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AAS and lowered HDL...not what you think?

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Reduced HDL levels are a commonly recognized side effect of androgen use. It is generally assumed that this is a bad thing because HDL levels are negatively correlated with CVD and HDL is believed to exert a protective effect on the circulatory system.

 

So I got wondering why is it that androgens decrease HDL levels. Turns out, this is pretty well understood: androgens increase the activity of hepatic triglyceride lipase, aka HTGL (PMID:4033402)...what makes this sort of interesting is that HTGL activity is believed to be protective against CVD (PMID:7853704)

 

So this begs the question, is the reduction in HDL levels seen with androgen use really indicative of an increased CVD risk? The available evidence seems to point to no because even though the number of HDL particles is reduced, the protective activity of some of the HDL fractions is not.

 

Clin Endocrinol (Oxf). 2003 Jan;58(1):49-58.

Tibolone lowers high density lipoprotein cholesterol by increasing hepatic lipase activity but does not impair cholesterol efflux.

von Eckardstein A, Crook D, Elbers J, Ragoobir J, Ezeh B, Helmond F, Miller N, Dieplinger H, Bennink HC, Assmann G.

Source

 

Institüt für Klinische Chemie und Laboratoriumsmedizin, Zentrallaboratorium, Westfälische Wilhelms-Universität Münster, Germany. arnold.voneckardstein@ikc.usz.ch

Abstract

OBJECTIVE:

 

Androgens and other drugs that reduce plasma concentrations of high density lipoprotein (HDL) cholesterol are often considered to be pro-atherogenic. Tibolone lowers HDL-cholesterol by 20% but the clinical significance of this effect is unknown.

METHODS:

 

In a randomized, double-blind study, 34 women received 2.5 mg tibolone daily and 34 women received placebo. Serum concentrations of lipids, lipoprotein subclasses and apolipoproteins, together with plasma activities of lipid transfer proteins and lipolytic enzymes and the capacity of plasma to induce cholesterol efflux from cultured cells, were measured.

RESULTS:

 

Compared to placebo, tibolone reduced serum concentrations of HDL-cholesterol (-14%), HDL phosphatidylcholine (-14%), apolipoprotein (apo)A-I (-12%), HDL subclasses lipoprotein (Lp)A-I (-20%), HDL-apoE (-16%), pre beta-LpA-I (-10%) and alpha-LpA-I (-12%) and increased hepatic lipase activity (+25%) and HDL sphingomyelin : phosphatidylcholine ratio (10.5%), but did not alter serum concentrations of HDL sphingomyelin, apoA-IV and LpA-I/A-II, lipoprotein lipase, the plasma activities of lecithin : cholesterol acyl transferase, cholesteryl ester transfer protein, phospholipid transfer protein or the plasma capacity to release cholesterol from cultured fibroblasts or Fu5AH hepatocytes.

CONCLUSIONS:

 

Tibolone lowers HDL-cholesterol in part by increasing hepatic lipase activity. Conservation of sphingomyelin and apoA-II in HDL, as well as cholesteryl ester transfer protein activity, preserves the capacity of plasma to release cholesterol, despite the lower concentrations of HDL-cholesterol. This may have important implications for the use of steroid effects on HDL concentrations as surrogates for atherosclerosis.

 

PMID: 12519412

 

 

Atherosclerosis. 2001 Dec;159(2):433-9.

Lowering of HDL cholesterol in post-menopausal women by tibolone is not associated with changes in cholesterol efflux capacity or paraoxonase activity.

von Eckardstein A, Schmiddem K, Hövels A, Gülbahçe E, Schuler-Lüttmann S, Elbers J, Helmond F, Bennink HJ, Assmann G.

Source

 

Institut für Klinische Chemie und Laboratoriumsmedizin, Zentrallaboratorium, Westfälische Wilhelms-Universität Münster, Albert-Schweitzer-Strasse 33, D-48129, Münster, Germany. vonecka@uni-muenster.de

Abstract

 

