Coronary artery calcium scan
Coronary artery calcium scan - Peter Attia
Coronary artery calcium scan - Peter Attia
MESO-Rx
Anabolic Steroids
AAS and Cardiovascular/Pulmonary Function
- Thread starter Michael Scally MD
- Start date
chocolatemalt
New Member
This is fantastic. Definitely worth keeping the link handy as an example for anyone's skepticism that the medical establishment has a strong, mindless bias against TRT and testosterone generally.
Biomarkers and Non-Calcified Coronary Artery Plaque Progression in Older Men Treated with Testosterone
Recent results from the Cardiovascular (CV) Trial of the Testosterone(T) Trials showed that T treatment of older men with low T was associated with greater progression of non-calcified plaque (NCP). We evaluated the effect of anthropometric measures and cardiovascular biomarkers on plaque progression in individuals in the T Trial.
The CV part of the trial included 170 men aged 65 years or older with low T. Participants received T gel or placebo gel for 12 months. The primary outcome was change in NCP volume from baseline to 12 months, as determined by coronary computed tomography angiography (CCTA). We assayed several markers of CV risk and analyzed each marker individually in a model as predictive variables and change in NCP as the dependent variable.
Of 170 enrollees, 138 (73 T, 65 placebo) completed the study and were available for the primary analysis. Of 10 markers evaluated, none showed a significant association with the change in NCP volume, but a significant interaction between treatment assignment and waist-hip ratio p-0.0014) indicated that this variable impacted the testosterone effect on non-calcified plaque volume.
The statistical model indicated that for every 0.1 change in the waist-hip ratio, the T-induced 12-month change in non-calcified plaque volume increased by 26.96 mm3 (95% confidence interval 7.72, 46.20). Among older men with low T treated for one year, greater waist-hip ratio was associated with greater NCP progression, as measured by CCTA.
Other biomarkers and anthropometric measures did not show statistically significant association with plaque progression.
Shaikh K, Ellenberg SS, Nakanishi R, et al. Biomarkers and Non-Calcified Coronary Artery Plaque Progression in Older Men Treated with Testosterone. The Journal of Clinical Endocrinology & Metabolism 2019. Biomarkers and Non-Calcified Coronary Artery Plaque Progression in Older Men Treated with Testosterone
Recent results from the Cardiovascular (CV) Trial of the Testosterone(T) Trials showed that T treatment of older men with low T was associated with greater progression of non-calcified plaque (NCP). We evaluated the effect of anthropometric measures and cardiovascular biomarkers on plaque progression in individuals in the T Trial.
The CV part of the trial included 170 men aged 65 years or older with low T. Participants received T gel or placebo gel for 12 months. The primary outcome was change in NCP volume from baseline to 12 months, as determined by coronary computed tomography angiography (CCTA). We assayed several markers of CV risk and analyzed each marker individually in a model as predictive variables and change in NCP as the dependent variable.
Of 170 enrollees, 138 (73 T, 65 placebo) completed the study and were available for the primary analysis. Of 10 markers evaluated, none showed a significant association with the change in NCP volume, but a significant interaction between treatment assignment and waist-hip ratio p-0.0014) indicated that this variable impacted the testosterone effect on non-calcified plaque volume.
The statistical model indicated that for every 0.1 change in the waist-hip ratio, the T-induced 12-month change in non-calcified plaque volume increased by 26.96 mm3 (95% confidence interval 7.72, 46.20). Among older men with low T treated for one year, greater waist-hip ratio was associated with greater NCP progression, as measured by CCTA.
Other biomarkers and anthropometric measures did not show statistically significant association with plaque progression.
Shaikh K, Ellenberg SS, Nakanishi R, et al. Biomarkers and Non-Calcified Coronary Artery Plaque Progression in Older Men Treated with Testosterone. The Journal of Clinical Endocrinology & Metabolism 2019. Biomarkers and Non-Calcified Coronary Artery Plaque Progression in Older Men Treated with Testosterone
Application of Non-HDL Cholesterol for Population-Based Cardiovascular Risk Stratification
Background - The relevance of blood lipid concentrations to long-term incidence of cardiovascular disease and the relevance of lipid-lowering therapy for cardiovascular disease outcomes is unclear.
We investigated the cardiovascular disease risk associated with the full spectrum of bloodstream non-HDL cholesterol concentrations.
We also created an easy-to-use tool to estimate the long-term probabilities for a cardiovascular disease event associated with non-HDL cholesterol and modelled its risk reduction by lipid-lowering treatment.
Methods - In this risk-evaluation and risk-modelling study, we used Multinational Cardiovascular Risk Consortium data from 19 countries across Europe, Australia, and North America. Individuals without prevalent cardiovascular disease at baseline and with robust available data on cardiovascular disease outcomes were included.
The primary composite endpoint of atherosclerotic cardiovascular disease was defined as the occurrence of the coronary heart disease event or ischaemic stroke. Sex-specific multivariable analyses were computed using non-HDL cholesterol categories according to the European guideline thresholds, adjusted for age, sex, cohort, and classical modifiable cardiovascular risk factors.
In a derivation and validation design, we created a tool to estimate the probabilities of a cardiovascular disease event by the age of 75 years, dependent on age, sex, and risk factors, and the associated modelled risk reduction, assuming a 50% reduction of non-HDL cholesterol.
Findings - Of the 524 444 individuals in the 44 cohorts in the Consortium database, we identified 398 846 individuals belonging to 38 cohorts (184 055 [48·7%] women; median age 51·0 years [IQR 40·7–59·7]). 199 415 individuals were included in the derivation cohort (91 786 [48·4%] women) and 199 431 (92 269 [49·1%] women) in the validation cohort.
During a maximum follow-up of 43·6 years (median 13·5 years, IQR 7·0–20·1), 54 542 cardiovascular endpoints occurred. Incidence curve analyses showed progressively higher 30-year cardiovascular disease event-rates for increasing non-HDL cholesterol categories (from 7·7% for non-HDL cholesterol <2·6 mmol/L to 33·7% for ≥5·7 mmol/L in women and from 12·8% to 43·6% in men; p<0·0001).
