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Title: The physiological and haematological effects associated with the abuse of recombinant human growth hormone and insulin in androgenic-anabolic steroid dependency
Author: Graham , Michael R.
Awarding Body: University of Glamorgan
Current Institution: University of South Wales
Date of Award: 2007
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Abstract:
Sports persons abuse androgenic-anabolic steroid (AAS) for cosmetic reasons (Pope et al., 2000) and to improve muscle mass and strength (Bhasin et al., 1996) with the intention of improving performance. MS abuse causes physiological and psychological dependence (Brower et al., 2002) and adverse cardiovascular effects (Graham et al., 2006b). sports persons also abuse recombinant human (rh) growth hormone (GH) and insulin for similar reasons and because it is still undetectable by urinalysis (Powrie et al., 2007). The purpose of this thesis was to determine the prevalence of abuse of rhGH and insulin with the intention of identifying any adverse physiological and haematological effects. The first study consisted of a questionnaire design that attempted to discover the prevalence of abuse of AAS. From the distribution of 210 questionnaires (response rate 70%) it was concluded that there were increases in the abuse of the drugs, growth hormone (24%) and insulin (14%) in comparison to earlier findings (Grace et al., 2001r The purpose of the second study was to investigate the effects of 30 days rhGH administration (0.013 mg.kg -I, n=36) in an abstinent AAS group (rhGH) compared with an exercise control group (BC) and a sedentary control group (SC). Packed cell volume (PCV) significantly decreased within the rhGH group (0.47±0.03 vs. 0.45±0.02, ratio; P<0.05) and was significantly greater than BC pre-rhGH administration (month 1; 0.47±0.03 vs. 0.44 ± 0.01; P<0.05). Triglycerides significantly decreased within the rhGH group (1.74 ± 0.4 vs. 1.4 ± OJ, mmol/L; P<0.05) and significantly decreased compared with SC on-rhGH administration (month 2; 1.4 ± 0.3 vs. 2.0 ± 0.6, mmol/L; P<0.05). The third study assessed the effects of 30 days insulin administration (0.12 IU.kg -I, n=36) in an abstinent AAS group (I-group) compared with an BC group and an SC group. Body mass index (BMI) significantly increased within the I-group (30.8 ± 3.2 vs. 31.2 ± 3.2, kg.m", P<0.05). PCV significantly increased within the I-group (0.45 ± 0.01 vs. 0.47 ± 0.02, ratio; P<0.05) and was significantly increased compared with BC on-insulin administration (month 2; 0.47 ± 0.02 vs. 0.44 ± 0.01, ratio; P<0.05). Triglycerides significantly increased within the I-group (1.78 ± 0.5 vs. 1.94 ± 0.5, mmol/L; P<0.05). Maximum inspiratory pressure (MIP) significantly increased within the I-group (MIP: 117 ± 32 vs. 122 ± 28, cm.H20; P<0.05). The fourth study assessed the effects of 30 days rhGH (0.017 mg.kg -1.dai1) and insulin (0.13 IU.kg -1, n=36) in an abstinent AAS group (rhGH-&-I group) compared with an BC group and anSCgroup. The arterial pulse wave velocity (APWV) significantly increased in the lower limb pre-occlusion velocity in the rhGH-&-I group compared with the BC group on rhGH-&-I administration (month 2; 10.8 ± 1.7 vs. 9.6 ± 0.9, m.s', P<0.05). The fifth study assessed the effects of 6 days rhGH administration (0.019 mg.kg -l.dail, n=48) in an abstinent AAS group (rhGH) compared with an abstinent AAS control group (C). Hospital Anxiety and Depression Scale (HADS) questionnaire significantly decreased in both anxiety (A) and depression (D) symptoms within the rhGH group (A: 6.8 ± 4.5 vs. 3.6 ± 3.5 vs. 4.1 ± 3.1; D: 4.5 ± 4.7 vs. 1.5 ± 2.5 vs. 2.5 ± 3.0, P<0.017) and compared with the C group (A: 3.6 ± 3.5 vs. 5.3 ± 2.1; D: 1.5 ± 2.5 vs. 3.0 ± 2.8, P<0.05). Body fat significantly decreased within the rhGH group (19.2 ± 6.3 vs. 20.2 ± 6.2, %, P<0.017). Resting heart rate (HR) and resting rate pressure product (RPP) significantly increased compared with the BC group (HR: 78 ± 11 vs. 67 ± 16, bpm; RPP: 97 ± 14 vs. 84 ± 24, bpm.mm.Hg X 10-2, P<0.05). APWV, lower limb pre-occlusion velocity, homocysteine (HCY) and C reactive protein (CRP) concentrations all significantly decreased within the rhGH administration group (APWV: 9.97 ± 1.38 vs. 9.18 ± 1.6, m.s"; HCY: 13.2 ± 4.0 vs. 11.5 ± 3.0, umol/L; CRP: 1.77 ± 2.1 vs. 1.26 ± 1.5 vs., mg/L, all P<0.017). Forced expiratory volume in 1 second/forced vital capacity (FEV I/FVC), MIP and maximum epiratory pressure (MEP) all significantly increased compared with the C group (FEV1/FVC: 85 ± 6 vs. 82 ± 5, %; MIP: 144 ± 24 vs. 129 ± 28, L; MEP: 179 ± 35 vs. 157 ± 32, L, all P<0.05). Strength (one repetition maximum; bench press [BePr] and squat [S]) and power (high intensity cycle ergometry) all significantly increased within the rhGH group (BePr: 106 ± 18 vs. 113 ± 19, S: 143 ± 27 vs. 164 ± 26, kg; Power: 1345 ± 216 vs. 1466 ± 257 vs. 1497 ± 253, W, all P<0.017) and BePr and S significantly increased compared with the C group (BePr; 113 ± 19 vs. 97 ± 24, kg; S; 164 ± 26 vs. 141 ± 34 kg, both P<0.05). Serum insulin-like growth factor (IGF-1) significantly increased within the rhGH group (159 ± 54 vs. 317 ± 91, ng.ml", P<0.017) and compared with the C group (317 ± 91 vs. 169 ± 50, ng.ml", P<0.05). RhGH administration for 30 days, in a dosage of 0.013 mg.kg -1.d-1, in abstinent AAS using weight lifters, appeared to offer no improvements in strength, but suggested an improvement in the specific cardiovascular risk marker, triglycerides. Insulin administration, for 30 days, in a dosage of 0.12 IU.kg -\, appeared to precipitate an adverse effect on the blood viscosity and lipoprotein profile, which may have a deleterious effect on an individual's risk of atherogenesis. The combination of rhGH-&-I, for 30 days, appeared to cause a significant increase in APWV, which may significantly increase cardiovascular risk in otherwise apparently healthy individuals However, 6 days use of rhGH in a dosage of 0.019 mg.kg -1.dai1 in apparently healthy abstinent AAS dependents, appeared to improve psychological profiles, alter body composition favourably, improve specific cardiovascular risk markers, improve respiratory function and increase strength and power. This suggested that the effects are dosage and time dependent. Despite this, the increase in resting heart rate and RPP may have an adverse effect on the cardiovascular system. Further work is required to establish any long term adverse effects before such therapy could be offered as a replacement treatment from AAS dependency.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.574488  DOI: Not available
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