Low HDL cholesterol increases the risk of coronary heart disease. Treatment of postmenopausal women with tibolone lowers HDL cholesterol. We elucidated the consequences of this unwanted side effect in a randomized, double-blind study, where 12 women received 2.5 mg tibolone per day and 6 women, placebo. Blood samples were collected on days -1 (i.e. baseline), 28, 56, and 84 for the analysis of various parameters of lipid metabolism and HDL function. Compared to placebo, treatment with tibolone led to statistically significant decreases of HDL cholesterol (-22% to -32%), apoA-I (-14% to -22%), and HDL subclass LpA-I (-30% to -40%) but to no significant changes in apoA-II and HDL subclass LpA-I,A-II. These changes were not associated with statistically significant changes in the activity of plasma to release 3H-cholesterol from radiolabeled fibroblasts or in the serum activity of the anti-oxidative enzyme paraoxonase/arylesterase. There were no significant changes in either serum levels of triglycerides, LDL cholesterol, apoB, and leptin, or in LDL size. We conclude that changes in insulin do not contribute to the lowering of HDL cholesterol by tibolone. Despite decreased HDL cholesterol, putatively anti-atherogenic activities of HDL remained unchanged.

 

PMID: 11730824

 

 

Interesting stuff.

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Growth Horm IGF Res. 2003 Aug;13 Suppl A:S72-84.

Testosterone and atherosclerosis.

Eckardstein A, Wu FC.

Source

 

Institute of Clinical Chemistry, University Hospital of Zurich, Raemistrasse 100, CH-8091, Zurich, Switzerland. arnold.voneckardstein@ikc.usz.ch

Abstract

 

Hypoandrogenemia in men and hyperandrogenemia in women are associated with increased risk of coronary artery disease but also with visceral obesity, insulin resistance, low high-density lipoprotein (HDL) cholesterol, elevated triglycerides, low-density lipoprotein (LDL) cholesterol and plasminogen activator inhibitor (PAI-1). These gender differences and confounders render the precise role of endogenous androgens in atherosclerosis unclear. Exogenous androgens, on the other hand, induce both apparently beneficial and deleterious effects on cardiovascular risk factors by decreasing serum levels of HDL-C, PAI-1 (apparently deleterious), Lp(a), fibrinogen, insulin, leptin and visceral fat mass (apparently beneficial) in men as well as women. However, androgen-induced declines in circulating HDL-C should not automatically be assumed to be pro-atherogenic, since it may reflect accelerated reverse cholesterol transport instead.Short-term application of supraphysiological doses of exogenous T can reduce the severity and frequency of angina pectoris and improve the electrocardiographic signs of myocardial ischaemia; long-term effects have not been investigated. Nonetheless, interpretations of the effects of pharmacological doses of androgens on arterial compliance and flow-mediated dilatation in particular must be treated with circumspection also because at physiological concentrations, beneficial, neutral, and detrimental effects on vascular reactivity can be observed.Testosterone exerts 'pro-atherogenic' effects on macrophage function by facilitating the uptake of modified lipoproteins and an 'anti-atherogenic' effect by stimulating efflux of cellular cholesterol to HDL. In the majority of animal experiments, exogenous testosterone exerted neutral or beneficial effects on the development of atherosclerosis. In conclusion, the overall effect of administration of testosterone on cardiovascular-disease risk is difficult to assess because androgens have such an extraordinary array of effects in vivo. When dealing with a complex multifactorial condition such as CAD, it is premature to assume that clinical benefits can be derived from manipulation of the sex steroid milieu - even when these assumptions are based on biologically plausible mechanisms or, indeed, on cross-sectional risk-factor observational data. Neither needs the therapeutic use of testosterone in men be restricted by concerns regarding cardiovascular side effects.

 

PMID:12914731

 

 

 

Endocr Rev. 2003 Apr;24(2):183-217.

Androgens and coronary artery disease.

Wu FC, von Eckardstein A.

Source

 

Department of Endocrinology, Manchester Royal Infirmary, University of Manchester, Manchester M13 9WL, United Kingdom. fredrick.wu@man.ac.uk

Abstract

 

