Why does testosterone therapy decrease HDL cholesterol in some men?

[Nelson Vergel]

This HDL lowering effect is seen at higher testosterone doses.


Relationship of plasma HDL-Cholesterol to testosterone, estradiol, and sex-hormone-binding globulin levels in men and women



James Semmens et al.
Metabolism
Volume 32, Issue 5, May 1983, Pages 428–432

Abstract

The significance of sex hormone levels in determining variation in high-density lipoprotein cholesterol (HDL-C) concentrations was studied in healthy Seventh Day Adventists (vegetarians) and Mormons. These groups were selected to avoid the confounding effects of alcohol consumption and cigarette smoking on HDL-C concentrations. Multivariate analysis showed that testosterone has a strong negative association with HDL-C in men (t = 3.99, P < 0.001) and women (t = 2.04, P < 0.05) when controlled for other variables including the concentration of sex-hormone-binding globulin (SHBG). Sex-hormone-binding globulin showed an independent positive association with HDL-C in men (P < 0.001). We postulate that the sex hormones affect HDL-C levels by regulating the activities of two important enzymes involved in the production and catabolism of HDL, namely, lipoprotein lipase and hepatic endothelial lipase. Other factors contributing independently to variation in HDL-C levels in this study were, in men, age and triglyceride, and in women, apoprotein-HDL, triglyceride, systolic blood pressure, heart rate, body mass index, and triceps skinfold thickness. Plasma estradiol concentrations were not significantly associated in either sex.

Testosterone (or Anastrozole?) Decreased my HDL: What Can I Do?

How to Increase Good Cholesterol (HDL)

 

[Nelson Vergel]

J Med Assoc Thai. 2008 Mar;91(3):400-7.

High-density lipoprotein cholesterol changes after continuous egg consumption in healthy adults.

Mayurasakorn K1, Srisura W, Sitphahul P, Hongto PO.


Abstract

OBJECTIVE:

To determine the relationship between continuous egg consumption with Thai life-style dietary and serum lipids of healthy young people.

MATERIAL AND METHOD:

Fifty-six participants with an average age of 35 were enrolled. In an experimental method of cholesterol intake, all participants were fed an additional egg per day to their basic diet. This project ran for 12 weeks.

RESULTS:

The 12-week egg consumption significantly increased serum total cholesterol by 0.27 +/- 0.15 mmol/L (10.43 +/- 5.80 mg/dL) (p < 0.05). The HDL-cholesterol (HDL-c) increased significant by 0.55 +/- 0.06 mmol/L (21.80 +/- 2.25 mg/dL) (p < 0.001) while the total cholesterol (TC) decreased as the HDL-c ratio was 0.94 +/- 1.1 (p < 0.001). No significant changes were found in LDL-cholesterol (LDL-c) and triglyceride levels. The present study showed that small serum LDL-c changed in response to change of egg consumption. Additionally, 12-week egg consumption also resulted in an increasing HDL-c level.

CONCLUSION:
In the majority of healthy adults, an addition of one egg per day to a normal fat diet could raise HDL-c levels and decreased the ratio of TC toHDL-c. Therefore, egg consumption might benefit blood cholesterol.

 

[Nelson Vergel]

Testosterone, HDL and cardiovascular risk in men: the jury is still out

Page, Stephanie T, and Katya B Rubinow. "Testosterone, HDL and cardiovascular risk in men: the jury is still out." Clinical Lipidology Aug. 2012: 363+. Health Reference Center Academic. Web. 7 July 2015.
Author(s): Katya B Rubinow 1 , Stephanie T Page
[*] 2


Testosterone-replacement therapy in older men with aging-associated hypogonadism remains an area of substantial clinical controversy. Although improvements in strength, quality of life and stamina have been observed [1] , reluctance to more broadly prescribe testosterone replacement derives, in part, from concern that replacement therapy may augment cardiovascular risk in men. One basis for this concern is the observation that exogenous testosterone can decrease serum levels of HDL-cholesterol (HDL-C). As low HDL-C is a well recognized risk factor for cardiovascular disease (CVD), this HDL-C-lowering effect could augment risk and therefore argue against widespread use of testosterone-replacement therapy in clinical practice. Importantly, however, the impact of exogenous testosterone on HDL-C levels is not uniform and appears to vary substantially with variables, including patient age and both the dose and route of androgen administration [2] . Thus, the HDL-C-lowering effects of testosterone observed in some clinical or research settings might not be relevant to the use of testosterone for physiologic replacement therapy in older men. Moreover, recent clinical data demonstrate the possible dissociation of HDL-C levels and cardiovascular risk, undermining the assumption that an intervention that reduces HDL-C necessarily translates into augmented risk. Finally, the historical focus on HDL-C alone fails to account for the remarkable complexity of HDL particle composition, particularly with regard to the modifiable protein cargo that likely confers the functional properties of HDL.

