Reta Too Effective?

DeliriousNatty

New Member
Hello everyone,

Just wanted to ask what your thoughts are regarding my bloods on 500T/30V. It appears my LDL is extremely low. I don’t take any citrus bergamot, statins or red yeast.

Current regiment at time of test:
Reta 2mg/wk
Fishoil
Coq-10
Glutathione 250mg IM Daily
Tudca, nac, yatata
Telm
Cialis

For background info, prior to this cycle and using glps, I was normally low end reference range, so pretty good.
These numbers are from a week ago and are day 4 into the Anavar portion, I think I actually took 10mg var before the test by happenstance lmao

Here’s the numbers:
Total Cholesterol: 57mg/dl
Hdl: 31
LDLc: 19mg/dl
Glucose: 80
Trig: 34

AST:48
ALT:43

If anyone has any expertise with something similar, I’d love to hear advice. Thanks
 
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Several mechanisms shown in early human trials translational data...
↓ Hepatic VLDL production
↑ LDL receptor expression
↑ hepatic fatty acid oxidation
↓ de novo lipogenesis
↑ bile acid turnover

In phase 2 obesity/metabolic trials, retatrutide produced...
Marked reductions in total cholesterol
Significant LDLC lowering independent of statins. Triglycerides often crashing into the 30s to 40s.

That last point is key...
When TGs are that low, LDL will often “collapse” numerically, because LDLC is downstream of VLDL output.

You didn’t just run retatrutide in isolation, you stacked several LDL lowering items, without realizing how additive they are.

Your regimen hits LDL from multiple angles. Retatrutide (primary driver), Telmisartan, Fish oil, Cialis, Glutathione.

LDL as low as 10 to 20 mg/dL has not shown harm in the short to medium term.
Neurologic or hormonal issues tend to appear only with chronic fat malabsorption or severe caloric deprivation.
 
Several mechanisms shown in early human trials translational data...
↓ Hepatic VLDL production
↑ LDL receptor expression
↑ hepatic fatty acid oxidation
↓ de novo lipogenesis
↑ bile acid turnover

In phase 2 obesity/metabolic trials, retatrutide produced...
Marked reductions in total cholesterol
Significant LDLC lowering independent of statins. Triglycerides often crashing into the 30s to 40s.

That last point is key...
When TGs are that low, LDL will often “collapse” numerically, because LDLC is downstream of VLDL output.

You didn’t just run retatrutide in isolation, you stacked several LDL lowering items, without realizing how additive they are.

Your regimen hits LDL from multiple angles. Retatrutide (primary driver), Telmisartan, Fish oil, Cialis, Glutathione.

LDL as low as 10 to 20 mg/dL has not shown harm in the short to medium term.
Neurologic or hormonal issues tend to appear only with chronic fat malabsorption or severe caloric deprivation.
Thankyou for this thorough reply. I can see how the multiple vectors contribute to a much lower ldl…but I was under the impression that ldl went up, even just marginally with orals and aas.

Am I off base here?

You def make me feel slightly better knowing that it’s not the worse thing ever to have it that low for a short time.

The worst side I’ve noticed ( that I’ve attributed to low lipids) is probably joint related. Had some bad tennis elbow after pushing shoulder press hard for a few weeks in a block.

Thanks again for all your help man! Anything immediate you’d suggest to raise it efficiently aside from eating high fats?
 
Thankyou for this thorough reply. I can see how the multiple vectors contribute to a much lower ldl…but I was under the impression that ldl went up, even just marginally with orals and aas.

Am I off base here?

You def make me feel slightly better knowing that it’s not the worse thing ever to have it that low for a short time.

The worst side I’ve noticed ( that I’ve attributed to low lipids) is probably joint related. Had some bad tennis elbow after pushing shoulder press hard for a few weeks in a block.

Thanks again for all your help man! Anything immediate you’d suggest to raise it efficiently aside from eating high fats?
Are you suffering any side effects currently? If you aren't I would not worry, again in the short term. Dependant how long you intend to run Reta.
 
Well not really anything out of ordinary, since I’m in a blast rn, I kind of attributed everything to estrogen lmao.

I’ve gotten bloods done recently now and it was high in the beginning, but good 2nd.

Soooo TLDR, small joint issues and dry ish skin but that’s about all. Some upping the fats things feel a lil better
 
Well not really anything out of ordinary, since I’m in a blast rn, I kind of attributed everything to estrogen lmao.

I’ve gotten bloods done recently now and it was high in the beginning, but good 2nd.

Soooo TLDR, small joint issues and dry ish skin but that’s about all. Some upping the fats things feel a lil better
What's your androgen load look like? And E2 in comparison? Reason I ask is I'm trying to compile some data on estrogen levels in relation to androgen load.

Joints and dry skin are inheritantly low E in reference to androgen burden. Not purely in each case but more often than not. Essentially stating that E2 numbers mean shit outside what the androgen load looks like. Often low and high E mimic each other, then we rely on a lab number to suggest what we do, and this is inheritantly wrong bro science, and irrelevant depending what compounds are being run, that is obviously absent negative sides, which again will be individual.

Thread 'Aromatase Inhibitors Fix the Number but Break the System, open discussion.' Aromatase Inhibitors Fix the Number but Break the System, open discussion.
 
At time of test it was 72mg test daily and I believe 1 week into 30mg Anavar(20mg pre-w, 10 seperate).