A significant and independent association between endogenous testosterone (T) levels and coronary events in men and women has not been confirmed in large prospective studies, although cross-sectional data have suggested coronary heart disease can be associated with low T in men. Hypoandrogenemia in men and hyperandrogenemia in women are associated with visceral obesity; insulin resistance; low high-density lipoprotein (HDL) cholesterol (HDL-C); and elevated triglycerides, low-density lipoprotein cholesterol, and plasminogen activator type 1. These gender differences and confounders render the precise role of endogenous T in atherosclerosis unclear. Observational studies do not support the hypothesis that dehydroepiandrosterone sulfate deficiency is a risk factor for coronary artery disease. The effects of exogenous T on cardiovascular mortality or morbidity have not been extensively investigated in prospective controlled studies; preliminary data suggest there may be short-term improvements in electrocardiographic changes in men with coronary artery disease. In the majority of animal experiments, exogenous T exerts either neutral or beneficial effects on the development of atherosclerosis. Exogenous androgens induce both apparently beneficial and deleterious effects on cardiovascular risk factors by decreasing serum levels of HDL-C, plasminogen activator type 1 (apparently deleterious), lipoprotein (a), fibrinogen, insulin, leptin, and visceral fat mass (apparently beneficial) in men as well as women. However, androgen-induced declines in circulating HDL-C should not automatically be assumed to be proatherogenic, because these declines may instead reflect accelerated reverse cholesterol transport. Supraphysiological concentrations of T stimulate vasorelaxation; but at physiological concentrations, beneficial, neutral, and detrimental effects on vascular reactivity have been observed. T exerts proatherogenic effects on macrophage function by facilitating the uptake of modified lipoproteins and an antiatherogenic effect by stimulating efflux of cellular cholesterol to HDL. In conclusion, the inconsistent data, which can only be partly explained by differences in dose and source of androgens, militate against a meaningful assessment of the net effect of T on atherosclerosis. Based on current evidence, the therapeutic use of T in men need not be restricted by concerns regarding cardiovascular side effects. Available data also do not justify the uncontrolled use of T or dehydroepiandrosterone for the prevention or treatment of coronary heart disease.

 

PMID:12700179

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Atherosclerosis. 2001 Dec;159(2):425-32.

Effects of androgen manipulation on postprandial triglyceridaemia, low-density lipoprotein particle size and lipoprotein(a) in men.

 

Hislop MS, St Clair Gibson A, Lambert MI, Noakes TD, Marais AD.

Source

 

Department of Internal Medicine, University of Cape Town Medical School, Anzio Road, Observatory, 7925, Cape Town, South Africa.

 

Abstract

 

Although androgenic hormones decrease HDLC concentration, no direct evidence has linked them to atherosclerosis. The present study was undertaken to extend our ability to assess risk associated with androgen induced lipoprotein(Lp) changes by simultaneously gathering information about postprandial triglyceridaemia (PPT), LDL particle size, HDL and Lp(a) in men either taking exogenous androgens or with suppressed endogenous androgen concentrations. The experimental groups comprised nine male bodybuilders who self-administered anabolic-androgenic steroids (AAS) for a mean period of 6.5 weeks, and 10 healthy men whose testosterone concentration had been reversibly suppressed for 5 weeks using the GnRH agonist triptorelin (Decapeptyl; D-Trp-6-LHRH). A separate group receiving no hormonal treatment provided analytical control (n=7). Lipoprotein size was assessed by gradient gel electrophoresis categorisation (GGE), lipoprotein concentrations by immuno and enzymatic assays and PPT by a standardised oral fat tolerance test (65g /m(2)). Testosterone concentration was significantly reduced on triptorelin from 7.32+/-1.92 to 1.15+/-0.57 ng/ml (P=0.002). High dose AAS use was confirmed by urinalysis. With AAS use, mean HDLC and Lp(a) concentrations and PPT decreased from 0.9+/-0.3 to 0.7+/-0.3 mmol/l (P=0.004), 125+/-128 to 69+/-73 U/l (P=0.008) and 11.6+/-10.0 mmol/l h to 7.5+/-5.4 mmol/l h (P=0.027) respectively. Mean total cholesterol and LDLC were unchanged. LDL size was unchanged in six AAS users, decreased in one but remaining in the normal size range, and increased in two from small LDL to the normal range. Size changes in the latter two subjects were associated with 42 and 58% reductions in PPT respectively. In the triptorelin group, mean total cholesterol, HDLC and Lp(a) were increased from 4.8+/-0.8 mmol/l to 5.2+/-1.0 mmol/l (P=0.039), 1.1+/-0.2 to 1.4+/-0.3 mmol/l (P=0.002) and 278+/-149 to 377+/-222 U/l (P=0.004) respectively. Mean LDLC concentration and PPT were unchanged. LDL particle size increased in four, decreased in two, and was unchanged in four subjects. LDL size decreased in two and showed no change in the other five control subjects. Other lipid measures were unchanged in the control group. Thus, apart from lowering HDLC concentrations, no other potentially atherogenic effects of endogenous androgens or AAS were observed. A suppression of Lp(a) as well as a reduced PPT and increased LDL size in predisposed individuals may be antiatherogenic effects of AAS.

 

PMID: 11730823

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J Investig Med. 2008 Oct;56(7):920-4.

