Jackolee’s Next Cycle Log

Can I just mix the powder into a drink as well? That’s what I do with my nac, arginine, leucine, and got pure powdered tudca on the way too. Seems easier than making pills

You can, but you won’t want to. It tastes very very unpleasant. It is extremely bitter. It’s the chemical that causes a grapefruit rind to taste the way it does. So whatever you mix it in will instantly be like the worst IPA ever brewed after it’s been sitting in the sun in Somalia for 30 years and is covered in taint sweat from the fat Kardashian.

Look, the point is it tastes really bad. I can’t stress that enough.

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Haha! In a strange way I kind want to see how bad it is now. Thanks man. It’s in the amazon shopping cart now

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Donating blood is only a short time fix. It last me about 4 months. I have a big issues with HCT anytime my TRT dose is over 120/wk. I assume your TRT is with UGL supples so you don’t have to worry about a doc yelling at you.
I just started my blast Mar1st my HCT was 50.3 I donated that will take me down to about 48 and I will have to donate again at the end of the blast.

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I’m on trt through my doc and test is pharma. I only have to do labs through him every 6 months though so gives me plenty of time to blast and then return back to trt dose. He writes me 400 mg weekly and enough anastrozole and nolva to always have it on hand. I typically take 250mg at cruise. That typically keeps me around 850 2-3 days after my shot.

Although I recently started supplementing boron which is supposed to help with test production and my last labs taken 3 days after my shot were 1180. Pretty cool.

My doc is real progressive so I’m not worried.

Any experience with naringin as mentioned above? I’ve read threads that being well hydrated effects hct also, but I’m super hydrated and it’s the same as always. Don’t have any bp symptoms though

How could Boron help with your Test production, if you are TrT along with blasting?

It was something that @physioLojik recommended. I looked it up and that was one of the listed benefits. It was really cheap off amazon so I decided to give it a try. I get it that I’m shut down, but that is literally the only variable that is changed. Same dosage of test, same frequency, same days out from the shot and almost a 400 point upward swing. I don’t know the science. Maybe he can chime in

Are you typically a high SHBG guy? I wonder if Boron helps reduce SHBG to wear Free T is more available thus higher? Very interesting.

No I’m on the lower side. Mid 20s I think I recall. I don’t seem to fluctuate much. I’ve had labs done 2, 3, and 7 days post shot and it’s always like 850, 750, 600. That’s why the 1180 caught me off guard

The post above was the first I had heard about naringin. I will try and do some more research. I live in Vail CO 8000ft so HCT has always been an issue for me. Pre TRT I was 49. My only symptom when my HCT goes over 53% is higher blood pressure. That is about the time I start worrying but my doc doesn’t like anything above 51.0%

My doc wasn’t concerned because my RBC is always in range. I asked him about it but he didn’t seem worried at all. Then I read on here that I’m gonna drop dead. Who knows. I’m going to look into donating blood belfries the blast though, to be safe

Funny I got the opposite feeling from reading this forum on the dangers of high HCT. Many here think it does no harm. My doc is Defy and they say anything above 52 is dangerous and that trumps anyone on this forum for me.

On naringin if found this. I eat a grapefruit a day and I have HCT issues so I don’t hold much hope that dried and groundup grapefruit rines would do much for me. YMMV. It also sounds like it can really mess with several drugs guys on TRT take like cialas and anastrozole.

Naringin

What is naringin? Why do we need it?

Naringin is a type of flavonoid, a water-soluble pigment, found in grapefruits. By itself, naringin has little nutritional value, other than being responsible for giving grapefruit its bitter flavor, and possibly enhancing one’s sense of taste. As a dietary supplement, however, naringin has a wide range of benefits.

Naringin appears to interfere with the activity of several enzymes that are responsible for the breakdown of certain nutrients in the intestines, along with many types of drugs, resulting in higher levels of those substances in the blood. As such, naringin is used to enhance the effectiveness and increase the half-life of several supplements and related substances, such as caffeine.