Direct evidence for the HDL-C-lowering effect of testosterone derives principally from observations of men using androgenic-anabolic steroids for athletic enhancement [3] . This effect has been achieved consistently with the administration of supraphysiologic doses of oral androgens to young men [2] , but has been far less consistent when testosterone therapy has been used at physiologic doses to restore eugonadal serum levels, particularly in older men [4,5] . Moreover, the lipid-related effects of exogenous testosterone appear highly contingent on whether parenteral or oral routes of administration are employed. Oral testosterone administration significantly reduced HDL-C levels in young, healthy men [6] , whereas when older, hypogonadal men were treated with transdermal testosterone, we found no significant changes in HDL-C after 3 months of therapy [5] . These disparate effects may be a consequence, in part, of first-pass hepatic metabolism that occurs with oral but not parenteral administration. In addition, the HDL-C-lowering effect of testosterone may be offset, at least partially, by aromatase-mediated conversion of testosterone to estradiol, as estradiol can raise HDL-C levels in men [7] , and coadministration of intramuscular testosterone with an aromatase inhibitor led to significant decreases in HDL-C [8] . Increased adiposity and associated aromatase activity in older men could thus play a mitigating role in the androgen-mediated reductions in HDL-C seen in this population. Accordingly, more clinical studies are necessary in order to better define those populations of men at greatest risk of lipid-related effects of testosterone therapy and to determine the testosterone regimens that are least likely to confer seemingly adverse changes in lipid profiles.

Even when reductions in HDL-C are observed as a consequence of androgen therapy, the implications for cardiovascular risk modification remain highly uncertain [2] . Whereas an inverse relationship between HDL-C levels and cardiovascular risk has been demonstrated clearly on a population basis [9] , the utility of HDL-C as a biomarker of individual cardiovascular risk has increasingly fallen into question. Underscoring the limitations of assessing HDL-C alone, recent clinical trials have found no decrease in cardiovascular event rate despite significant and substantial increments in HDL-C after treatment intervention in subjects with pre-existing CVD; indeed, the CETP inhibitor torcetrapib raised HDL-C levels by 72% but was associated with an increased rate of cardiovascular events [10] . Conversely, no long-term data have established that the reduced HDL-C levels observed in men receiving testosterone lead to an increased incidence of CVD. Rather, clinical data strongly suggest that men with low circulating levels of testosterone are at greater risk of CVD [11] . These apparently discrepant findings regarding HDL-C and CVD risk may eventually be resolved as the complexity of HDL biology becomes better understood. Currently, research efforts are expanding to incorporate alternative metrics of HDL composition and function, such that HDL-C content is incorporated into a larger context of particle protein, triglyceride and phospholipid content, as well as quantitative measures of HDL's pleiotropic functions.

A primary role of HDL-C is that of reverse cholesterol transport, the process whereby HDL particles accept cholesterol from peripheral tissues and transport it to the liver for excretion in bile. These peripheral cholesterol donors include lipid-laden macrophages, which may otherwise deposit cholesterol in the artery wall and contribute to atherogenesis. Rader, Rothblat and colleagues have developed an assay that measures the capacity of serum HDL to efflux cholesterol from macrophages and demonstrated reduced efflux capacity in patients with existing coronary artery disease [12] . Furthermore, investigators found marked interindividual variation in HDL-mediated efflux among subjects with identical HDL-C levels, underscoring the potential dissociation between HDL-C and HDL function [13] . As in vitro data suggest mechanisms by which testosterone could accelerate reverse cholesterol transport [14] , a lower HDL-C level could reflect altered kinetics of cholesterol transport that would actually reduce cardiovascular risk. Thus, these data illustrate the difficulty of drawing inferences about HDL function on the basis of HDL-C alone.