Oxandrolone enhances hepatic ketogenesis in adult men.

Vega GL, Clarenbach JJ, Dunn F, Grundy SM.

Source

 

Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA. Gloria.Vega@utsouthwestern.edu

Abstract

BACKGROUND:

 

Immediate administration of oxandrolone markedly increases hepatic lipase activity and reduces levels of plasma high-density lipoprotein.

RATIONALE FOR THE STUDY:

 

We postulated that oxandrolone should increase hepatic lipase and that the nonesterified fatty acids generated would enhance hepatic ketogenesis during an extended fat tolerance test.

MAIN RESULTS:

 

Eighteen men participated in the study using short-term administration of oxandrolone (10 mg/d) over a week. Subjects had evaluation of hepatic ketogenesis at baseline and after 7 days of administration of oxandrolone. Ketogenesis was assessed by measuring plasma levels of 3-hydroxybutyrate during a fat tolerance test. Oxandrolone increased fasting levels of 3-hydroxybutyrate by 70%, and increased the area under the curve during an FFT by 53% above pretreatment levels without affecting the areas under the curve for nonesterified fatty acids, glycerol, or triglycerides. Fasting 3-hydroxybutyrate levels correlated with nonesterified fatty acids and with triglycerides; however, there were no significant correlations with any other parameter.

CONCLUSIONS:

 

This study shows that short-term administration of oxandrolone results in marked increases in hepatic ketogenesis. This finding is consistent with an increased influx of fatty acids into the liver secondary to lipoprotein lipolysis by increased hepatic lipase. However, the possibility cannot be ruled out that oxandrolone acts directly in the liver to stimulate fatty acid oxidation. Therefore, the observation of increased ketogenesis will require further studies to determine the molecular basis of the response.

 

PMID:18797410

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Is their a test to get our lipoprotein lipase/hepatic triglyceride lipase (LPL/HTGL) ratio? Privatemdlabs didnt have a test that measured HTGL activity listed in their blood work options so was wondering is this even something we can measure with bloods?

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You have to wonder about the multiple body builders that have died in their 30's and 40's from heart attacks and strokes. Their diet and exercise was perfect... I think there is still increased risk with lowered HDL and with orals even more with increased LDL.

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You have to wonder about the multiple body builders that have died in their 30's and 40's from heart attacks and strokes. Their diet and exercise was perfect... I think there is still increased risk with lowered HDL and with orals even more with increased LDL.

 

"their diet was perfect" is a very dubious statement. You know how those guys got their 10,000+ calories in mass gain phases? How they abused diuretics, etc.?

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You have to wonder about the multiple body builders that have died in their 30's and 40's from heart attacks and strokes. Their diet and exercise was perfect... I think there is still increased risk with lowered HDL and with orals even more with increased LDL.

 

Selection bias. Male basketball players in their teens and twenties have a much higher risk of sudden cardiac death than BB of any age.

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Reduced HDL levels are a commonly recognized side effect of androgen use. It is generally assumed that this is a bad thing because HDL levels are negatively correlated with CVD and HDL is believed to exert a protective effect on the circulatory system.--So I got wondering why is it that androgens decrease HDL levels. Turns out, this is pretty well understood: androgens increase the activity of hepatic triglyceride lipase, aka HTGL (PMID:4033402)...what makes this sort of interesting is that HTGL activity is believed to be protective against CVD (PMID:7853704)--So this begs the question, is the reduction in HDL levels seen with androgen use really indicative of an increased CVD risk?" <<< ----As usual, another well-articulated thread birthed by Benson... :)...

This one was on my radar for a long time also, and its clear that there simply is no evidence to support the idea that the reductions in HDL levels noted with androgen use are in anyway indicative of an increased CVD risk...

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"the cardiovascular impact of HDL is not simply related to its abundance"

also note that sometimes "HDL from stable coronary artery disease (CAD) or acute coronary syndrome patients inhibits rather than stimulates endothelial NO synthesis and endothelial repair"

 

 

J Clin Invest. 2011 Jul;121(7):2545-8. doi: 10.1172/JCI57671. Epub 2011 Jun 23.

 

PON-dering differences in HDL function in coronary artery disease.

Mineo C, Shaul PW.

Source

Division of Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9063, USA.