Total T: 4220
Free T: 1230
E2: 140

The joint issues were occurring around the time I started using ai, but I didn’t have any estrogenic symptoms aside from slightly high bp.

Ai used since: .25mg twice a week

I have another blood test scheduled for March 1st, so I’ll keep yal updated with what happens.

I also got a 23 and me coming in a few weeks, so I’d be interested in seeing if perhaps I have some predisposition or something cool along those lines.

Thanks again for all your help.
 
Reading through this it looks blatantly obvious I had low e2 issues…I’d lean otherwise as .5mg arimidex isn’t enough at all to crash me prior to this so maybe it’s just all cumulative with the reta, lowering of e2 and other ancillaries.

Thus allowing for perfect storm at time of blood test? Idfk hhahaha
 
aside from making bulking on slight surplus really easy, I like the side benefits( or thought I did), such as renal protection lipid improvenent.

It def helps with insulin sensitivity as well, even with pushing cals a little too far xD

Why are you tempted to try reta? If so I’d prob start on the lower end and go up slower than me lol
 
At time of test it was 72mg test daily and I believe 1 week into 30mg Anavar(20mg pre-w, 10 seperate).

Total T: 4220
Free T: 1230
E2: 140

The joint issues were occurring around the time I started using ai, but I didn’t have any estrogenic symptoms aside from slightly high bp.

Ai used since: .25mg twice a week

I have another blood test scheduled for March 1st, so I’ll keep yal updated with what happens.

I also got a 23 and me coming in a few weeks, so I’d be interested in seeing if perhaps I have some predisposition or something cool along those lines.

Thanks again for all your help.
AI tolerance is not static. It changes with total androgen load, DHT burden (Var matters here), bodyfat, GLP use, liver metabolism, cumulative suppression over weeks.

Reading through this it looks blatantly obvious I had low e2 issues…I’d lean otherwise as .5mg arimidex isn’t enough at all to crash me prior to this so maybe it’s just all cumulative with the reta, lowering of e2 and other ancillaries.

Thus allowing for perfect storm at time of blood test? Idfk hhahaha

A few things jump out immediately.
First, E2, 140 with TT, 4220 / Free T, 1230 is not high estrogen in context. That ratio is totally reasonable for that androgen load. On paper, that’s protective estrogen, not problematic estrogen.

Now the important part...your joint issues lining up with the introduction of the AI is the biggest tell here. BP was the only noticeable thing, because this time, the environment is different.

Why this likely was low E2 signaling even with E2 140. You basically created a perfect little storm.

Anavar dries joints, reduces collagen synthesis, increases stiffness. AI introduced reduces local estrogen signaling (serumtissue). Retatrutide GLP effects lowered aromatization and reduced inflammatory response. With high androgens joints rely even more on estrogen for lubrication and cartilage health.

aside from making bulking on slight surplus really easy, I like the side benefits( or thought I did), such as renal protection lipid improvenent.

It def helps with insulin sensitivity as well, even with pushing cals a little too far xD

Why are you tempted to try reta? If so I’d prob start on the lower end and go up slower than me lol
Keeping in mind retatrutide studies are controlled. Nobody is being studied taking super physiological doses of AAS in conjunction with the studies.

The studies clearly indicate what doses are effective in which groups based off collective data. Anything we determine here is anecdotal, but remarkably helpful in the sense it's treated with caution person to person. I'm currently cruising on 500 to 600mg T, 10iu HGH, and occasional 3x weekly TNE at 100 to 150mg pre-workout. Reta I am at taking 11mg every Sunday.
 
Extremely helpful bro, you put a lot of stuff in perspective. Completely slipped my mind that maybe Anavar played an impact on shbg or something.

As for your reta being 11mg, is this because you’ve experienced diminished success with it? How long have you been running ur current protocol?

Thanks again man
 
Extremely helpful bro, you put a lot of stuff in perspective. Completely slipped my mind that maybe Anavar played an impact on shbg or something.

As for your reta being 11mg, is this because you’ve experienced diminished success with it? How long have you been running ur current protocol?

Thanks again man
No diminished success at all. As a matter of fact it was successful at targeting my BG and lipids at 6mg. At 11mg the BG control is incredible, I never venture over 115 to 120 on a verio meter. And post meal I'm back to sub 100 within 1.5 to 2hrs. The includes heavy carbohydrate meals, and also supplemental glycogen. Conveniently enough this has allowed a larger window for the 10iu HGH.

I initially titrated from 1mg, to 6mg. At 1mg per week. I don't know why I did this, other than an abundance of caution as I was fully aware of the research, and typically refer to that for guidance. For me essentially nothing drastic occurred until 6mg and much of the research shows that dose to be where BG control takes maximum effect. Again the research isn't testing other factors such as AAS use, HGH implementation. From there I jumped face first into the empty pool of 11mg. This is where I also started to have negative side effects, burping, allodynia, and a really hard time consuming enough calories. I decided to take 1 week off from week 12 to 13, and once again dosed on last Sunday week 13 start. Strangely enough zero side effects to report this week at all.
 
I see, have you had any heart rate increase? My heart rate is already up from trt levels by quite a bit. I attribute this to the aas obv, but once I added in reta it went up another 5bpm.

Has the fat loss linerearly matched the increase in dose? If not what would u recommend as highest efficacious before diminishing returns?
 
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