Ongoing research efforts are similarly exploring alternative strategies for assessing the relationship between HDL and CVD, including measurement of HDL particle number and size, determination of HDL protein cargo and assays of other HDL functions [5,15] . For example, our research has generated the novel finding that testosterone replacement in older, hypogonadal men confers changes in the protein composition of HDL particles in the absence of changes in HDL-C [5] . Although we did not observe attendant changes in HDL-cholesterol-efflux capacity, HDL particles also mediate lipid peroxidation, endothelial cell nitric oxide production and immunomodulatory functions [15,16] . The development of new methods to examine the variable composition of HDL therefore promises to offer more nuanced insights into HDL biology overall and, specifically, into the undoubtedly intricate relationships between circulating androgens and HDL composition and function.

In contrast to the historical concern that testosterone might increase cardiovascular risk in men, mounting data now demonstrate elevated risk to be associated with low androgen states [17,18] . This elevated risk is strikingly prominent among men who have undergone androgen-deprivation therapy (ADT) for treatment of prostate cancer, as these men exhibit a two- to three-fold higher incidence of stroke and myocardial infarction, as well as an increased risk of cardiovascular-related mortality after ADT exposures as brief as 6 months [19] . Furthermore, this elevated risk is manifested despite the inconsistent but not infrequent observation of increased HDL-C levels with ADT [19] . However, intervention trials have yielded inconsistent findings. In one study of frail, elderly men, those who received testosterone replacement experienced significantly more cardiovascular events despite gains in mobility and strength [20] . Nonetheless, no increased cardiovascular risk was evident in a similarly designed trial [1] . These conflicting data thus highlight the importance of extending our focus beyond a single HDL-associated metric in order to understand the full scope of testosterone's effects on HDL and the associated implications for cardiovascular risk. In addition, analogous to the Women's Health Initiative, large-scale clinical studies in men are needed to help define specific populations of men who are most likely to benefit from replacement therapy and, further, to establish optimal parameters for the timing, dose and duration of testosterone treatment. As yet, however, the role of testosterone in modifying lipoprotein function and cardiovascular risk in men remains highly uncertain and constitutes an intriguing area of emergent research.

References

1 Srinivas-Shankar U, Roberts SA, Connolly MJ et al. Effects of testosterone on muscle strength, physical function, body composition, and quality of life in intermediate-frail and frail elderly men: a randomized, double-blind, placebo-controlled study. J. Clin. Endocrinol. Metab. 95, 639-650 (2010).

2 Shabsigh R, Katz M, Yan G, Makhsida N. Cardiovascular issues in hypogonadism and testosterone therapy. Am. J. Cardiol. 96, M67-M72 (2005).

3 Basaria S. Androgen abuse in athletes: detection and consequences. J. Clin. Endocrinol. Metab. 95, 1533-1543 (2010).

4 Ozata M, Yildirimkaya M, Bulur M et al. Effects of gonadotropin and testosterone treatments on lipoprotein(a), high density lipoprotein particles, and other lipoprotein levels in male hypogonadism. J. Clin. Endocrinol. Metab. 81, 3372-3378 (1996).

5 Rubinow KB, Vaisar T, Tang C et al. Testosterone replacement in hypogonadal men alters the HDL proteome but not HDL cholesterol efflux capacity. J. Lipid Res. 53(7), 1376-1383 (2012).

6 Amory JK, Kalhorn TF, Page ST. Pharmacokinetics and pharmacodynamics of oral testosterone enanthate plus dutasteride for 4 weeks in normal men: implications for male hormonal contraception. J. Androl. 29, 260-271 (2008).

7 Bagatell CJ, Knopp RH, Rivier JE, Bremner WJ. Physiological levels of estradiol stimulate plasma high density lipoprotein 2 cholesterol levels in normal men. J. Clin. Endocrinol. Metab. 78, 855-861 (1994).

8 Friedl KE, Hannan CJ Jr, Jones RE, Plymate SR. High-density lipoprotein cholesterol is not decreased if an aromatizable androgen is administered. Metabolism 39, 69-74 (1990).