How much naringin should I take?

Most studies have shown that a dose of 25 milligrams of naringin is enough to increase the bioavailability and half-life of certain nutrients and/or drugs consumed with it.

What forms of naringin are available?

The main source of naringin is pure grapefruit juice. However, many types of grapefruit juice are either blended with other juices, or use grapefruits that have low naringin levels, to help remove bitterness and improve taste. Naringin supplements are also available, and are sold in pill, liquid and capsule form.

What can happen if I take too much naringin? Are there any interactions I should be aware of? What precautions should I take?

Because naringin can alter the metabolism of certain drugs so that they remain in the bloodstream longer, taking naringin supplements can result in higher-than-expected levels of those drugs in the blood, which may cause a variety of unwanted side-effects. As a result, patients should not take any drugs with naringin or grapefruit juice without first consulting a licensed health care provider. In addition, the effects of taking naringin and/or drinking grapefruit juice are cumulative; the more naringin that is ingested, the greater its interaction with certain drugs and other nutrients.

Among the drugs known to be affected by naringin are calcium channel blockers; estrogen supplements; sedatives; high blood pressure medications; and cholesterol-lowering medications. As always, make sure to consult with a licensed health care provider before taking naringin or any other herbal remedy or dietary supplement.

References

  • Balestrieri ML, Castaldo D, Balestrieri C, et al. Modulation by flavonoids of PAF and related phospholipids in endothelial cells during oxidative stress. J Lipid Res Feb 2003;44(2):380-7.
  • Fuhr U, Klittich K, Staib AH. Inhibitory effect of grapefruit juice and its bitter principal, naringenin, on CYP1A2 dependent metabolism of caffeine in man. British Journal of Clinical Pharmacology 1993;35:431-436

Thanks man! It was like 18 bucks so I’ll take it while on blast and then get labs again after donating. Appreciate your input!

https://academic.oup.com/ajh/article/12/7/739/112746

https://academic.oup.com/ajh/article-pdf/12/7/739/262823/12_7_739.pdf

Most doctors aren’t trained as scientists or engineers. Or they may have learned it and forgot it. You are fortunate to be working with Defy and Dr. Saya. Read the link above if you want to understand why increased hematocrit causes your heart to work harder (see Fig. 2 of pdf link for synopsis). Blood viscosity is non-linear function of Hct. I cringe when I see videos/posts stating that you actually are just fine in the mid to upper 50s. That’s why those truly informed start talking about protective measures when you start using TRT/AAS to counteract these issues. Some of these have been mentioned. Others that bear discussion include losartan (ARB), taurine, alpha-lipoic acid, etc.

Do you really want your heart working 20% harder all the time when it’s avoidable. Integrate that work over a significant time span and you start to see potential for early (earlier than it needs to be) heart failure.

When discussing oral AAS, research hepatic lipase and reverse cholesterol transport. If you naturally run high in triglycerides, you may be inviting significant issues when using oxandrolone. Taurine seems like a prudent supplement regardless.

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@readalot thank you for these articles. Hopefully the words aren’t too big for some of the guys here that push a high HCT is not only fine but better.

@hrdlvn Hey, thanks for your articles and references as well. I’ve only seen Dr. Saya come out and mention on forum (the other forum) it isn’t just about clotting/strokes which is a function of platelets as well. Even if your platelets are fine you are still putting more work on your heart by pushing Hct. If you’re after performance then maybe acceptable risk, but for longevity then not the best idea. Like alot of these markers, there’s a U shape between level and mortality risk. Actually listening to podcast the other day where the well-meaning fellow was suggesting shooting for a Hct of 55 and we should all have E2 above 80! I wonder how much of LVH associated with AAS/nandrolone is really just uncontrolled BP as opposed to a primary mechanism @unreal24278. I’ve read the speculation on endothelial injury with nandrolone in animal models. But again these are astronomical serum levels you just can’t get in reality unless injecting more oil than you could handle. Hence, good idea to bring in the losartan to control BP when needed.

