• All new members please introduce your self here and welcome to the board:
    http://www.professionalmuscle.com/forums/showthread.php?t=259
Buy Needles And Syringes With No Prescription
M4B Store Banner
intex
Riptropin Store banner
Generation X Bodybuilding Forum
Buy Needles And Syringes With No Prescription
Buy Needles And Syringes With No Prescription
Mysupps Store Banner
IP Gear Store Banner
PM-Ace-Labs
Ganabol Store Banner
Spend $100 and get bonus needles free at sterile syringes
Professional Muscle Store open now
sunrise2
PHARMAHGH1
kinglab
ganabol2
Professional Muscle Store open now
over 5000 supplements on sale at professional muscle store
boslabs1
granabolic1
napsgear-210x65
monster210x65
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
DeFiant
UGFREAK-banner-PM
STADAPM
yms-GIF-210x65-SB
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
wuhan2
dpharma
marathon
zzsttmy
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
azteca
crewguru
advertise1x
advertise1x
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store

AAS and lipoprotein a

Johan

New member
Registered
Joined
Jun 5, 2002
Messages
240
Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a).

Hartgens F, Rietjens G, Keizer HA, Kuipers H, Wolffenbuttel BH.

Netherlands Centre for Doping Affairs, Capelle aan den IJssel, The Netherlands. [email protected]

OBJECTIVES: To investigate the effects of two different regimens of androgenic-anabolic steroid (AAS) administration on serum lipid and lipoproteins, and recovery of these variables after drug cessation, as indicators of the risk for cardiovascular disease in healthy male strength athletes. METHODS: In a non-blinded study (study 1) serum lipoproteins and lipids were assessed in 19 subjects who self administered AASs for eight or 14 weeks, and in 16 non-using volunteers. In a randomised double blind, placebo controlled design, the effects of intramuscular administration of nandrolone decanoate (200 mg/week) for eight weeks on the same variables in 16 bodybuilders were studied (study 2). Fasting serum concentrations of total cholesterol, triglycerides, HDL-cholesterol (HDL-C), HDL2-cholesterol (HDL2-C), HDL3-cholesterol (HDL3-C), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), and lipoprotein (a) (Lp(a)) were determined. RESULTS: In study 1 AAS administration led to decreases in serum concentrations of HDL-C (from 1.08 (0.30) to 0.43 (0.22) mmol/l), HDL2-C (from 0.21 (0.18) to 0.05 (0.03) mmol/l), HDL3-C (from 0.87 (0.24) to 0.40 (0.20) mmol/l, and Apo-A1 (from 1.41 (0.27) to 0.71 (0.34) g/l), whereas Apo-B increased from 0.96 (0.13) to 1.32 (0.28) g/l. Serum Lp(a) declined from 189 (315) to 32 (63) U/l. Total cholesterol and triglycerides did not change significantly. Alterations after eight and 14 weeks of AAS administration were comparable. No changes occurred in the controls. Six weeks after AAS cessation, serum HDL-C, HDL2-C, Apo-A1, Apo-B, and Lp(a) had still not returned to baseline concentrations. Administration of AAS for 14 weeks was associated with slower recovery to pretreatment concentrations than administration for eight weeks. In study 2, nandrolone decanoate did not influence serum triglycerides, total cholesterol, HDL-C, HDL2-C, HDL3-C, Apo-A1, and Apo-B concentrations after four and eight weeks of intervention, nor six weeks after withdrawal. However, Lp(a) concentrations decreased significantly from 103 (68) to 65 (44) U/l in the nandrolone decanoate group, and in the placebo group a smaller reduction from 245 (245) to 201 (194) U/l was observed. Six weeks after the intervention period, Lp(a) concentrations had returned to baseline values in both groups. CONCLUSIONS: Self administration of several AASs simultaneously for eight or 14 weeks produces comparable profound unfavourable effects on lipids and lipoproteins, leading to an increased atherogenic lipid profile, despite a beneficial effect on Lp(a) concentration. The changes persist after AAS withdrawal, and normalisation depends on the duration of the drug abuse. Eight weeks of administration of nandrolone decanoate does not affect lipid and lipoprotein concentrations, although it may selectively reduce Lp(a) concentrations. The effect of this on atherogenesis remains to be established.
[/QUOTE}

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

Cohen LI, Hartford CG, Rogers GG.