9 Boden WE. High-density lipoprotein cholesterol as an independent risk factor in cardiovascular disease: assessing the data from Framingham to the veterans affairs high - density lipoprotein intervention trial. Am. J. Cardiol. 86, 19L-22L (2000).

10 Barter PJ, Caulfield M, Eriksson M et al. Effects of torcetrapib in patients at high risk for coronary events. N. Engl. J. Med. 357, 2109-2122 (2007).

11 Keating NL, O'Malley AJ, Freedland SJ, Smith MR. Diabetes and cardiovascular disease during androgen deprivation therapy: observational study of veterans with prostate cancer. J. Natl Cancer Inst. 102, 39-46 (2010).

12 Khera AV, Cuchel M, de la Llera-Moya M et al. Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. N. Engl. J. Med. 364, 127-135 (2011).

13 de la Llera-Moya M, Drazul-Schrader D, Asztalos BF et al. The ability to promote efflux via ABCA1 determines the capacity of serum specimens with similar high-density lipoprotein cholesterol to remove cholesterol from macrophages. Arterioscler. Thromb. Vasc. Biol. 30, 796-801 (2010).

14 Langer C, Gansz B, Goepfert C et al. Testosterone up-regulates scavenger receptor BI and stimulates cholesterol efflux from macrophages. Biochem. Biophys. Res. Commun. 296, 1051-1057 (2002).

15 Besler C, Heinrich K, Rohrer L et al. Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease. J. Clin. Invest. 121, 2693-2708 (2011).

16 Gordon SM, Hofmann S, Askew DS, Davidson WS. High density lipoprotein: it's not just about lipid transport anymore. Trends Endocrinol. Metab. 22, 9-15 (2010).

17 Laughlin GA, Barrett-Connor E, Bergstrom J. Low serum testosterone and mortality in older men. J. Clin. Endocrinol. Metab. 93, 68-75 (2008).

18 Vikan T, Johnsen SH, Schirmer H et al. Endogenous testosterone and the prospective association with carotid atherosclerosis in men: the Tromsø study. Eur. J. Epidemiol. 24, 289-295 (2009).

19 Shahani S, Braga-Basaria M, Basaria S. Androgen deprivation therapy in prostate cancer and metabolic risk for atherosclerosis. J. Clin. Endocrinol. Metab. 93, 2042-2049 (2008).

20 Basaria S, Coviello AD, Travison TG et al. Adverse events associated with testosterone administration. N. Engl. J. Med. 363, 109-122 (2010).

 

[Nelson Vergel]

This study used a 1% T gel product and may have not attained high enough T levels.

J Lipid Res. 2012 Jul; 53(7): 1376–1383.

Testosterone replacement in hypogonadal men alters the HDL proteome but not HDL cholesterol efflux capacity


Katya B. Rubinow,1,* Tomas Vaisar,† Chongren Tang,† Alvin M. Matsumoto,§** Jay W. Heinecke,† and Stephanie T. Page*
*Center for Research in Reproduction and Contraception, Department of Medicine, University of Washington School of Medicine, Seattle, WA
†Diabetes and Obesity Center of Excellence, Division of Metabolism, Endocrinology, and Nutrition, and Department of Medicine, University of Washington School of Medicine, Seattle, WA
§Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, WA
**the Geriatric Research, Education, and Clinical Center, V. A. Puget Sound Health Care System, Seattle, WA



Abstract

The effects of androgens on cardiovascular disease (CVD) risk in men remain unclear. To better characterize the relationship between androgens and HDL, we investigated the effects of testosterone replacement on HDL protein composition and serum HDL-mediated cholesterol efflux in hypogonadal men. Twenty-three older hypogonadal men (ages 51–83, baseline testosterone < 280 ng/dl) were administered replacement testosterone therapy (1% transdermal gel) with or without the 5α-reductase inhibitor dutasteride. At baseline and after three months of treatment, we determined fasting lipid concentrations, HDL protein composition, and the cholesterol efflux capacity of serum HDL. Testosterone replacement did not affect HDL cholesterol (HDL-C) concentrations but conferred significant increases in HDL-associated paraoxonase 1 (PON1) and fibrinogen α chain (FGA) (P = 0.022 and P = 0.023, respectively) and a decrease in apolipoprotein A-IV (apoA-IV) (P = 0.016). Exogenous testosterone did not affect the cholesterol efflux capacity of serum HDL. No differences were observed between men who received testosterone alone and those who also received dutasteride. Testosterone replacement in older hypogonadal men alters the protein composition of HDL but does not significantly change serum HDL-mediated cholesterol efflux. These effects appear independent of testosterone conversion to dihydrotestosterone. Further research is needed to determine how changes in HDL protein content affect CVD risk in men.