Multivariable adjusted Cox models with non-HDL cholesterol lower than 2·6 mmol/L as reference showed an increase in the association between non-HDL cholesterol concentration and cardiovascular disease for both sexes (from hazard ratio 1·1, 95% CI 1·0–1·3 for non-HDL cholesterol 2·6 to <3·7 mmol/L to 1·9, 1·6–2·2 for ≥5·7 mmol/L in women and from 1·1, 1·0–1·3 to 2·3, 2·0–2·5 in men).
The derived tool allowed the estimation of cardiovascular disease event probabilities specific for non-HDL cholesterol with high comparability between the derivation and validation cohorts as reflected by smooth calibration curves analyses and a root mean square error lower than 1% for the estimated probabilities of cardiovascular disease.
A 50% reduction of non-HDL cholesterol concentrations was associated with reduced risk of a cardiovascular disease event by the age of 75 years, and this risk reduction was greater the earlier cholesterol concentrations were reduced.
Interpretation - Non-HDL cholesterol concentrations in blood are strongly associated with long-term risk of atherosclerotic cardiovascular disease. We provide a simple tool for individual long-term risk assessment and the potential benefit of early lipid-lowering intervention. These data could be useful for physician–patient communication about primary prevention strategies.
Brunner FJ, Waldeyer C, Ojeda F, et al. Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. The Lancet. Redirecting
Background - The relevance of blood lipid concentrations to long-term incidence of cardiovascular disease and the relevance of lipid-lowering therapy for cardiovascular disease outcomes is unclear.
We investigated the cardiovascular disease risk associated with the full spectrum of bloodstream non-HDL cholesterol concentrations.
We also created an easy-to-use tool to estimate the long-term probabilities for a cardiovascular disease event associated with non-HDL cholesterol and modelled its risk reduction by lipid-lowering treatment.
Methods - In this risk-evaluation and risk-modelling study, we used Multinational Cardiovascular Risk Consortium data from 19 countries across Europe, Australia, and North America. Individuals without prevalent cardiovascular disease at baseline and with robust available data on cardiovascular disease outcomes were included.
The primary composite endpoint of atherosclerotic cardiovascular disease was defined as the occurrence of the coronary heart disease event or ischaemic stroke. Sex-specific multivariable analyses were computed using non-HDL cholesterol categories according to the European guideline thresholds, adjusted for age, sex, cohort, and classical modifiable cardiovascular risk factors.
In a derivation and validation design, we created a tool to estimate the probabilities of a cardiovascular disease event by the age of 75 years, dependent on age, sex, and risk factors, and the associated modelled risk reduction, assuming a 50% reduction of non-HDL cholesterol.
Findings - Of the 524 444 individuals in the 44 cohorts in the Consortium database, we identified 398 846 individuals belonging to 38 cohorts (184 055 [48·7%] women; median age 51·0 years [IQR 40·7–59·7]). 199 415 individuals were included in the derivation cohort (91 786 [48·4%] women) and 199 431 (92 269 [49·1%] women) in the validation cohort.
During a maximum follow-up of 43·6 years (median 13·5 years, IQR 7·0–20·1), 54 542 cardiovascular endpoints occurred. Incidence curve analyses showed progressively higher 30-year cardiovascular disease event-rates for increasing non-HDL cholesterol categories (from 7·7% for non-HDL cholesterol <2·6 mmol/L to 33·7% for ≥5·7 mmol/L in women and from 12·8% to 43·6% in men; p<0·0001).
Multivariable adjusted Cox models with non-HDL cholesterol lower than 2·6 mmol/L as reference showed an increase in the association between non-HDL cholesterol concentration and cardiovascular disease for both sexes (from hazard ratio 1·1, 95% CI 1·0–1·3 for non-HDL cholesterol 2·6 to <3·7 mmol/L to 1·9, 1·6–2·2 for ≥5·7 mmol/L in women and from 1·1, 1·0–1·3 to 2·3, 2·0–2·5 in men).
The derived tool allowed the estimation of cardiovascular disease event probabilities specific for non-HDL cholesterol with high comparability between the derivation and validation cohorts as reflected by smooth calibration curves analyses and a root mean square error lower than 1% for the estimated probabilities of cardiovascular disease.
A 50% reduction of non-HDL cholesterol concentrations was associated with reduced risk of a cardiovascular disease event by the age of 75 years, and this risk reduction was greater the earlier cholesterol concentrations were reduced.
Interpretation - Non-HDL cholesterol concentrations in blood are strongly associated with long-term risk of atherosclerotic cardiovascular disease. We provide a simple tool for individual long-term risk assessment and the potential benefit of early lipid-lowering intervention. These data could be useful for physician–patient communication about primary prevention strategies.
Brunner FJ, Waldeyer C, Ojeda F, et al. Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. The Lancet. Redirecting
[RUFKM] [OA] A Tumultuous Course of Exogenous Testosterone by a Bodybuilder Causing a Catastrophic Hypercoagulable State in the Surgical Intensive Care Unit
This is the extent of the testosterone history: “Upon review of his social history, the patient did admit to using exogenous testosterone in the past. The exact dose and duration of his testosterone use was not fully clarified with the patient directly.”
Present literature demonstrates an equivocal relationship between testosterone and thrombogenicity.
Herein, we describe a case in which a patient used an unspecified amount and duration of exogenous testosterone injections, subsequently developing thrombotic events in his: right radial artery, right iliac artery, superficial femoral artery, splenic artery and a bilateral lower lobe pulmonary embolism.
As a result, clinicians should consider exogenous testosterone use as a potential risk factor when the etiology of a patient’s thrombotic events are not clear.
We also completed a literature review of the molecular mechanisms in which testosterone can increase the clot burden through an increases human platelet thromboxane A2 receptor density and an increase in erythropoiesis.
Lee K, Toraby S, Cotterman R, Oriowo B, Fish J. A Tumultuous Course of Exogenous Testosterone by a Bodybuilder Causing a Catastrophic Hypercoagulable State in the Surgical Intensive Care Unit. Case Reports in Vascular Medicine 2019;2019:5. https://doi.org/10.1155/2019/3097865
This is the extent of the testosterone history: “Upon review of his social history, the patient did admit to using exogenous testosterone in the past. The exact dose and duration of his testosterone use was not fully clarified with the patient directly.”