Abstract

HDL cholesterol activates endothelial cell production of the atheroprotective signaling molecule NO, and it promotes endothelial repair. In this issue of the JCI, Besler et al. provide new data indicating that HDL from stable coronary artery disease (CAD) or acute coronary syndrome patients inhibits rather than stimulates endothelial NO synthesis and endothelial repair. This may be related to decreased HDL-associated paraoxonase 1 (PON1) activity. These observations support the concept that the cardiovascular impact of HDL is not simply related to its abundance, and the translation of the present findings to prospective studies of CAD risk and to evaluations of HDL-targeted therapeutics is a logical future goal.

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It's also worth noting that AIs can sock the lipid profile pretty hard' date=' most notably HDL. [/quote']

 

This is commonly held wisdom but check out this chart from a 12 month study of letrozole (2.5g/day) in post-menopausal women.

 

onc0111006940001.jpg

 

TC fell, HDL increased and LDL decreased from baseline over 12 months.

 

http://www.ncbi.nlm.nih.gov/pubmed/20980416

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Ok, again, re: Testosterone's effects on HDL levels and CAD/CVD risk, the following is very clear IMHO...-- Testosterone consistently Decreases CAD/CVD risk by its ability to specifically augment/increase levels of - 1-hepatic lipase, 2- HDL- efficiency/functionality - (despite occasionally decreasing total HDL number), and finally- 3- Activity of the liver protein Scavenger Receptor B1. These testosterone-mediated effects all improve reverse cholesterol transport (RCT) - all of which greatly decreases CAD/CVD risk in men.

 

The often overlooked aspect of HDL-C seems to be that of not focusing on the small subclass of HDL-C lipoproteins....The large and medium HDL cholesterol subtypes or classes are the ones that well known to prevent CVD/CAD in men. However, among these 3 classes in the HDL "family"...ONLY the the small subtype of HDL DOES NOT prevent CVD/CAD...

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JAMA. 1989 Feb 24;261(8):1165-8.

Contrasting effects of testosterone and stanozolol on serum lipoprotein levels.

Thompson PD, Cullinane EM, Sady SP, Chenevert C, Saritelli AL, Sady MA, Herbert PN.

Source

 

Department of Medicine, Miriam Hospital, Providence, RI 02906.

Abstract

 

Oral anabolic steroids produce striking reductions in serum concentrations of high-density lipoprotein (HDL) cholesterol. We hypothesized that this effect related to their route of administration and was unrelated to their androgenic potency. We administered oral stanozolol (6 mg/d) or supraphysiological doses of intramuscular testosterone enanthate (200 mg/wk) to 11 male weight lifters for six weeks in a crossover design. Stanozolol reduced HDL-cholesterol and the HDL2 subfraction by 33% and 71%, respectively. In contrast, testosterone decreased HDL-cholesterol concentration by only 9% and the decrease was in the HDL3 subfraction. Apolipoprotein A-I level decreased 40% during stanozolol but only 8% during testosterone treatment. The low-density lipoprotein cholesterol concentration increased 29% with stanozolol and decreased 16% with testosterone treatment. Stanozolol, moreover, increased postheparin hepatic triglyceride lipase activity by 123%, whereas the maximum change during testosterone therapy (+25%) was not significant. Weight gain was similar with both drugs, but testosterone was more effective in suppressing gonadotropic hormones. We conclude that the undesirable lipoprotein effects of 17-alpha-alkylated steroids given orally are different from those of parenteral testosterone and that the latter may be preferable in many clinical situations.

 

PMID: 2915439

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Metabolism. 1997 Sep;46(9):992-6.

Effects of short-term stanozolol administration on serum lipoproteins in hepatic lipase deficiency.

Bausserman LL, Saritelli AL, Herbert PN.

Source

 

Lipid Research Laboratory, Miriam Hospital, Brown University Medical School, Providence, RI, USA.

Abstract

 

We have identified a kindred in Providence, RI, deficient in hepatic triglyceride lipase (HL). The two affected brothers have coronary heart disease and elevated levels of triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, and apolipoprotein [apo] A-I. The lipoprotein lipase (LPL) activity is normal. We and others have postulated that the effects of oral anabolic steroids on HDL metabolism are mediated by HL. To test this hypothesis, we treated these two men and two controls with the oral androgen stanozolol (6 mg/d) for 2 weeks. Consistent with other reports, HL activity increased a mean of 277% in controls with a concomitant decrease in HDL cholesterol (49%), HDL2 cholesterol (90%), HDL3 cholesterol (16%), and apo A-I (41%) and no change in apo A-II. Although stanozolol failed to induce HL activity in the HL-deficient man, HDL cholesterol, HDL2 cholesterol, and apo A-I were reduced a mean of 20%, 48%, and 32%, respectively. In contrast to controls, HDL3 cholesterol (46%) and apo A-II (14%) increased in HL-deficient subjects. Stanozolol treatment also increased LPL activity (124% +/- 86%, n = 4) and decreased lipoprotein(a) ([Lp(a)] 66% +/- 3%, n = 3) in the three men with detectable levels. The data indicate that in addition to stimulation of HL activity, stanozolol treatment changes HDL cholesterol concentration and subfraction distribution by other mechanisms.