 

[Nelson Vergel]

Effects of testosterone replacement on HDL subfractions and apolipoprotein A-I containing lipoproteins.

Authors:
Tan, K et al

Clinical Endocrinology. Feb98, Vol. 48 Issue 2, p187-194. 8p.


OBJECTIVES Gonadal steroids are important regulators of lipoprotein metabolism. The aims of this study were to determine the effects of a minimum effective dose of testosterone replacement on high density lipoprotein (HDL) subfractions and apolipoprotein (apo) A-I containing particles (lipoprotein (Lp)A-I) and LpA-I:A-II) in hypogonadal men with primary testicular failure and to investigate the underlying mechanisms of these changes. MEASUREMENTS Eleven Chinese hypogonadal men were started on testosterone enanthate 250 mg intramuscularly at 4-weekly intervals. HDL was subfractionated by density gradient ultracentrifugation and LpA-I was analysed by electro-immunodiffusion after 3, 6 and 12 weeks of treatment. Plasma cholesteryl ester transfer protein (CETP) activity and lipolytic enzymes activities in post-heparin plasma were measured to determine the mechanisms underlying testosterone-induced changes in HDL. RESULTS The dosage of testosterone enanthate used in the present study resulted in suboptimal trough testosterone levels. No changes were seen in plasma total cholesterol, triglyceride, low density lipoprotein cholesterol (LDL-C,) apo B and apo(a) after 12 weeks. There was a drop in HDL3 -C compared to baseline (0.82 ± 0.17 mmol/l vs . 0.93 ± 0.13, P < 0.01) whereas a small but significant increase was seen in HDL2 -C (0.21 ± 0.13 mmol/l vs . 0.11 ± 0.09, P < 0.05). Plasma apo A-I decreased after treatment (1.34 ± 0.25 g/l vs . 1.50 ± 0.29, P < 0.01), due to a reduction in LpA-I:A-II particles (0.86 ± 0.18 g/l vs . 0.99 ± 0.24, P < 0.01). No changes were observed in the levels of LpA-I particles. No significant changes were seen in plasma CETP and lipoprotein lipase activities after testosterone replacement but there was a transient increase in hepatic lipase (HL) activity at weeks 3 and 6. The decrease in HDL correlated with the increase in HL activity (r = 0.62, P < 0.05).

 

[GEORGE TOULIATOS]

I was surprised when i first started TRT one year ago and i realised that withing one month or so,my HDL was going down.Six months later i switched to transdermal application and it was stabilised,same occured with my hematocrite.

 

[Sakuraba39]

Mine was low before I started and has varied a bit (yet still low) over the last decade.

 

[Nelson Vergel]

Researchers link high levels of 'good' cholesterol with excessive mortality

It has been accepted wisdom for many years that the more good cholesterol people have in their blood, the better. But the good cholesterol, also known as HDL, might not be as good as we think.

In any case, the results of a new study from the University of Copenhagen seriously contradict the assumption that high levels of HDL in the blood are only a good thing. The researchers have shown that people with extremely high levels of good cholesterol have a higher mortality rate than people with normal levels. For men with extremely high levels, the mortality rate was 106 per cent higher than for the normal group. For women with extremely high levels, the mortality rate was 68 per cent higher.

"These results radically change the way we understand 'good' cholesterol. Doctors like myself have been used to congratulating patients who had a very high level of HDL in their blood. But we should no longer do so, as this study shows a dramatically higher mortality rate," says Børge Nordestgaard, Professor at the Department of Clinical Medicine and one of the authors of the study.

Source

 

[Nelson Vergel]

Click here: Should we not worry about decreased HDL caused by higher-dose testosterone replacement?

