Water Retention Caused by Testosterone May Have Nothing to Do with Estradiol

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Digghy said:
Hi Nelson, actually liver and kidneys work well, and I never had this bloating before December 2017, yes I had sometimes some water retention but due to stress, climate changes or diet, disappearing in couple of days.

No alcohol (never in my life), and yes, I have a low carb diet: from monday to sunday I eat only low fat proteic food (meat and fish) and a lot of vegetables, including some carbs only in my post workout breakfast (but it's only 2 apples and 40 grams of oat meat). On sunday I have a high sugar cheat meal (usually with a lot of icecream), but have this diet scheme since 5 years ago and never never had water retention issues.

I definetly think MR receptors are the problem, binding my high cortisol and making me retaining water. In fact I am especially bloated after workout, in particular after doing cardio, when my cortisol levels raises. And I am bloated only in my abdomen, where cortisol receptors and MR intestinal receptors are high. I am 8-10% bodyfat, but look like I am 14% now with all this water retention!

I am a little bit puzzled because I tried with Eplenerone which should bind MR receptors, but was uneffective at all.

My question is: how long does it take to my 11 HSD2 enzimes to make their job again deactivating my periferic cortisol and avoiding it to bind to my MR receptors? I am 2 months off my TRT (and having done it for a short time frame, only 3 months, and with super low dose, apart from that I never used AAS) but no progress so far, and I am becoming scared.

I do not think this can be due to something other than TRT, as I had no food intolerances before and my diet and training is always the same.

Cheers
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What is your most recent HgbA1c? Do you donate blood or undergo medical phlebotomy? What is your waking fasting glucose? What is your blood glucose reading one hour after your "cheat" meal? Two hours? Three hours?

Although perhaps lower in carbs than the Standard American Diet, the diet described is not low-carb.
 
Defy Medical TRT clinic doctor
dnfuss said:
What is your most recent HgbA1c? Do you donate blood or undergo medical phlebotomy? What is your waking fasting glucose? What is your blood glucose reading one hour after your "cheat" meal? Two hours? Three hours?

Although perhaps lower in carbs than the Standard American Diet, the diet described is not low-carb.
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Hi dnfuss, my HgbA1c is 36 mmol/mol on a range of 20-40. My blood glucose early morning with empty stomach is 94 mg/dl on a range 70-110, with blood glucose being little high if considered my diet as I have cortisol in the high range and this increase blood glucose even if I eat low carb.

My carb daily intake from monday to saturday ranges between 80 and 120 gr, considering I am 190 cm for 90 kg and training at least 3 hours per day with good intensity, my glicogen store are quite depleted on saturday when I cheat. And my carbs are taken almost entirely by vegetables.

I have never donated blood or had any medical phlebotomy.

I never did glucose reading after my cheat as I cheat on sunday dinner and no labs can take my blood at that time.

What I have noticed, by the way, is that on monday morning after my sunday cheat, I look much better than the other days. Maybe because my carb intake fill my muscles with glycogen taking also water with it, or because on sunday afternoon I relax and feel less stressed so this plus the big meal lower my cortisol. Don't know, but on monday morning I look better, even if still bloated in comparison to my usual level.

What is strange is that it since 2013 that I have more or less the same dietary scheme and similar training scheme, and never feel bloated and retaining water since I started TRT!
 
I remember patrick arnold talking about this like 10 or 15 years ago. was this written lately or does he even write anymore?
 
Digghy said:
Hi dnfuss, my HgbA1c is 36 mmol/mol on a range of 20-40. My blood glucose early morning with empty stomach is 94 mg/dl on a range 70-110, with blood glucose being little high if considered my diet as I have cortisol in the high range and this increase blood glucose even if I eat low carb.

My carb daily intake from monday to saturday ranges between 80 and 120 gr, considering I am 190 cm for 90 kg and training at least 3 hours per day with good intensity, my glicogen store are quite depleted on saturday when I cheat. And my carbs are taken almost entirely by vegetables.

I have never donated blood or had any medical phlebotomy.

I never did glucose reading after my cheat as I cheat on sunday dinner and no labs can take my blood at that time.