Present literature demonstrates an equivocal relationship between testosterone and thrombogenicity.
Herein, we describe a case in which a patient used an unspecified amount and duration of exogenous testosterone injections, subsequently developing thrombotic events in his: right radial artery, right iliac artery, superficial femoral artery, splenic artery and a bilateral lower lobe pulmonary embolism.
As a result, clinicians should consider exogenous testosterone use as a potential risk factor when the etiology of a patient’s thrombotic events are not clear.
We also completed a literature review of the molecular mechanisms in which testosterone can increase the clot burden through an increases human platelet thromboxane A2 receptor density and an increase in erythropoiesis.
Lee K, Toraby S, Cotterman R, Oriowo B, Fish J. A Tumultuous Course of Exogenous Testosterone by a Bodybuilder Causing a Catastrophic Hypercoagulable State in the Surgical Intensive Care Unit. Case Reports in Vascular Medicine 2019;2019:5. https://doi.org/10.1155/2019/3097865
The 2018 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on the management of blood cholesterol endorsed the coronary artery calcium score as a tiebreaker in the decision to withhold, postpone, or initiate statin therapy for adults at intermediate or borderline risk of atherosclerotic cardiovascular disease (ASCVD).1 We disagree and will make a case against the use of coronary artery calcium scoring for any reason.
Suspected Reactivation of Extrapulmonary Tuberculosis Focus After Non-Medical Abuse of Anabolic Androgenic Steroids: A Case Report
Background Youth population has a common tendency to use androgenic steroids. The reasons for such abuse vary from performance enhancement to muscle building in order to enhance physical appearance. Such rampant abuse, aided by fitness centers and gym trainers, has a huge risk of side effects such as hepatic dysfunctions and increased risk of infections.
Case presentation We report a case of 21-year-old man who started with anabolic steroids, namely testosterone enanthate, nandrolone decanoate and boldenone undecylenate injections, for the purpose of muscle building and strength training at his fitness center. He presented to his family physician after 2 months with upper neck swelling on right side 5 x 4 cm for 15-20 days.
He was started on Augmentin 625 mg tablet three times a day for 7 days. On seventh day, swelling persisted, and fine needle aspiration cytology (FNAC) was performed, which was suggestive of granulomatous lesion likely to be tuberculosis. The patient was started with anti-tubercular therapy (ATT) under category A, but swelling did not improve and repeated FNAC was advised. The ATT was withheld and Augmentin tablet was restarted for another 3 days.
A revised diagnosis of acute suppurative lymphadenitis was made, and an incision and drainage of the abscess was performed. The patient was started on Amikacin 500 intramuscular injection for 5 days along with faropenem and cefuroxime axetil tablets for 14 days. He initially started recovering but returned with pustular discharge from the incision mark. It was decided to reinitiate the ATT-intensive phase medication for another 2 months.
The patient finally recovered with complete healing of the wound. The frequent change of treating physician and misuse of antimicrobials made the diagnosis tougher, contributing to delay in the optimum therapy.
Conclusion This case highlights the abuse of multiple steroids together in the form of stacking by a young adult, which leads to a rare serious adverse effect such as suspected tubercular reactivation.
Singh V, Batta A. Suspected reactivation of extrapulmonary tuberculosis focus after non-medical abuse of anabolic androgenic steroids: a case report. Journal of basic and clinical physiology and pharmacology 2019. https://www.degruyter.com/view/j/jbcpp.ahead-of-print/jbcpp-2019-0167/jbcpp-2019-0167.xml
Background Youth population has a common tendency to use androgenic steroids. The reasons for such abuse vary from performance enhancement to muscle building in order to enhance physical appearance. Such rampant abuse, aided by fitness centers and gym trainers, has a huge risk of side effects such as hepatic dysfunctions and increased risk of infections.
Case presentation We report a case of 21-year-old man who started with anabolic steroids, namely testosterone enanthate, nandrolone decanoate and boldenone undecylenate injections, for the purpose of muscle building and strength training at his fitness center. He presented to his family physician after 2 months with upper neck swelling on right side 5 x 4 cm for 15-20 days.
He was started on Augmentin 625 mg tablet three times a day for 7 days. On seventh day, swelling persisted, and fine needle aspiration cytology (FNAC) was performed, which was suggestive of granulomatous lesion likely to be tuberculosis. The patient was started with anti-tubercular therapy (ATT) under category A, but swelling did not improve and repeated FNAC was advised. The ATT was withheld and Augmentin tablet was restarted for another 3 days.
A revised diagnosis of acute suppurative lymphadenitis was made, and an incision and drainage of the abscess was performed. The patient was started on Amikacin 500 intramuscular injection for 5 days along with faropenem and cefuroxime axetil tablets for 14 days. He initially started recovering but returned with pustular discharge from the incision mark. It was decided to reinitiate the ATT-intensive phase medication for another 2 months.
The patient finally recovered with complete healing of the wound. The frequent change of treating physician and misuse of antimicrobials made the diagnosis tougher, contributing to delay in the optimum therapy.
Conclusion This case highlights the abuse of multiple steroids together in the form of stacking by a young adult, which leads to a rare serious adverse effect such as suspected tubercular reactivation.
Singh V, Batta A. Suspected reactivation of extrapulmonary tuberculosis focus after non-medical abuse of anabolic androgenic steroids: a case report. Journal of basic and clinical physiology and pharmacology 2019. https://www.degruyter.com/view/j/jbcpp.ahead-of-print/jbcpp-2019-0167/jbcpp-2019-0167.xml
Leukemic phase of ALK-negative anaplastic large cell lymphoma in a patient who is on androgenic steroids: A case report.
Highlights
· Clinicopathological correlation is imperative in the diagnosis of leukemic phase ALK-negative anaplastic large cell lymphoma.
· Leukemic phase ALK-negative anaplastic large cell lymphoma progresses rapidly if the diagnosis is delayed.