 

[Nelson Vergel]

Testosterone and Estradiol Mediate Discrete Effects on High-density Lipoprotein Particle Size and Sterol Efflux Capacity in Healthy Men

Originally published 8 Jun 2018 Circulation. 2018;136:A14585


A low plasma level of high-density lipoprotein (HDL) cholesterol (HDL-C) is associated with cardiovascular risk. A key cardioprotective property of HDL is cholesterol efflux capacity (CEC), the ability of HDL to accept cholesterol from macrophages. A meta-analysis suggested that HDL-mediated CEC is inversely associated with cardiovascular risk, which appears to be independent of HDL concentration.

Abstract
Introduction: Exogenous testosterone decreases serum levels of high-density lipoprotein cholesterol (HDL-C) in men, but whether this reflects altered HDL function is uncertain.

Hypothesis: Testosterone-mediated changes in serum HDL-C do not predict changes in HDL cholesterol efflux capacity (CEC).

Methods: Healthy men (n=45, 19-55 years of age) were rendered medically castrate with the GnRH antagonist acyline for 4 weeks and administered either 1) placebo gel, 2) low-dose testosterone gel (1.62%, 1.25 g), 3) full replacement dose testosterone gel (5 g) or 4) full replacement dose testosterone gel with an aromatase inhibitor. At baseline and end-of-treatment, serum total and ABCA1-specific CEC were quantified, and HDL particle size and concentration were measured through calibrated ion mobility analysis.

Results: As expected, a significant time-by-group interaction was observed for serum levels of HDL-C (p=0.01 in overall RM-ANOVA), with significant increases in HDL-C evident after both complete and partial testosterone deprivation. Medical castration also increased total HDL particle concentration (median(IQR) 19.1(1.8) nmol/L at baseline vs. 21.3(3.1) nmol/L at week 4, p=0.006). However, time-by-group interactions were not found for either total or ABCA1-specific CEC (p=0.17 and p=0.34 in overall RM-ANOVA, respectively), nor did change in serum testosterone level associate with changes in CEC. In contrast, change in serum 17β-estradiol level exhibited an inverse association with ABCA1-specific efflux (β=-0.48 per 10 pg/mL change in serum 17β-estradiol, p=0.002). When expressed as a percentage of total HDL particle number, significant time-by-group interactions were found for both small (s-HDL-P%) and large (l-HDL-P%) HDL particles (p=0.009 and p=0.03, respectively, in overall RM-ANOVA). Change in l-HDL-P% correlated inversely with change in serum testosterone level (β=-0.40 per 1 ng/dL change in serum testosterone, p=0.01) but positively with change in serum 17β-estradiol level (β=0.50 per 10 pg/mL change in serum 17β-estradiol, p=0.001).

Conclusions: Testosterone-mediated changes in serum HDL-C may not reflect changes in HDL CEC. Testosterone and estradiol both may contribute to the regulation of HDL particle size in men.

Message: Testosterone may decrease HDL but its effect on CEC is not as clear. Estradiol increases HDL.

 

[Nelson Vergel]

Arterioscler Thromb Vasc Biol. 2018 Mar;38(3):669-672. doi: 10.1161/ATVBAHA.117.310587. Epub 2018 Jan 11.

High-Density Lipoprotein Cholesterol and Mortality: Too Much of a Good Thing?

Hamer M1, O'Donovan G2, Stamatakis E2.

Abstract
OBJECTIVE:
The objective of this study was to examine the shape of the association between high-density lipoprotein cholesterol (HDL-C) and mortality in a large general population sample.

APPROACH AND RESULTS:
Adult participants (n=37 059; age=57.7±11.9 years; 46.8% men) were recruited from general population household-based surveys (Health Survey for England and Scottish Health Survey). Individual participant data were linked with the British National Health Service Central Registry to record mortality. There were 2250 deaths from all causes during 326 016 person-years of follow-up. When compared with the reference category (HDL-C=1.5-1.99 mmol/L), a U-shaped association was apparent for all-cause mortality, with elevated risk in participants with the lowest (hazard ratio=1.23; 95% confidence interval, 1.06, 1.44) and highest (1.25; 0.97, 1.62) HDL-C concentration. Associations for cardiovascular disease were linear, and elevated risk was observed in those with the lowest HDL-C concentration (1.49; 1.15, 1.94).