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

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.

Hormonal agents used in lowering lipoprotein(a).

Soma MR, Meschia M, Bruschi F, Morrisett JD, Paoletti R, Fumagalli R, Crosignani P.

Institute of Pharmacological Sciences, University of Milan, Italy.

Lipoprotein(a) (Lp(a)) plasma concentrations in Caucasian populations are classified as a quantitative genetic trait. Although the prevailing view has been that Lp(a) levels are affected by age and gender, recent data are beginning to indicate otherwise. Lp(a) levels change throughout life especially in females after menopause. Lp(a) levels decrease in women treated with anabolic steroids such as stanozolol and danazol. The Lp(a) plasma concentration is also profoundly affected by sex hormone variations during pregnancy. In men with prostatic cancer Lp(a) levels are reduced about 50% by estrogen therapy, and increased 20% by orchidectomy. We have evaluated the changes in Lp(a) and lipid levels in postmenopausal women following estrogen/progestogen replacement therapy. The mean level of Lp(a) in treated women was about 50% lower after 6 and 12 months of replacement therapy. A significant correlation between basal Lp(a) levels and the changes at either 6 or 12 months was observed, suggesting that therapy was particularly efficacious in those women with high basal Lp(a) levels. One year after therapy cessation, Lp(a) concentrations tended to return to pre-therapy values. In addition estrogen-progestogen treatment significantly lowered total-cholesterol (12%) and LDL-cholesterol (28%), and increased HDL-cholesterol (18%). From these studies it appears that sex hormones are actively involved in the modulation of plasma Lp(a) levels and that both female and male sex hormones possess a lowering effect. The results confirm a direct effect of sex hormones on Lp(a) metabolism and suggest that estrogen-progestogen treatment of postmenopausal women can improve the lipid profile not only by lowering total- and LDL-cholesterol and raising HDL cholesterol, but also by lowering plasma Lp(a).

Lipoprotein Lp(a) levels are reduced by danazol, an anabolic steroid.

Crook D, Sidhu M, Seed M, O'Donnell M, Stevenson JC.

Wynn Institute for Metabolic Research, London, U.K.

Serum levels of lipids, lipoproteins and apolipoproteins were measured in 26 premenopausal women with endometriosis both before and after six months therapy with the anabolic steroid danazol (600 mg/day) and in 15 untreated women who acted as controls. No changes were seen in the control group over six months. In women treated with danazol, mean levels of low density lipoprotein (LDL) cholesterol increased by 36% while those of high density lipoprotein (HDL) cholesterol decreased by 46%, changes characteristic of androgenic steroids. In contrast to this potentially detrimental lipoprotein profile, lipoprotein(a) [Lp(a)] levels were reduced by 78.6% +/- 24.0% (mean +/- S.D.) in women taking danazol. These dramatic changes in Lp(a) levels correlated with baseline Lp(a) levels but not with changes in LDL or HDL. Anabolic steroids such as danazol appear to be powerful modulators of serum Lp(a) concentrations. This could be due to direct effects on Lp(a) metabolism, or secondary to the effects of these steroids on insulin metabolism or on the coagulation and fibrinolysis system.

I guess the effects on homocystein is what we should be most concerned about

Hyperhomocysteinemia in bodybuilders taking anabolic steroids.

Ebenbichler CF, Kaser S, Bodner J, Gander R, Lechleitner M, Herold M, Patsch JR.

