Low testosterone is also linked to heart problems, coming off may not be the best idea.
Yes, SERMs are better on lipids than AIs are. Going one step further, Raloxifene is the safest SERM in terms of cholesterol damage because it does not impair macrophage-specific reverse cholesterol transport (M-RCT), unlike Tamoxifen.
This can be seen in this study:
Sci Rep. 2016 Sep 7;6:32105. doi: 10.1038/srep32105.
Clinically used selective estrogen receptor modulators affect different steps of macrophage-specific reverse cholesterol transport.
Fernández-Suárez ME1,2,
Escolà-Gil JC3,4,5,
Pastor O2,6,
Dávalos A7,
Blanco-Vaca F3,4,5,
Lasunción MA1,2,
Martínez-Botas J1,2,
Gómez-Coronado D1,2.
Author information
1Servicio de Bioquímica-Investigación, Hospital Universitario Ramón y Cajal, IRYCIS, Madrid, Spain.2CIBER de Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Madrid, Spain.3Institut d'Investigacions Biomèdiques (IIB) Sant Pau, Barcelona, Spain.4Departament de Bioquímica i Biología Molecular, Universitat Autònoma de Barcelona, Bellaterra, Spain.5CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Spain.6Servicio de Bioquímica Clínica, Hospital Universitario Ramón y Cajal, IRYCIS, Madrid, Spain.7Instituto Madrileño de Estudios Avanzados (IMDEA)-Alimentación, Madrid, Spain.
Abstract
Selective estrogen receptor modulators (SERMs) are widely prescribed drugs that alter cellular and whole-body cholesterol homeostasis. Here we evaluate the effect of SERMs on the macrophage-specific reverse cholesterol transport (M-RCT) pathway, which is mediated by HDL. Treatment of human and mouse macrophages with tamoxifen, raloxifene or toremifene induced the accumulation of cytoplasmic vesicles of acetyl-LDL-derived free cholesterol. The SERMs impaired cholesterol efflux to apolipoprotein A-I and HDL, and lowered ABCA1 and ABCG1 expression. These effects were not altered by the antiestrogen ICI 182,780 nor were they reproduced by 17β-estradiol. The treatment of mice with tamoxifen or raloxifene accelerated HDL-cholesteryl ester catabolism, thereby reducing HDL-cholesterol concentrations in serum. When [(3)H]cholesterol-loaded macrophages were injected into mice intraperitoneally, tamoxifen, but not raloxifene, decreased the [(3)H]cholesterol levels in serum, liver and feces. Both SERMs downregulated liver ABCG5 and ABCG8 protein expression, but tamoxifen reduced the capacity of HDL and plasma to promote macrophage cholesterol efflux to a greater extent than raloxifene. We conclude that SERMs interfere with intracellular cholesterol trafficking and efflux from macrophages. Tamoxifen, but not raloxifene, impair M-RCT in vivo. This effect is primarily attributable to the tamoxifen-mediated reduction of the capacity of HDL to promote cholesterol mobilization from macrophages.
PMID: 27601313 PMCID:
PMC5013287 DOI:
10.1038/srep32105
Source:
https://www.ncbi.nlm.nih.gov/pubmed/27601313
Again, go down to 10mg ED or EOD of TE or Test CYP injected subq in your stomach, then get BW done after 5-6 weeks and see where free and TT are.