CONCLUSIONS:
A U-shaped association was observed between HDL-C and mortality in a large general population sample.

 

[Nelson Vergel]

Why does testosterone therapy decrease HDL cholesterol in some men


How to Increase Good Cholesterol (HDL) | Excel Male


Zinc Supplements Can Lower Good (HDL) Cholesterol | Excel Male



Effect of Diet on HDL | Excel Male

 

[Nelson Vergel]

Should we not worry about decreased HDL caused by higher-dose ...



NAC Benefits: HDL and More | Excel Male

 

[Nelson Vergel]

Supplements that lower LDL cholesterol and triglycerides and increase HDL.

 

[Nelson Vergel]

Lipids. 2019 May 29. doi: 10.1002/lipd.12155. [Epub ahead of print]

Aerobic Training in Young Men Increases the Transfer of Cholesterol to High Density Lipoprotein In Vitro: Impact of High Density Lipoprotein Size.

da Silva JL1, Maranhão RC1,2, Silva MSM3, Dias RG3, Freitas FR1, Bolani W3, Lemos Junior JR3,4, Alves CR5, Oliveira PA6, Alves GB6, Oliveira EM5, Negrao CE5,6, Krieger JE3, Pereira AC3, Silva GA1, Souza JP7, Vinagre CGC1,7.

Abstract
Exercise training not only improves the plasma lipid profile but also reduces risk of developing coronary heart disease. We investigate whether plasma lipids and high density lipoprotein (HDL) metabolism are affected by aerobic training and whether the high-density lipoprotein cholesterol (HDL-C) levels at baseline influence exercise-induced changes in HDL. Seventy-one male sedentary volunteers were evaluated and allocated in two subgroups, according to the HLD-C levels (< or >40 mg/dL). Participants underwent an 18-week aerobic training period. Blood was sampled before and after training for biochemical analysis. Plasma lipids, apolipoproteins, HDL diameter, and VO2 peak were determined. Lipid transfers to HDL were determined in vitro by incubating plasma samples with a donor lipid artificial nanoemulsion. After the 18-week period of aerobic training, the VO2 peak increased, while the mean body mass index (BMI) decreased. HDL-C concentration was higher after the training period, but low-density lipoprotein cholesterol (LDL-C) and non-HDL-C did not change. The transfer of esterified cholesterol and phospholipids was greater after exercise training, but the triacylglycerol and unesterified cholesterol transfers were unchanged. The HDL particle diameter increased after aerobic training in all participants. When the participants were separated in low-HDL and normal-HDL groups, the postaerobic exercise increment in HDL-C was higher in the low-HDL group, while the transfer of esterified cholesterol was lower. In conclusion, aerobic exercise training increases the lipid transfers to HDL, as measured by an in vitro method, which possibly contributes to the classical elevation of the HDL-C associated with training.

 

[Nelson Vergel]

Investigating The U-Shaped Link Between HDL Cholesterol And Adverse Outcomes

Despite historical evidence suggesting an inverse association between HDL cholesterol (HDL-C) and adverse cardiovascular events, pharmacological efforts to increase HDL-C and improve outcomes have not been successful. Recently, a U-shaped association between HDL-C and adverse events has been demonstrated in several population cohorts, further complicating our understanding of the clinical significance of HDL. Potential explanations for this finding include genetic mutations linked to very high HDL-C, impaired HDL function at high HDL-C levels, and residual confounding. However, our understanding of this association remains premature and needs further investigation.

 

[Nelson Vergel]

HDL Cholesterol Linked to Parkinson's Disease

Population study shows relationships between HDL levels and variability with incident PD

www.medpagetoday.com

 

[Nelson Vergel]

ORAL TESTOSTERONE VERSUS TOPICAL TESTOSTERONE: LARGER DECREASES IN HDL

CHANGES IN METABOLIC PARAMETERS AND BONE MARKERS WITH ORAL VERSUS TOPICAL TESTOSTERONE (2022) Fiona Yuen, Ronald S Swerdloff, Robert Dudley, and Christina Wang The Lundquist Institute at Harbor-UCLA Medical Center, Torrance, CA; Clarus Therapeutics, Northbrook, IL Background: Oral testosterone...

www.excelmale.com