Understood, I’m off the var train.
I was going to share my results at the end of my run but this is the end now.
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Doing great. Keep going. You can get way leaner and get your lipids in check with or without TRT and continued training and eating plan. TRT will obviously give you another knob to target higher LBM at given BF%.
Like I mentioned once the oxandrolone washes out reassess your lipids and target macros/eating plan that work with your system.
Another good read:
https://t-nation.com/t/realistic-trt-recomp-progress/253389/3729
Washout estimation…more correctly “duration of effect” once you’ve stopped the medication:
https://t-nation.com/t/realistic-trt-recomp-progress/253389/3697
https://t-nation.com/t/oxandrolone-troche-experience-potential-atherosclerosis-marker-wmd/254627/49
I am definitely no doctor, but when I saw your blood work results the first thought I had was if there was a family history of heart disease.
I lost a good friend who knew his father died of heart disease in his 40’s. My friend didn’t want insurance and didn’t get checked out. He lived into his late 50’s and died of heart failure.
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With those baseline lipids I would have worked on dialing in eating and training to bring Trig/HDL-c ratio under 2 (along with body recomp goal). Under 1 is even better but not everyone has OCD :-).
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https://www.nature.com/articles/s41598-021-00020-3
Discussion
The TG/HDL-C ratio describes a specific lipid and glucose metabolic profile which was able to predict CHD events and progression of coronary atherosclerosis in patients with stable angina and without known disease enrolled in a prospective, multicenter international study. In this population at intermediate-low risk, patients with a higher TG/HDL-C ratio had clinical and bio-humoral features of atherogenic dyslipidemia, insulin resistance, metabolic syndrome and diabetes together with a higher coronary atherosclerosis burden at CTA. Both a higher TG/HDL-C ratio and the coronary CTA score were additional predictors of worse outcome, independently of other cardiovascular risk factors, the presence of obstructive CAD or ischemia. This residual risk was not modified by conventional medical treatments or revascularization procedures. In those patients who were submitted to a clinical and bio-humoral re-evaluation and a follow-up CTA scan over a 6 years period, the specific cardio-metabolic disorder identified by higher values of TG/HDL-C ratio at baseline remained stable over time while it progressed in the other patients. The coronary atherosclerotic process also evolved in both groups, as indicated by increase in markers of endothelial activation, systemic inflammation and of the coronary CTA score, despite increasing use of medications and lowering of LDL-C levels. Nevertheless, most of these changes were more prominent in patients who had a higher TG/HDL-C ratio already at baseline and thus a more prolonged exposure to this specific cardiometabolic risk.
The relationship between TG/HDL-C ratio, the specific cardio-metabolic profile known as atherogenic dyslipidemia and CAD related clinical outcomes has been previously described either in general populations7,8,9,10 or in high risk patients with known CAD or acute coronary syndromes11,12,13,14,15. In particular, in two gender-specific12 or country-specific14 populations of high-risk patients referred for ICA, the highest values of the TG/HDL-C distribution were associated with twofold increase in all-cause mortality and 1.5- to threefold increase in cardiovascular events during a 5–6 years follow-up, independently of traditional coronary risk factors and angiographic CAD severity. Our results now expand these and other observations in a prospective European multicenter population of intermediate-low risk patients with stable angina, without previous CAD and a low prevalence of obstructive disease (25% at ICA). All-cause mortality and the rate of non-fatal myocardial infarction (2% and 5% at 4.5 years) were much lower than in previous studies. However, also in this population, a higher TG/HDL-C ratio (>3.38, IV quartile) was associated with an almost twofold increase in the risk of non-fatal myocardial infarction and of the composite outcome end-point (all-cause death and non-fatal myocardial infarction). Even more importantly, the prognostic role of higher TG/HDL-C ratio was additive to that of the well-established coronary CTA atherosclerosis risk score (18) and was independent of other cardiovascular risk factors, biomarkers and the presence of more severe symptoms, inducible ischemia and/or obstructive CAD at ICA. The combined model including TG/HDL-C ratio and the CTA score predicted residual CHD risk also independently of revascularization procedures and medical treatments.The addition to the prognostic model of the CTA score attenuated the hazard ratio of TG/HDL-C alone suggesting a causal link between this variable and CAD related outcome. A possible causal relationship between the cardio-metabolic profile, expressed by TG/HDL-C ratio, and residual CHD risk, not tackled by current treatments, was also suggested in the present study by the observations collected in a subgroup of patients who were re-evaluated at follow up receiving a second blood sampling and a second CTA scan. Despite a more frequent use of cardioactive and risk controlling medications, including statins and anti-diabetics, and the improvement of circulating LDL-C levels, the specific lipid and glucose disorder associated with higher TG/HDL-C ratio either remained unaltered or worsened. This behavior was paralleled by an overall increase in the bio-humoral markers of endothelial activation and systemic inflammation and more importantly by a worsening of the coronary atherosclerotic burden described by the CTA score. The effects on systemic inflammation and coronary atherosclerotic risk pattern were even more pronounced in patients with a TG/HDL-C ratio already elevated at baseline who were possibly exposed to an adverse cardio-metabolic condition for longer periods.