· Anabolic steroids compromises the immune system and depletes the ability of lymphocytes to remove tumour producing cells.
ALK-negative anaplastic large cell lymphoma (ALCL) is a peripheral T-cell lymphoma that usually involves lymph nodes or extranodal sites. Leukemic phase of ALK-negative ALCL is exceedingly rare and often carries a poor prognosis. Androgenic steroids have gained popularity among the young, and at higher doses, it can result in immune dysregulation and may be potentially carcinogenic.
Case presentation: A 30-year-old gentleman of Malay ethnicity presented to the hematology department with night fevers, loss of weight and bony pain for the past 6 weeks. He is a gymnasium instructor with a history of chronic usage of intramuscular testosterone enanthate. Physical examination revealed ecchymosis over the left elbow and hepatomegaly. A complete blood count depicted anemia, thrombocytopenia and leucocytosis.
An 18-Fluorodeoxyglucose positron emission tomography (18-FDG PET/CT) imaging showed a hypermetabolic anterior mediastinal mass of 6.8 x 7.0 x 6.5 cm with diffuse hypermetabolism in the liver, spleen and axial skeleton. The bone marrow trephine and mediastinal tissue histology were consistent with leukemic ALK-negative ALCL.
He was treated with CHOEP (cyclophosphamide, doxorubicin, vincristine, etoposide, prednisolone) induction chemotherapy in which he required intensive antibiotic and blood support. He progressed with worsening B symptoms and new diffuse lymphadenopathies suggesting rapid dissemination of the disease. He subsequently succumbed to multiorgan failure with disseminated intravascular coagulopathy at the intensive care unit.
Conclusion: Leukemic phase ALK-negative ALCL often carries a complex karyotype and requires early intensive polychemotherapy. Use of anabolic steroids depletes the ability of defending lymphocytes to remove tumour producing cells.
Kasinathan G. Leukemic phase of ALK-negative anaplastic large cell lymphoma in a patient who is on androgenic steroids: A case report. Annals of medicine and surgery (2012) 2020;49:1-4. Leukemic phase of ALK-negative anaplastic large cell lymphoma in a patient who is on androgenic steroids: A case report - ScienceDirect
Highlights
· Clinicopathological correlation is imperative in the diagnosis of leukemic phase ALK-negative anaplastic large cell lymphoma.
· Leukemic phase ALK-negative anaplastic large cell lymphoma progresses rapidly if the diagnosis is delayed.
· Anabolic steroids compromises the immune system and depletes the ability of lymphocytes to remove tumour producing cells.
ALK-negative anaplastic large cell lymphoma (ALCL) is a peripheral T-cell lymphoma that usually involves lymph nodes or extranodal sites. Leukemic phase of ALK-negative ALCL is exceedingly rare and often carries a poor prognosis. Androgenic steroids have gained popularity among the young, and at higher doses, it can result in immune dysregulation and may be potentially carcinogenic.
Case presentation: A 30-year-old gentleman of Malay ethnicity presented to the hematology department with night fevers, loss of weight and bony pain for the past 6 weeks. He is a gymnasium instructor with a history of chronic usage of intramuscular testosterone enanthate. Physical examination revealed ecchymosis over the left elbow and hepatomegaly. A complete blood count depicted anemia, thrombocytopenia and leucocytosis.
An 18-Fluorodeoxyglucose positron emission tomography (18-FDG PET/CT) imaging showed a hypermetabolic anterior mediastinal mass of 6.8 x 7.0 x 6.5 cm with diffuse hypermetabolism in the liver, spleen and axial skeleton. The bone marrow trephine and mediastinal tissue histology were consistent with leukemic ALK-negative ALCL.
He was treated with CHOEP (cyclophosphamide, doxorubicin, vincristine, etoposide, prednisolone) induction chemotherapy in which he required intensive antibiotic and blood support. He progressed with worsening B symptoms and new diffuse lymphadenopathies suggesting rapid dissemination of the disease. He subsequently succumbed to multiorgan failure with disseminated intravascular coagulopathy at the intensive care unit.
Conclusion: Leukemic phase ALK-negative ALCL often carries a complex karyotype and requires early intensive polychemotherapy. Use of anabolic steroids depletes the ability of defending lymphocytes to remove tumour producing cells.
Kasinathan G. Leukemic phase of ALK-negative anaplastic large cell lymphoma in a patient who is on androgenic steroids: A case report. Annals of medicine and surgery (2012) 2020;49:1-4. Leukemic phase of ALK-negative anaplastic large cell lymphoma in a patient who is on androgenic steroids: A case report - ScienceDirect
[Mice] Evolutions in Cardiac and Gonadal Ultra-Structure During a "Cycle" Of Androgenic Anabolic Abuse
Highlights
· The purpose of this study is to apply the manner of taking anabolic androgenic steroids by the abusers in the most simple administration: deca-dorabolin (nandrolone decanoate) taken in dose estimated to be 10 times supra-medical (30mg / kg of BW /IM per week, for 3 months) well stopped treatment for 6 weeks; what constitutes a cycle of use frequently used by the abuser and follow the evolution of cardiac and gonadal cyto-architecture under these conditions.
· This study is among the few studies done on the reverbability of the effects of androgen doping on cardiac pathology,
· This is among the very few morphometric studies done for this purpose, as well as on testicular pathology,
· And the only one reported by the evolution of the morphometric data mentioned in the manuscript during a whole cycle of androgen doping.
· These results ported that the use of AAS with “Cycling” may lead to irreversibly destroy the heart tissue. Either, “Cycling” does not ensure the complete recovery of fertility in AAS abusers.
· So, physicians should take these damages in mind seriously as a predictable and potential complication cardiac function and fertility resulting from abusing these drugs. At the same time, the official and medical control and restrictions on these drugs should be increased to prevent the abusers from obtaining these drugs.
BACKGROUND: The importance of the present study comes from the lack of sufficient information about the reversibility of the potential histopathological alterations which may result from anabolic androgenic drugs abuse by "Cycling" protocol. So, the aim of this study is to explore the negative effects of Deca-Durabolin abuse in cardiac and gonadal ultra-structures during an administration cycle.