More on naringin:

https://en.wikipedia.org/wiki/Naringin

Naringin inhibits some drug-metabolizing cytochrome P450 enzymes, including CYP3A4 and CYP1A2, which may result in drug-drug interactions.[5] Ingestion of naringin and related flavonoids can also affect the intestinal absorption of certain drugs, leading to either an increase or decrease in circulating drug levels. To avoid interference with drug absorption and metabolism, the consumption of citrus (especially grapefruit) and other juices with medications is advised against.[6]

@jackolee Wow, I’ve really been impressed with all your efforts! Amazing what can be accomplished when dialing in the eating/training BEFORE TRT/tools get used. Good luck with your competition. Absolutely awesome work.

Before you consider oxandrolone, other 17-AA orals, here’s some good material to check out:

https://academic.oup.com/jcem/article/86/11/5108/2849115

There has been some concern over the use of AAS in patients with AIDS, as many of these patients have subclinical hepatic disease. As protease inhibitors and oxandrolone are metabolized by cytochrome P450 3A4 enzyme system, combined use of these drugs may result in elevation of the oxandrolone concentration to harmful levels.

Just a word of caution that multiple drugs will have interaction/most likely synergistic effect with naringin. Hence, naringin (and caffeine) have been shown to enhance serum levels of oxandrolone for a given oral dosage by retarding metabolism.

Really nice (can be counterintuitive) discussion on hepatic lipase wrt to CAD:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3288605/

Increased or decreased hepatic lipase (HL) activity has been associated with coronary artery disease (CAD). This is consistent with the findings that gene variants that influence HL activity were associated with increased CAD risk in some population studies but not in others. In this review, we will explain the conditions that influence the effects of HL on CAD. Increased HL is associated with smaller and denser LDL (sdLDL) and HDL (HDL3) particles, while decreased HL is associated with larger and more buoyant LDL and HDL particles. The effect of HL activity on CAD risk is dependent on the underlying lipoprotein phenotype or disorder. Central obesity with hypertriglyceridemia (HTG) is associated with high HL activity that leads to the formation of sdLDL that is proatherogenic. In the absence of HTG, where large buoyant cholesteryl ester-enriched LDL is prominent, elevation of HL does not raise the risk for CAD. In HTG patients, drug therapy that decreases HL activity selectively decreases sdLDL particles, an antiatherogenic effect. Drug therapy that raises HDL2 cholesterol has not decreased the risk for CAD. In trials where inhibition of cholesterol ester transfer protein (CETP) or HL occurs, the increase in HDL2 most likely is due to inhibition of catabolism of HDL2 and impairment of reverse cholesterol transport (RCT). In patients with isolated hypercholesterolemia, but with normal triglyceride levels and big-buoyant LDL particles, an increase in HL activity is beneficial; possibly because it increases RCT. Drugs that lower HL activity might decrease the risk for CAD only in hypertriglyceridemic patients with sdLDL by selectively clearing sdLDL particles from plasma, which would override the potentially pro-atherogenic effect on RCT.

Note than oxandrolone will significantly increase hepatic lipase. Whether that is of significant concern to CAD seems to be related to your genetics and triglyceride metabolism:

https://jim.bmj.com/content/56/7/920.long

Thank you very much for all the info. That’s a lot to read up on. Luckily I’m not planning on starting for another month or so. Thank you for the good luck wishes. I’m as ready as I’m gonna be so we’ll hope it’s enough. I didn’t use any AAS other than my TRT dose for this contest prep. I’m sure others will have so hopefully I’ll come in pretty competitive none the less. Have s good one man!

Not to derail your thread, but curious how much and when your taking the boron. I’m going to start as well, but curious about starting dose and timing. Thanks

I’ll check when I get home. I don’t remember. It’s a liquid and I take 1.25 ml but can’t remember how many mg that is