 

PMID:9284885

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just out and somewhat related (+ confirms that common practice makes sense ;))

 

Mol Nutr Food Res. 2012 Jun;56(6):900-11. doi: 10.1002/mnfr.201100611.

Taurine is a liver X receptor-α ligand and activates transcription of key genes in the reverse cholesterol transport without inducing hepatic lipogenesis.

Hoang MH, Jia Y, Jun HJ, Lee JH, Hwang KY, Choi DW, Um SJ, Lee BY, You SG, Lee SJ.

Source

 

Department of Biotechnology, Graduate School of Life Sciences and Biotechnology, Korea University, Seoul, South Korea.

Abstract

SCOPE:

 

Taurine, which is abundant in seafood, has antiatherogenic activities in both animals and humans; however, its molecular target has been elusive. We examined whether taurine could activate liver X receptor-α (LXR-α), a critical transcription factor in the regulation of reverse cholesterol transport in macrophages.

METHODS AND RESULTS:

 

Taurine bound directly to LXR-α in a reporter gene assay, time-resolved fluorescence resonance energy transfer analysis, and limited protease digestion experiment. Macrophage cells incubated with taurine showed reduced cellular cholesterol and induced medium cholesterol in a dose-dependent manner with the induction of ATP-binding cassette transporter A1 and G gene and protein expression. In hepatocytes, taurine significantly induced Insig-2a levels and delayed nuclear translocation of the sterol regulatory element-binding protein 1 (SREBP-1) protein, resulting in a dose-dependent reduction in the cellular lipid levels without inducing the expression of fatty acid synthesis genes.

CONCLUSION:

 

Taurine is a direct LXR-α ligand, represses cholesterol accumulation, and modulates the expression of genes involved in reverse cholesterol transport in macrophages, without inducing hepatic lipogenesis. The induction of Insig-2a suppressed the nuclear translocation of SREBP-1c.

 

© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

 

edit: CAN WE PLEASE SWITCH THE ITALICS BACK OFF (its simply not legible and unnecessary if quotes are already in a box!)

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Med Sci Sports Exerc. 1996 Feb;28(2):176-9.

Lipoprotein (a) and cholesterol in body builders using anabolic androgenic steroids.

Cohen LI, Hartford CG, Rogers GG.

Source

 

Department of Physiology, University of the Witwatersrand Medical School, Parktown, Johannesburg, South Africa.

Abstract

 

We examined the influence of self-administered anabolic androgenic steroids (AAS) on the lipogram of male body builders. Serum lipoprotein (a) (Lp(a)), total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels were measured in 10 experimental and 8 control male competitive body builders. The proportion of subjects with serum Lp(a) levels above 30 mg.dl-1 was significantly lower in the AAS group than the non-AAS group. HDL-C levels were significantly lower and LDL-C levels significantly higher in the AAS group than the non-AAS group. These data suggest that AAS in male body builders have a beneficial effect on serum Lp(a) levels but reduce the HDL-C:LDL-C ratio.

 

PMID: 8775151

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Aside from niacin, this is the only thing I've ever seen that significantly lowered LPa...and there are a couple of other studies that showed that AAS lowered it quite substantially...

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Their diet and exercise was perfect...

 

 

Was it? I've seen quite a few high level bodybuilders who couldn't exercise their way out a paper bag if the routine was anything beyond split bodyparts, low intensity cardio. And the diet, well sometimes the diet is just about manipulation of macros, with little else to be concerned about. Also, let's not forget about their dieting drugs, diuretics etc. Not to mention recreational drugs.

 

Also, another important aspect. A lot of bodybuilders ignore their high hematocrit levels. I think that is just as detrimental as anything else.

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Also, another important aspect. A lot of bodybuilders ignore their high hematocrit levels. I think that is just as detrimental as anything else.

 

Another reason to give blood regularly.

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