METHODS: For our purpose, study was performed on 40 male adult mices. Animals were divided into five groups of 8 animals each treated weekly by Deca-Durabolin (nandrolone decanoate) at 30g/kg of BW during one month (GI); during two months (GII); during three months (GIII); during three months followed by six weeks of treatment discontinuation (GIV) and Control (C). Cytohistological examinations to determine the histopathological damage properties of the heart and tests were performed.
RESULTS: Our results showed that the animals supported very well the administrated substance. Our study showed important degenerative changes in cardiac and gonadal tissues after one months of androgen abuse. These damages increases with the duration of treatment with well marked cell lesions, and worsen again 6 weeks after stopping treatment in cardiac tissue, whereas the gonadal tissue does not recover completely during this period.
CONCLUSION: These results ported that the use of AAS with "Cycling" may lead to irreversibly destroy the heart tissue. Either, "Cycling" does not ensure the complete recovery of fertility in AAS abusers.
Kahal A, Allem R, Zahzeh T, et al. Evolutions in cardiac and gonadal ultra-structure during a "Cycle" of androgenic anabolic abuse in adult male mice. Steroids 2019:108571. Evolutions in cardiac and gonadal ultra-structure during a “Cycle” of androgenic anabolic abuse in adult male mice - ScienceDirect
Highlights
· The purpose of this study is to apply the manner of taking anabolic androgenic steroids by the abusers in the most simple administration: deca-dorabolin (nandrolone decanoate) taken in dose estimated to be 10 times supra-medical (30mg / kg of BW /IM per week, for 3 months) well stopped treatment for 6 weeks; what constitutes a cycle of use frequently used by the abuser and follow the evolution of cardiac and gonadal cyto-architecture under these conditions.
· This study is among the few studies done on the reverbability of the effects of androgen doping on cardiac pathology,
· This is among the very few morphometric studies done for this purpose, as well as on testicular pathology,
· And the only one reported by the evolution of the morphometric data mentioned in the manuscript during a whole cycle of androgen doping.
· These results ported that the use of AAS with “Cycling” may lead to irreversibly destroy the heart tissue. Either, “Cycling” does not ensure the complete recovery of fertility in AAS abusers.
· So, physicians should take these damages in mind seriously as a predictable and potential complication cardiac function and fertility resulting from abusing these drugs. At the same time, the official and medical control and restrictions on these drugs should be increased to prevent the abusers from obtaining these drugs.
BACKGROUND: The importance of the present study comes from the lack of sufficient information about the reversibility of the potential histopathological alterations which may result from anabolic androgenic drugs abuse by "Cycling" protocol. So, the aim of this study is to explore the negative effects of Deca-Durabolin abuse in cardiac and gonadal ultra-structures during an administration cycle.
METHODS: For our purpose, study was performed on 40 male adult mices. Animals were divided into five groups of 8 animals each treated weekly by Deca-Durabolin (nandrolone decanoate) at 30g/kg of BW during one month (GI); during two months (GII); during three months (GIII); during three months followed by six weeks of treatment discontinuation (GIV) and Control (C). Cytohistological examinations to determine the histopathological damage properties of the heart and tests were performed.
RESULTS: Our results showed that the animals supported very well the administrated substance. Our study showed important degenerative changes in cardiac and gonadal tissues after one months of androgen abuse. These damages increases with the duration of treatment with well marked cell lesions, and worsen again 6 weeks after stopping treatment in cardiac tissue, whereas the gonadal tissue does not recover completely during this period.
CONCLUSION: These results ported that the use of AAS with "Cycling" may lead to irreversibly destroy the heart tissue. Either, "Cycling" does not ensure the complete recovery of fertility in AAS abusers.
Kahal A, Allem R, Zahzeh T, et al. Evolutions in cardiac and gonadal ultra-structure during a "Cycle" of androgenic anabolic abuse in adult male mice. Steroids 2019:108571. Evolutions in cardiac and gonadal ultra-structure during a “Cycle” of androgenic anabolic abuse in adult male mice - ScienceDirect
[19972] Randomized Controlled Trial of Testosterone Treatment on Left Ventricular Mass in Older Men With Low Testosterone
https://www.ahajournals.org/doi/10.1161/CIR.0000000000000742
Background: Left ventricular hypertrophy is an independent predictor of myocardial infarction, heart failure, and sudden cardiac death. Based on animal and observational studies, testosterone has been hypothesized to act as a hypertrophic stimulus on cardiac muscle. There have been no randomized controlled trials measuring the effect of testosterone treatment on left ventricular mass in humans.
Methods: The Testosterone Trials (TTrials) are a set of seven randomized, double-blind, placebo-controlled trials of testosterone gel in older men with low testosterone. The Cardiovascular Trial is a substudy of TTrials in which participants underwent coronary CT angiography at baseline and after one year of treatment to determine the effect of testosterone treatment on coronary artery plaque.
The current analysis considers the effect of testosterone on cardiac chamber size. The primary end-point of this analysis is change in body surface area (BSA)-indexed left ventricular mass (LVMI) by randomization status. Secondary endpoints were changes in cardiac chamber volumes indexed by BSA.
Results: Baseline characteristics are shown in Table 1. Testosterone treatment significantly increased serum testosterone levels into the mid-normal range for young men (Figure 1); levels in the placebo arm did not change. At month 12, testosterone treatment was associated with a significantly increased LVMI compared to placebo treatment; p=0.033. The average magnitude of change was 3.09 ml/m2 (95% CI 0.26, 5.92). The differences in change in all other chamber measurements were not significant between groups (Table 2).
Conclusion: Testosterone is widely used to treat male hypogonadism, but its effects on the heart have not been fully delineated. In this study, testosterone treatment was associated with a significant increase in left ventricular mass. This supports previous observations that testosterone acts as a hypertrophic stimulus on cardiac myocytes, which should be considered as part of the safety profile of testosterone treatment.
https://www.ahajournals.org/doi/10.1161/CIR.0000000000000742
Background: Left ventricular hypertrophy is an independent predictor of myocardial infarction, heart failure, and sudden cardiac death. Based on animal and observational studies, testosterone has been hypothesized to act as a hypertrophic stimulus on cardiac muscle. There have been no randomized controlled trials measuring the effect of testosterone treatment on left ventricular mass in humans.
