0.32≤
r≤−0.43;
P<0.005). Statistical adjustment for visceral AT area, fasting insulin, fasting free fatty acid (FFA) levels and total body fat mass eliminated most of the correlations between steroid and lipoprotein levels, while SHBG remained significantly correlated with lipoprotein concentrations after such adjustments. Multivariate analyses revealed that SHBG, Δ[SUP]4[/SUP]-DIONE, Δ[SUP]5[/SUP]-DIOL and metabolic variables all contributed to the variance in plasma lipoprotein concentrations (from 10 to 29% of explained variance). Visceral AT, fasting FFA and insulin levels as well as SHBG concentrations appeared to be independent correlates of lipoprotein concentrations. Thus, metabolic and anthropometric variables examined in the present study could have represented important confounding factors in previous studies which have examined the relationship of steroid hormones to plasma lipoprotein concentrations.
This one links low DHT with low SHBG.
Maturitas. Volume 2, Issue 2, July 1980, Pages 109–118
Interrelationships between sex hormone-binding globulin and testosterone, 5α-dihydrotestosterone and oestradiol- 7β in blood of normal men [SUP]☆[/SUP]
Abstract
Sex hormone-binding globulin (SHBG), testosterone (T), 5α-dihydrotestosterone (DHT) and 17β-oestradiol (E[SUB]2[/SUB]) were measured in 93 men in the age range 36–80 yr. Assuming that the binding of the steroids to blood albumin and SHBG follows the law of mass action, non-SHBG bound steroid concentrations (T[SUB]n[/SUB], DHT[SUB]n[/SUB], E[SUB]2n[/SUB]) were calculated from the SHBG and the respective total hormone values. The main results were: (1) Mean T[SUB]n[/SUB], DHT[SUB]n[/SUB], E[SUB]2n[/SUB] and SHBG remained on a constant level until the age of 65 yr. In men 66–80 yr old T[SUB]n[/SUB] and DHT[SUB]n[/SUB] were found to be significantly lower (
P<0.001), whereas E[SUB]2n[/SUB] and SHBG were elevated (
P < 0.05,
P < 0.001, respectively) when compared with men age 36–55 yr. (2) In contrast to total T and DHT, which correlated positively with SHBG (
P < 0.001) in Group I (age 36–55 yr) and also when eliminating the influence of age (
P < 0.05,
P < 0.01,
P < 0.01 for T, DHT and E[SUB]2[/SUB]) in Group II (age 56–80 yr), the correlation between T[SUB]n[/SUB] and SHBG was insignificant, whereas a negative correlation between DHT[SUB]n[/SUB] and SHBG (
P < 0.01) was present in Group I. (3) The age dependent increase of SHBG in Group II can be best explained by the respective alterations of the E[SUB]2n[/SUB]/DHT[SUB]n[/SUB] ratio. These results are discussed with respect to the relation between the SHBG, the total steroid and the non-SHBG bound steroid concentrations.
This one links higher growth hormone levels with higher SHBG.
Journal of Steroid Biochemistry
Volume 32, Issue 2, February 1989, Pages 327–334
On the regulation of sex-hormone-binding globulin—A challenge of an old dogma and outlines of an alternative mechanism
Abstract
In this review, the different factors known to affect SHBG levels are discussed with respect to their possible significance in the physiological regulation of this protein: Sex steroids, puberty, nutritional status, thyroid hormones and liver disease. It is concluded that the serum levels of SHBG are related rather to general metabolic factors, nutritional status, growth and ageing than to the estrogen/androgen balance. The authors suggest that SHBG is regulated primarily by growth hormone, somatomedin-C and possibly other growth factors. Growth hormone may promote SHBG synthesis in the liver while somatomedin-C may stimulate its extravasation and uptake in target tissues. It is suggested that sex steroids merely have an indirect, modulating influence.
I wonder if using growth hormone releasing peptides will increase SHGB.