The pathophysiological implications of elevated TG and low HDL-C levels, as well as of the associated lipid and glucose profile in atherogenesis have been widely explored and reported19 and are consistent with the results of the present study. In the present population, higher TG/HDL-C values were associated with the bio-humoral features of atherogenic dyslipidemia11, the metabolic syndrome, insulin resistance7,12 and more in general of a diabetic or pre-diabetic state20. Patients with higher values of TG/HDL-C ratio had also higher values of remnant-C, which has been recently implicated in atherogenesis, inflammation and prediction of CHD risk4,5,6, and of the TyG index, which has been proposed as a surrogate indicator of “insulin resistance” and related with CHD risk21,22 and progression of coronary atherosclerosis23. Interestingly, in the present low risk population of patients without previous disease, the TG/HDL-C ratio was a better predictor of CAD related outcomes than either remnant-C or the TyG index. This observation suggests that, at least in these patients, both TGs and HDL-C function may have an interactive role19,24. TG-rich lipoproteins carry cholesterol in addition to TGs and this, together with LDL-C is considered to be the atherogenic agent that feeds the development of arterial wall plaques4,5,25. Elevated TG and VLDL levels, are associated with lower levels of HDL-C and formation of small, dense HDL and small, dense LDL particles19. Cholesteryl ester transfer protein (CETP) catalyzes the transfer of cholesteryl esters (CE) from HDL to ApoB-containing lipoproteins (VLDL and LDL) in exchange for TG. In the context of higher levels of TGs and VLDL, this exchange results in higher proportion of TG-rich small, dense HDL which are catabolized more rapidly, leading to low levels of HDL-C, reduction of reverse cholesterol transport (RCT) and reduced antioxidant and anti-inflammatory properties24,25,26. On the other hand, when TG levels are high, ApoB particles are more TG-enriched. The hydrolysis of the TGs within the TG-rich LDL by hepatic lipase remodels the LDL particles which become smaller and denser and can enter the arterial intima more easily and are more atherogenic. Small, dense LDL particles also bind weakly to the LDL receptor, thus increasing their half-life in the plasma and being more subject to oxidative damage and to subsequent uptake by the macrophage scavenger receptors19.Moreover, our patients were characterized by an extensive bio-humoral evaluation. Higher values of TG/HDL-C ratio were associated with lower circulating levels of ApoA1, higher levels of hs-cTnI and, over time, of IL-6 and VCAM1. Thus, the cardiometabolic risk profile defined by TG/HDL-C was associated with a downregulation of endothelial protective mechanisms and an upregulation of systemic and vascular inflammatory processes, translating into progressive coronary atherosclerosis and subclinical myocardial damage27. In this context, a reduced functionality of HDL particles might contribute to the coronary atherogenic risk19,28. This may explain why, besides the TG/HDL-C ratio and CTA score, circulating ApoA1 levels were the only additional independent predictors of adverse outcome in our population.
We recognize some limitations of the present study.LDL-C was not determined directly but was calculated with the Friedewald formula. It was computed in 352/355 patients since in 3 cases TG levels were higher than 400 mg/dL. The study population was well characterized but was relatively small and included only symptomatic patients with suspected obstructive CAD but at intermediate-low risk. We used a composite outcome end-point since our ability to separately model mortality was limited by the small number of deaths. Cardiac death occurred in only one patient thus only all-cause death could be considered. Lack of statistical significance for some covariates usually associated with risk of death may thus reflect low power rather than lack of prognostic value. The number of patients with repeated CTA scans was not sufficient to estimate the independent association between changes in biomarkers and in specific CTA parameters such as plaque features.Moreover, not all biomarkers were measured at follow-up in this subpopulation, thus changes in some biomarkers could not be assessed. On the other hand, ICAM1 and VCAM1 levels were not available for association analysis with the TG/HDL-C ratio in the entire population. The study included a highly selected population of patients who presented for a clinically indicated diagnostic work-up for stable angina with normal cardiac function. Thus, it is unknown whether our findings extend to a general population of asymptomatic subjects with similar risk factors or to higher risk populations with known acute or chronic coronary syndromes or with cardiac dysfunction and heart failure.
In conclusion, obesity, insulin resistance and metabolic syndrome are emerging conditions in contemporary populations of symptomatic patients with suspected CAD29; the present results suggest that the TG/HDL-C ratio is a simple method to identify among these patients, independently of the severity of symptoms or the presence of obstructive disease and inducible ischemia, those individuals with a substantial residual coronary risk not tackled by current treatments. The underlying genetic and molecular pathways are complex and deserve continuing mechanistic research to develop new targeted nutritional, lifestyle and drug strategies beyond the established LDL-C lowering interventions. Some pharmacological approaches are already promising in this context, including omega 3-fatty acids, PCSK9 inhibitors, PPAR-alfa agonists and ATP-citrate lyase inhibitors30,31. Most of these drugs have been tested in primary or secondary prevention studies but their efficacy in improving outcome in selected patients with suspected CAD and high cardiometabolic risk, such as those associated with the highest TG/HDL-C ratio has not been established.
I’m going to get the NMR lipid panel drawn this afternoon.
I’ll be fasted for 18-20hrs by that time.
As pointed out I doubt it will change much but I’m hung up on it. Its fair to say the var is the main culprit.
I’ve been 180ish lbs @10 - 12% bf doing only 100mgs test every 5 days and carb cycling diet. So I feel I can get some great results I just got sucked into wanting to get back fast.
I didn’t expect trenbolone like lab results though.
I’ll share the NMR fasted labs soon as I get em.
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Good job pulling this test and getting the data. No, it doesn’t make it less dramatic. These are horrendous results consistent with your lipid-c tests and should tell you to stop what you are doing.
Nice job advocating for yourself!
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Thanks all for reading and sharing feedback.
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