Methods: The Testosterone Trials (TTrials) are a set of seven randomized, double-blind, placebo-controlled trials of testosterone gel in older men with low testosterone. The Cardiovascular Trial is a substudy of TTrials in which participants underwent coronary CT angiography at baseline and after one year of treatment to determine the effect of testosterone treatment on coronary artery plaque.
The current analysis considers the effect of testosterone on cardiac chamber size. The primary end-point of this analysis is change in body surface area (BSA)-indexed left ventricular mass (LVMI) by randomization status. Secondary endpoints were changes in cardiac chamber volumes indexed by BSA.
Results: Baseline characteristics are shown in Table 1. Testosterone treatment significantly increased serum testosterone levels into the mid-normal range for young men (Figure 1); levels in the placebo arm did not change. At month 12, testosterone treatment was associated with a significantly increased LVMI compared to placebo treatment; p=0.033. The average magnitude of change was 3.09 ml/m2 (95% CI 0.26, 5.92). The differences in change in all other chamber measurements were not significant between groups (Table 2).
Conclusion: Testosterone is widely used to treat male hypogonadism, but its effects on the heart have not been fully delineated. In this study, testosterone treatment was associated with a significant increase in left ventricular mass. This supports previous observations that testosterone acts as a hypertrophic stimulus on cardiac myocytes, which should be considered as part of the safety profile of testosterone treatment.
Testosterone Gel Increases LV Mass In Older Men
Testosterone gel increases LV mass in older men
Testosterone gel for treatment of hypogonadism in older men boosted their left ventricular mass by 3.5% in a single year in the multicenter, double-blind, placebo-controlled Testosterone Cardiovascular Trial, although the clinical implications of this impressive increase remain unclear, Elizabeth Hutchins, MD, reported at the American Heart Association scientific sessions.
...
The key study finding was that LV mass indexed to body surface area rose significantly in the testosterone gel group, from an average of 71.5 g/m2 at baseline to 74.8 g/m2 at 1 year. That’s a statistically significant 3.5% increase. In contrast, LV mass remained flat across the year in controls: 73.8 g/m2 at baseline and 73.3 g/m2 at 12 months.
Dr. Hutchins noted that this was the first-ever randomized controlled trial to measure the effect of testosterone therapy on LV mass in humans. The documented increase achieved with 1 year of testosterone gel doesn’t come close to reaching the threshold of LV hypertrophy, which is about 125 g/m2 for men. But evidence from animal and observational human studies suggests that even in the absence of LV hypertrophy, increases in LV mass are associated with increased mortality, she added.
[OA] Rate and Extent of Recovery from Reproductive and Cardiac Dysfunction Due to Androgen Abuse
Context: Androgen abuse impairs male reproductive and cardiac function but the rate, extent and determinants of recovery are not understood.
Objective: To investigate recovery of male reproductive and cardiac function after ceasing androgen intake in current and past androgen abusers compared with healthy non-users.
Methods: Cross-sectional, observational study recruited via social media 41 current and 31 past users (≥3 months since last use, median 300 days since last use) with 21 healthy, eugonadal non-users. Each provided a history, examination, serum and semen sample and underwent testicular ultrasound, body composition analysis and cardiac function evaluation.
Results: Current abusers had suppressed reproductive function, impaired cardiac systolic function and lipoprotein parameters compared with non or past users. Past users did not differ from non-users suggesting full recovery of suppressed reproductive and cardiac functions after ceasing androgen abuse, other than residual reduced testicular volume. Mean time to recovery was faster for reproductive hormones (AMH, 7.3 months; LH, 10.7 months) than for sperm variables (output, 14.1 months) whereas spermatogenesis (serum FSH, inhibin B, inhibin) took longer. The duration of androgen abuse was the only other variable associated with slower recovery of sperm output (but not hormones).
Conclusion: Suppressed testicular and cardiac function due to androgen abuse is effectively fully reversible (apart from testis volume and serum SHBG) with recovery taking between 6 to 18 months after ceasing androgen intake with possible cumulative effects on spermatogenesis. Suppressed serum AMH, LH and FSH represent convenient, useful and underutilized markers of recovery from androgen abuse.
Shankara-Narayana N, Yu C, Savkovic S, et al. Rate and Extent of Recovery from Reproductive and Cardiac Dysfunction Due to Androgen Abuse in Men [published online ahead of print, 2020 Feb 7]. J Clin Endocrinol Metab. 2020;dgz324. https://academic.oup.com/jcem/advance-article/doi/10.1210/clinem/dgz324/5729047
Context: Androgen abuse impairs male reproductive and cardiac function but the rate, extent and determinants of recovery are not understood.
Objective: To investigate recovery of male reproductive and cardiac function after ceasing androgen intake in current and past androgen abusers compared with healthy non-users.
Methods: Cross-sectional, observational study recruited via social media 41 current and 31 past users (≥3 months since last use, median 300 days since last use) with 21 healthy, eugonadal non-users. Each provided a history, examination, serum and semen sample and underwent testicular ultrasound, body composition analysis and cardiac function evaluation.
Results: Current abusers had suppressed reproductive function, impaired cardiac systolic function and lipoprotein parameters compared with non or past users. Past users did not differ from non-users suggesting full recovery of suppressed reproductive and cardiac functions after ceasing androgen abuse, other than residual reduced testicular volume. Mean time to recovery was faster for reproductive hormones (AMH, 7.3 months; LH, 10.7 months) than for sperm variables (output, 14.1 months) whereas spermatogenesis (serum FSH, inhibin B, inhibin) took longer. The duration of androgen abuse was the only other variable associated with slower recovery of sperm output (but not hormones).
Conclusion: Suppressed testicular and cardiac function due to androgen abuse is effectively fully reversible (apart from testis volume and serum SHBG) with recovery taking between 6 to 18 months after ceasing androgen intake with possible cumulative effects on spermatogenesis. Suppressed serum AMH, LH and FSH represent convenient, useful and underutilized markers of recovery from androgen abuse.