Universitatsklinik fur Innere Medizin, Universitat Innsbruck, Anichstrasse 35, 6010, Innsbruck, Austria

Background: Hyperhomocysteinemia has been accepted as an independent risk factor for atherosclerosis and atherothrombosis. In recent years, several reports have appeared in the literature linking the use of anabolic steroids with acute vascular events in bodybuilders. In this study, we investigated whether hyperhomocysteinemia could contribute to the high vascular risk in bodybuilders taking anabolic steroids. Methods and results: Twenty-three bodybuilders in different phases of their training cycle and six control athletes participated in our study. Anthropomorphic measures displayed a higher body mass index for bodybuilders in the competition phase than for bodybuilders in the work-out and build-up phases, and for control athletes. Homocysteine levels were 8.7+/-1.6 micromol/l (mean+/-S.D.) in control athletes, 8.5+/-2.8 micromol/l in work-out phase bodybuilders, and 8.3+/-1.5 micromol/l in competition phase bodybuilders, but 11.9+/-3.1 micromol/l in build-up phase bodybuilders (P<0.05 for build-up phase bodybuilders vs. control athletes, work-out phase bodybuilders, and competition phase bodybuilders, respectively). Vitamin B12 and folate levels did not differ significantly between the four groups. Conclusion: Our study shows that intake of anabolic steroids, as used typically by bodybuilders in the build-up phase, induces acute hyperhomocysteinemia and is likely to initiate an additional, potentially atherothrombotic mechanism in this group of athletes.

PMID: 11173010 [PubMed - as supplied by publisher]

this might explain why estrogen is so important for cardio health when cycling

Effects of sex steroids on plasma total homocysteine levels: a study in transsexual males and females.

Giltay EJ, Hoogeveen EK, Elbers JM, Gooren LJ, Asscheman H, Stehouwer CD.

Department of Endocrinology, Division of Andrology, Hospital Vrije Universiteit, Amsterdam, The Netherlands.

Plasma total homocysteine (tHcy) levels are higher in men vs. premenopausal women, but it is not known whether this difference is related to sex steroids. The effects of cross-sex hormone administration on plasma tHcy levels were therefore investigated. Plasma tHcy levels were measured at baseline and after 4 months of treatment in 17 male-to-female (M-->F) transsexuals treated with ethinyl estradiol (100 micrograms/day), in combination with the antiandrogen, cyproterone acetate (100 mg/day), and in 17 female-to-male (F-->M) transsexuals treated with testosterone esters (250 mg/2 weeks, im). In M-->F transsexuals, the plasma tHcy level decreased from geometric mean 8.2 mumol/L to 5.7 mumol/L (P < 0.001); and in F-->M transsexuals, it increased from 7.7 mumol/L to 9.0 mumol/L (P = 0.005). In M-->F transsexuals, changes in serum sex hormone-binding globulin levels correlated negatively, and changes in plasma creatinine and albumin levels correlated positively, with changes in plasma tHcy levels. In F-->M transsexuals, changes in serum 17 beta-estradiol levels correlated negatively, and changes in plasma creatinine levels correlated positively, with changes in plasma tHcy levels. We conclude that tHcy levels decrease after estrogen + antiandrogen administration to male (transsexual) subjects, and levels increase after androgen administration to female (transsexual) subjects. These changes may be both primary and secondary to the anabolic/catabolic effects, as reflected by changes of creatinine and albumin levels after cross-sex hormone administration.

PMID: 9467573 [PubMed - indexed for MEDLINE]
 
Would I be correct to assume that controling homocystein would be a far more important issue especialy for us bodybuilders compered to controling LDL? After all Lp(a) is a bigger risk factor then LDL and LDL isnt all that bad if it doesnt oxidize(easily prevented by vitamin c for instance)??

If that is true then cardiovascular health is just a vitamin b supplement away :confused: since 5-10mg folicacid, 300-600mcg vitamin B12 and 300-500mg vitamin B6 effectly lowers homocystein.
 

Forum statistics

Total page views
575,926,600
Threads
138,421
Messages
2,856,321
Members
161,433
Latest member
TheTruth777
NapsGear
HGH Power Store email banner
yourdailyvitamins
Prowrist straps store banner
yourrawmaterials
3
raws
Savage Labs Store email
Syntherol Site Enhancing Oil Synthol
aqpharma
yms-GIF-210x131-Banne-B
hulabs
ezgif-com-resize-2-1
MA Research Chem store banner
MA Supps Store Banner
volartek
Keytech banner
thc
Godbullraw-bottom-banner
Injection Instructions for beginners
YMS-210x131-V02
Back
Top