What I have noticed, by the way, is that on monday morning after my sunday cheat, I look much better than the other days. Maybe because my carb intake fill my muscles with glycogen taking also water with it, or because on sunday afternoon I relax and feel less stressed so this plus the big meal lower my cortisol. Don't know, but on monday morning I look better, even if still bloated in comparison to my usual level.

What is strange is that it since 2013 that I have more or less the same dietary scheme and similar training scheme, and never feel bloated and retaining water since I started TRT!
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I will defer to others far more qualified than I am to comment on your water retention question.

Your HgbA1c and fasting glucose are at the higher end of normal (especially given your exercise level and relative youth); please keep an eye on them. You can purchase a glucose meter and strips without a prescription and see what your blood glucose is one and two hours after your Sunday dinner.

What has been described is NOT a low-carb diet by almost any definition.
 
im kind of worried when you mention about eplerones effect on kidneys? GFR under 30? I wouldn't want to mess with my kidneys
 
Look up fodmap, there may be a high fodmap food that you take consistently that may contribute to your bloating. Apples are one of the worst culprits, as are onions, mushrooms and some grains. I saw low potassium is also a culprits, so good low fodmap foods with high potassium include spinach, kale and cabbage. Check it out.
 
maxadvance said:
Look up fodmap, there may be a high fodmap food that you take consistently that may contribute to your bloating. Apples are one of the worst culprits, as are onions, mushrooms and some grains. I saw low potassium is also a culprits, so good low fodmap foods with high potassium include spinach, kale and cabbage. Check it out.
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I have done the Fodmap, didnt do much really, as fodmap is good for IBS and bloating of the gut from gas build up. My bloating is about water edema especially on my chest, love handles and face. I am normally pretty shredded person and witg trt I am balooning up.

But nolvadex 20 mg ED in 5 days done the deal right away. So it seems like estrogen is the problem in the end of the day, just gotta find a way to get rid of it. I lost so much water weight and my body changed drastically on Nolvadex literally within days. My face got chiselled again as my usual face off of trt.
 
tylermax said:
I have done the Fodmap, didnt do much really, as fodmap is good for IBS and bloating of the gut from gas build up. My bloating is about water edema especially on my chest, love handles and face. I am normally pretty shredded person and witg trt I am balooning up.

But nolvadex 20 mg ED in 5 days done the deal right away. So it seems like estrogen is the problem in the end of the day, just gotta find a way to get rid of it. I lost so much water weight and my body changed drastically on Nolvadex literally within days. My face got chiselled again as my usual face off of trt.
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Im jsut going to note here that you keep on posting yet have no labs to show us. Going by feel which you seem in tune to your body but knowing your SHBG, E2 sensitive while you're having these symptoms...can be very useful. Just because a number on a lab test is in range, etc etc often does NOT mean its good for you. For instance, the water retention is a key component of Estrogen (can be...).
 
Vince Carter said:
Im jsut going to note here that you keep on posting yet have no labs to show us. Going by feel which you seem in tune to your body but knowing your SHBG, E2 sensitive while you're having these symptoms...can be very useful. Just because a number on a lab test is in range, etc etc often does NOT mean its good for you. For instance, the water retention is a key component of Estrogen (can be...).
Click to expand...


I agree, unfortunately I am in Canada and can not get the sensitive test. So I am kinda stuck, as most I read states that unless it is the senstive test it is useless.
 
Is the bloating/Swelling in just the lower extremities or has anyone experienced it in the mid section. Just started TRT and I feel bloated quite a bit bear lately. After I eat even small amounts of food. Any possible answers...
 
About to start an experiment with this drug. It seems to prevent insulin resistance of
hydrochlorothiazide. It also reduces sodium retention.