Shankara-Narayana N, Yu C, Savkovic S, et al. Rate and Extent of Recovery from Reproductive and Cardiac Dysfunction Due to Androgen Abuse in Men [published online ahead of print, 2020 Feb 7]. J Clin Endocrinol Metab. 2020;dgz324. https://academic.oup.com/jcem/advance-article/doi/10.1210/clinem/dgz324/5729047
Physique Demon
Member
When something like this happens over time can it return to normal? Or is this permanent...?
[OA] Inferior Vena Cava Occlusion in Retroperitoneal Fibrosis and Exogenous Testosterone Administration
Retroperitoneal fibrosis (RPF) causing large vessel stenosis and thrombosis is rare but well-described.
We describe a 50-year-old man with rapid progression of central venous thrombosis in the presence of RPF and exogenous testosterone use.
Therapeutic anticoagulation was initiated and catheter directed thrombolysis was performed after placement of an inferior vena cava (IVC) filter.
Repeat venogram revealed severe focal retrohepatic IVC stenosis, which was treated with serial venoplasty and stenting. Clinical improvement was significant 48 hours after intervention.
This case represents a rare presentation of IVC occlusion in the setting of RPF and exogenous testosterone administration successfully treated with endovascular interventions.
Kirby DT, Dilday JC, Muir KB, Young AG, Aidinian G. Inferior vena cava occlusion in retroperitoneal fibrosis and exogenous testosterone administration. Journal of Vascular Surgery Cases and Innovative Techniques 2020;6:34-7. Inferior vena cava occlusion in retroperitoneal fibrosis and exogenous testosterone administration - ScienceDirect
Retroperitoneal fibrosis (RPF) causing large vessel stenosis and thrombosis is rare but well-described.
We describe a 50-year-old man with rapid progression of central venous thrombosis in the presence of RPF and exogenous testosterone use.
Therapeutic anticoagulation was initiated and catheter directed thrombolysis was performed after placement of an inferior vena cava (IVC) filter.
Repeat venogram revealed severe focal retrohepatic IVC stenosis, which was treated with serial venoplasty and stenting. Clinical improvement was significant 48 hours after intervention.
This case represents a rare presentation of IVC occlusion in the setting of RPF and exogenous testosterone administration successfully treated with endovascular interventions.
Kirby DT, Dilday JC, Muir KB, Young AG, Aidinian G. Inferior vena cava occlusion in retroperitoneal fibrosis and exogenous testosterone administration. Journal of Vascular Surgery Cases and Innovative Techniques 2020;6:34-7. Inferior vena cava occlusion in retroperitoneal fibrosis and exogenous testosterone administration - ScienceDirect
No PR yet, but I am sure there will be shortly. ESPERION | The Lipid Management Company
FDA approves ESPR’s Nexletol (bempedoic acid): https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/211616s000lbl.pdf
FDA approves ESPR’s Nexletol (bempedoic acid): https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/211616s000lbl.pdf
ESPR—FDA approves Nexletol/Zetia FDC called Nexlizet:
Esperion Announces FDA Approval of the NEXLIZET™ (bempedoic acid and ezetimibe) Tablet, an Oral, Once-Daily, Non-Statin LDL-Cholesterol Lowering Medicine
By incorporating a dual LDL-lowering MoA, Nexlizet can reduce LDL for some patients beyond what can be accomplished with Nexletol monotherapy.
Each Nexlizet tablet contains 180mg of Nexletol and 10mg (generic) Zetia. (Zetia has been off-patent in the US for several years.)
FDA Approves Bempedoic Acid-Ezetimibe Combination for ASCVD, Heterozygous FH
FDA Approves Bempedoic Acid-Ezetimibe Combo for ASCVD, HeFH
Esperion Announces FDA Approval of the NEXLIZET™ (bempedoic acid and ezetimibe) Tablet, an Oral, Once-Daily, Non-Statin LDL-Cholesterol Lowering Medicine
By incorporating a dual LDL-lowering MoA, Nexlizet can reduce LDL for some patients beyond what can be accomplished with Nexletol monotherapy.
Each Nexlizet tablet contains 180mg of Nexletol and 10mg (generic) Zetia. (Zetia has been off-patent in the US for several years.)
FDA Approves Bempedoic Acid-Ezetimibe Combination for ASCVD, Heterozygous FH
FDA Approves Bempedoic Acid-Ezetimibe Combo for ASCVD, HeFH
kosp
Member
Is AAS-Induced Left Ventricular Hypertrophy reversible after time off?
[OA] [PhD Thesis] Testosterone - Of Importance in Patients with Dysglycemia and Cardiovascular Disease?
Background: Testosterone has been associated with cardiovascular (CV) health in men and women with or without diabetes. There are however conflicting results which warrant further investigations to understand if testosterone is important for prognosis, in particular in relation to diabetes and cardiovascular disease (CVD). To gain further insight, several aspects such as when and which testosterone fraction to assess as well as genetic variations in the androgen receptor are of interest to study.
Aims: To study the role of testosterone in men and women with different levels of dysglycemia and CVD by investigating:
1. the dynamics of testosterone levels up to a year following an acute myocardial infarction (AMI) in men with and without dysglycemia
2. the relation between the androgen receptor gene CAG repeat length, testosterone levels and prognosis
3. the prognostic implications of total testosterone, free testosterone and the binding protein sex hormone-binding globulin (SHBG) in patients with AMI compared to healthy controls as well as in men and women with dysglycemia and high CV risk
Methods: Studies I and II were based on data from the GAMI study, a prospective cohort study of patients with AMI providing blood samples at four time points up to a year post-infarction, and healthy, age-matched controls.
Study participants were classified as having normal (NGT) or abnormal glucose tolerance (AGT) based on oral glucose tolerance tests and followed for about 11 years for CV events, and CV and all-cause mortality; Study I comprised male patients (n=123) and controls (n=124), Study II comprised male patients (n=121) with blood samples available for DNA analyses.
Studies III and IV were based on a biomarker substudy of ORIGIN which was a large, multicenter randomized controlled trial following patients with dysglycemia and high CV risk for about six years for CV events and all-cause mortality. Study III comprised all male patients (n=5 553) and Study IV all female patients (n=2 848) in the biomarker substudy.
Results: In Study I, median testosterone levels were lower immediately after an AMI compared to controls at baseline (243 ng/dl vs. 380 ng/dl; p<0.01) but increased at discharge, three months and 12 months to 311, 345 and 357 ng/dl respectively. Patients with AGT had the lowest levels at the first timepoint (230 ng/dl). Total and free testosterone did not predict CV events or all-cause mortality in men with AMI but CV and all-cause mortality in controls.
In Study II, contrary to the hypothesis, there was no correlation between CAG repeat length and testosterone and moreover CAG repeat length did not predict CV events or all-cause mortality.
In Study III, total and free testosterone did not predict prognosis in Cox regression analyses by one standard deviation increment but low free testosterone (≤7 ng/dl) was associated with increased allcause mortality. Additionally, increasing SHBG was related to a higher risk of CV events (HR 1.07; 95% CI 1.00–1.14; p<0.03) and all-cause mortality (HR 1.13; 95% CI 1.06–1.21; p<0.01).
Finally, in Study IV, total and free testosterone did not predict any outcomes in women but SHBG was related to increased all-cause mortality (HR 1.14; 95% CI 1.05-1.24; p<0.01).
Conclusions: Low testosterone was common in patients hospitalized with AMI, in particular in those with AGT, but increased over time indicating that samples taken in close proximity to AMI should be interpreted with caution.
In contrast to healthy controls where low total and free testosterone was predictive of prognosis, only free testosterone ≤7 ng/dl was associated with all-cause mortality in patients. This suggests that testosterone may be a mediator in CVD and prognosis rather than a traditional risk factor.
The potential importance of CAG repeat length in this context was not confirmed. Interestingly, SHBG was an independent predictor for CV events and all-cause mortality in men and for all-cause mortality in women with dysglycemia. This warrants further study to clarify whether the actions of SHBG are mediated through an impact on the distribution of testosterone or if SHBG is a direct prognostic marker.
Wang A. Testosterone - of importance in patients with dysglycemia and cardiovascular disease? Thesis for Doctoral Degree (Ph.D.) Akademisk Avhandling. https://openarchive.ki.se/xmlui/handle/10616/47004
Background: Testosterone has been associated with cardiovascular (CV) health in men and women with or without diabetes. There are however conflicting results which warrant further investigations to understand if testosterone is important for prognosis, in particular in relation to diabetes and cardiovascular disease (CVD). To gain further insight, several aspects such as when and which testosterone fraction to assess as well as genetic variations in the androgen receptor are of interest to study.
Aims: To study the role of testosterone in men and women with different levels of dysglycemia and CVD by investigating:
1. the dynamics of testosterone levels up to a year following an acute myocardial infarction (AMI) in men with and without dysglycemia
2. the relation between the androgen receptor gene CAG repeat length, testosterone levels and prognosis
3. the prognostic implications of total testosterone, free testosterone and the binding protein sex hormone-binding globulin (SHBG) in patients with AMI compared to healthy controls as well as in men and women with dysglycemia and high CV risk
Methods: Studies I and II were based on data from the GAMI study, a prospective cohort study of patients with AMI providing blood samples at four time points up to a year post-infarction, and healthy, age-matched controls.
Study participants were classified as having normal (NGT) or abnormal glucose tolerance (AGT) based on oral glucose tolerance tests and followed for about 11 years for CV events, and CV and all-cause mortality; Study I comprised male patients (n=123) and controls (n=124), Study II comprised male patients (n=121) with blood samples available for DNA analyses.
Studies III and IV were based on a biomarker substudy of ORIGIN which was a large, multicenter randomized controlled trial following patients with dysglycemia and high CV risk for about six years for CV events and all-cause mortality. Study III comprised all male patients (n=5 553) and Study IV all female patients (n=2 848) in the biomarker substudy.
Results: In Study I, median testosterone levels were lower immediately after an AMI compared to controls at baseline (243 ng/dl vs. 380 ng/dl; p<0.01) but increased at discharge, three months and 12 months to 311, 345 and 357 ng/dl respectively. Patients with AGT had the lowest levels at the first timepoint (230 ng/dl). Total and free testosterone did not predict CV events or all-cause mortality in men with AMI but CV and all-cause mortality in controls.
In Study II, contrary to the hypothesis, there was no correlation between CAG repeat length and testosterone and moreover CAG repeat length did not predict CV events or all-cause mortality.
In Study III, total and free testosterone did not predict prognosis in Cox regression analyses by one standard deviation increment but low free testosterone (≤7 ng/dl) was associated with increased allcause mortality. Additionally, increasing SHBG was related to a higher risk of CV events (HR 1.07; 95% CI 1.00–1.14; p<0.03) and all-cause mortality (HR 1.13; 95% CI 1.06–1.21; p<0.01).
Finally, in Study IV, total and free testosterone did not predict any outcomes in women but SHBG was related to increased all-cause mortality (HR 1.14; 95% CI 1.05-1.24; p<0.01).
Conclusions: Low testosterone was common in patients hospitalized with AMI, in particular in those with AGT, but increased over time indicating that samples taken in close proximity to AMI should be interpreted with caution.
In contrast to healthy controls where low total and free testosterone was predictive of prognosis, only free testosterone ≤7 ng/dl was associated with all-cause mortality in patients. This suggests that testosterone may be a mediator in CVD and prognosis rather than a traditional risk factor.
The potential importance of CAG repeat length in this context was not confirmed. Interestingly, SHBG was an independent predictor for CV events and all-cause mortality in men and for all-cause mortality in women with dysglycemia. This warrants further study to clarify whether the actions of SHBG are mediated through an impact on the distribution of testosterone or if SHBG is a direct prognostic marker.
Wang A. Testosterone - of importance in patients with dysglycemia and cardiovascular disease? Thesis for Doctoral Degree (Ph.D.) Akademisk Avhandling. https://openarchive.ki.se/xmlui/handle/10616/47004
Similar threads