Amiloride - Wikipedia

Effect of amiloride, or amiloride plus hydrochlorothiazide, versus hydrochlorothiazide on glucose tolerance and blood pressure (PATHWAY-3): a parallel-group, double-blind randomised phase 4 trial

Background: Potassium depletion by thiazide diuretics is associated with a rise in blood glucose. We assessed whether addition or substitution of a potassium-sparing diuretic, amiloride, to treatment with a thiazide can prevent glucose intolerance and improve blood pressure control. MethodsWe did a parallel-group, randomised, double-blind trial in 11 secondary and two primary care sites in the UK. Eligible patients were aged 18–80 years; had clinic systolic blood pressure of 140 mm Hg or higher and home systolic blood pressure of 130 mmHg or higher on permitted background drugs of angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, β blockers, calcium-channel blockers, or direct renin inhibitors (previously untreated patients were also eligible in specific circumstances); and had at least one component of the metabolic syndrome in addition to hypertension. Patients with known diabetes were excluded. Patients were randomly assigned (1:1:1) to 24 weeks of daily oral treatment with starting doses of 10 mg amiloride, 25 mg hydrochlorothiazide, or 5 mg amiloride plus 12·5 mg hydrochlorothiazide; all doses were doubled after 12 weeks. Random assignment was done via a central computer system. Both participants and investigators were masked to assignment. Our hierarchical primary endpoints, assessed on a modified intention-to-treat basis at 12 and 24 weeks, were the differences from baseline in blood glucose measured 2 h after a 75 g oral glucose tolerance test (OGTT), compared first between the hydrochlorothiazide and amiloride groups, and then between the hydrochlorothiazide and combination groups. A key secondary endpoint was change in home systolic blood pressure at 12 and 24 weeks. This trial is registered with ClinicalTrials.gov, number NCT00797862, and the MHRA, Eudract number 2009-010068-41, and is now complete. FindingsBetween Nov 18, 2009, and Dec 15, 2014, 145 patients were randomly assigned to amiloride, 146 to hydrochlorothiazide, and 150 to the combination group. 132 participants in the amiloride group, 134 in the hydrochlorothiazide group, and 133 in the combination group were included in the modified intention-to-treat analysis. 2 h glucose concentrations after OGTT, averaged at 12 and 24 weeks, were significantly lower in the amiloride group than in the hydrochlorothiazide group (mean difference −0·55 mmol/L [95% CI −0·96 to −0·14]; p=0·0093) and in the combination group than in the hydrochlorothiazide group (−0·42 mmol/L [–0·84 to −0·004]; p=0·048). The mean reduction in home systolic blood pressure during 24 weeks did not differ significantly between the amiloride and hydrochlorothiazide groups, but the fall in blood pressure in the combination group was significantly greater than that in the hydrochlorothiazide group (p=0·0068). Hyperkalaemia was reported in seven (4·8%) patients in the amiloride group and three (2·3%) patients in the combination group; the highest recorded potassium concentration was 5·8 mmol/L in a patient in the amiloride group. 13 serious adverse events occurred but the frequency did not differ significantly between groups. InterpretationThe combination of amiloride with hydrochlorothiazide, at doses equipotent on blood pressure, prevents glucose intolerance and improves control of blood pressure compared with montherapy with either drug. These findings, together with previous data about morbidity and mortality for the combination, support first-line use of amiloride plus hydrochlorothiazide in hypertensive patients who need treatment with a diuretic. FundingBritish Heart Foundation and National Institute for Health Research.
 
Testosterone-Induced Water Retention - How to Combat It

From Muscular Development Magazine


Connect the dots— a child’s game where a random-appearing collection of darkened circles on paper suddenly generates a favorite cartoon character or animal when the dots are connected by a pencil line in proper order. Innovation in science is a game of “connect the dots.” Clinical trials look primarily at outcome and results, while the real “sexiness” of research is finding out why and how, rather than what.



Bodybuilding represents the epitome of “what” science. For generations, a lore of training, nutrition, supplements and drugs has evolved from the combined experience of tens of thousands, maybe as many as a million bodybuilders— who have tried, tracked, studied and in some cases, suffered from being an “experiment of one” or “human guinea pigs,” as some refer to the iron culture. Only in the last decade or so has basic and abstract science come forward to attempt to determine the “why and how” of bodybuilding. Some scientists refer to bodybuilding lore as “broscience” in a condescending manner, perhaps to generate a YouTube persona, provide the gratification of self-grandeur or to resolve a deep-seated belief that they have always disappointed their father.



Unfortunately, there is very little direct research into bodybuilding, but related research can be applied if there is enough familiarity with the topic to recognize when seemingly disconnected findings are published. This paper may represent such an apocalyptic revelation. For the record, apocalypse is not a term of catastrophe or end times, but discovery as it translates to “lifting of the veil.”



Water Retention

One adverse effect of testosterone use and misuse is edema— particularly, dependent edema— a condition more common in older men.1 Edema means water retention, and dependent refers to water retention “toward the ground” like when you can see the imprint of your socks around your ankles after you take them off. This is a sign of fluid retention, often associated with elevated sodium and potassium in the serum (blood). A study looking at various doses of testosterone enanthate in older men revealed nearly half experienced leg edema in the groups provided with supraphysiologic testosterone (300 and 600 milligrams per week of testosterone enanthate).2



Sodium and potassium are usually maintained in a balanced range through the actions of a multitude of hormones and chemokines that act primarily on the kidneys. Obviously, adequate water consumption plays a role as well, maintained by other hormones that stimulate thirst. Liver function also contributes, due to the osmotic (water-pulling) effect of various proteins produced by the blood, such as albumin. Hyperglycemia (elevated blood sugar) can factor in if it reaches pathologic concentrations, such as in type 1 diabetes, or perhaps following an extreme sugar binge.



Yet, many bodybuilders and lifters using anabolic-androgenic steroids (AAS), or men beginning testosterone replacement therapy (TRT), develop edema within a matter of days or weeks of beginning use, despite having previously been free of any such symptom. In TRT, dependent edema can lead to discontinuing treatment that is necessary to correct a hormonal deficiency that has direct consequences on metabolic health and even longevity. Certain gyms are filled with young men with transiently large, but doughy arms. Yet, what if this edema is not a significant adverse event that requires discontinuation of treatment (in the case of TRT), but a physiologic event that arises in men who generate an abnormal but treatable response to certain androgens? What if this treatment was not only safe and effective, but also may be instituted to treat a common condition that may pre-exist or develop over time eventually, regardless of exposure to or absence of TRT or AAS?



Regulating Blood Pressure

There is a responsive pathway that regulates blood pressure by increasing the reuptake of sodium from urine after it has been filtered from the blood. This causes sodium in the blood (serum) to go up, resulting in an increase in blood pressure and fluid retention. The pathway, CYP4A11 and CYP4F2, are enzyme systems in the liver, blood vessels and kidney cells that generate an active chemokine— a hormone-like messenger called 20-HETE.3 CYP4A11 and CYP4F2 convert arachadonic acid into 20-HETE using an enzyme called a monooxygenase.4 20-HETE generates numerous effects that cause an increase in both blood volume and resistance.4 This is like turning up the water flow on a garden hose and narrowing the opening. The water is discharged at a much greater pressure. This is great if you are pressure-washing your deck, but in your arteries and capillaries it causes damage and can lead to cardiovascular disease, organ damage and even death. An increase in blood pressure, alongside an increase in blood volume, causes extra “fluid” to be pushed from within blood vessels to the area between cells called the interstitial space. This is the beginning of one cause of androgen-associated edema.



To combat the effect of 20-HETE on the blood vessels requires a drug that antagonizes the CYP4A11 system, or competes with the enzyme to generate a non-harmful prostaglandin rather than 20-HETE. There are also antagonists to the 20-HETE receptor are in development. Unfortunately, none of these options are approved as of this time. However, the effect of 20-HETE on the kidneys can be managed using a common and inexpensive treatment. One possible strategy that may have value is increasing consumption of fish oil, as EPA and DHA (the omega-3 fatty acids) compete with arachadonic acid in the monooxygenase reaction. In test-tube studies, EPA and DHA in various concentrations reduced 20- HETE production by 15-65 percent.5



Drawing Sodium Back Into the Bloodstream

When blood volume is too high, sodium is elevated or hypertension (high blood pressure) exists. Sodium is usually excreted from the blood and NOT reabsorbed from the urine— as it is one of the main determinants of how much “fluid” is in the blood. However, 20-HETE stimulates an increase in special transporters that draw sodium (and chloride) back into the bloodstream from the newly filtered urine. This may occur through 20-HETE’s stimulation of an enzyme that generates the hormone angiotensin II. These transporters, called NCC, have been shown to be more abundant and more active as well when levels of angiotensin II are elevated.6 Angiotensin II is a hormone that is created through multiple converting enzymes, and stimulates the release and action of aldosterone. The function of aldosterone is to retain sodium. However, as angiotensin II is generated locally in the kidneys when stimulated by 20-HETE, it is a direct link to the increase in NCC transporter activity. It has been reported in mouse models that were genetically altered to have the more blood pressure-prone form of the human CYP4A11 gene that NCC transporters increased by 50 percent.3



Treating mice (and likely humans) with increased NCC activity, potentially due to increased 20-HETE production, is achieved by simple mechanisms. As stated earlier, inhibiting CYP4A11 or 20-HETE receptor antagonists will likely enter the pharmaceutical arsenal in the future.3 However, for now, established and inexpensive drugs and even supplements may offer much of the same benefits. Fish oil, sesamin, low sodium and a low-carb diet may be helpful.4 There are blood pressure drugs that work by acting directly upon the NCC to block sodium reuptake, as well as drugs that inhibit the production of angiotensin II (e.g., captopril, lisinopril, enalapril) or block angiotensin II’s action at its receptor (e.g., losartan). Another option is the diuretic hydrochlorothiazide (Dyazide), which acts directly on the NCC transporter. Given the prevalence of edema in older men started on TRT in the high-normal range or greater, it may be prudent to monitor their blood pressure frequently, or even consider administering an ACE inhibitor or losartan if their blood pressure is already in the prehypertensive range.



AAS Use and Edema

Now, the only thing lacking is the connection to AAS use, and what drugs may be most relevant to causing edema. AAS-associated edema is common among those using testosterone esters or oral AAS that aromatize easily, and rarely associated with DHT-based AAS such as stanozolol (aka Winstrol) or mesterolone (aka Proviron). One would then think that the estrogenic metabolites are causing the puffiness, and Winstrol and Proviron are cutting drugs that provide a hard, dry physique. Yet, it appears that DHT is the main culprit in AAS-associated edema, and estrogens get a pass this time.7 This may be relevant when choosing treatment modality in TRT, as topical agents have been shown to increase serum DHT over twice what was seen with injected testosterone.8



CYP4A11 and CYP4F2 are androgen regulated in mice and men. Increased androgen signaling results in an increase in CYP4F2, directly leading to an increase in 20-HETE in the kidneys’ microcirculation.4,5,7,9 This leads to many questions, of course, as this is a novel area of investigation. Is there an increase in blood pressure in men using predominantly DHT-derived AAS cycles (e.g., Winstrol)? Does the use of an aromatase inhibitor increase the risk of an elevation in blood pressure in AAS users of testosterone or aromatizable AAS, or men on TRT? Does suppressing estrogen via an aromatase inhibitor increase risk, or does adding an aromatizable AAS to a cycle decrease risk? Why are drugs such as Winstrol and Proviron “hardening” AAS— are they metabolized differently or generate a different response? Would a 5-alpha reductase drug reduce androgen-associated hypertension?



The purpose of this article is to make the reader aware of the presence of androgen-associated hypertension, so that he will be better prepared to make an informed decision about the choice of illicit AAS use and another relevant risk. For men on TRT or seeking treatment, as well as AAS users, blood pressure should be monitored throughout the exposure to the drug(s). Some individuals are more prone to this adverse effect due to one’s specific CYP4A11 or CYP4F2 gene.10 If one’s blood pressure increases, or is already high, then appropriate conversations should be initiated with one’s personal physician. Hypertension is known as one of the “silent killers,” as it can be without symptoms— but it also causes vascular and organ damage over time that can result in greatly impaired health, or even death.



References:

1. Chahla EJ, Hayek ME, et al. Testosterone replacement therapy and cardiovascular risk factors modification. Aging Male 2011;14:83-90.

2. Bhasin S, Woodhouse L, et al. Older men are as responsive as young men to the anabolic effects of graded doses of testosterone on the skeletal muscle. J Clin Endocrinol Metab 2005;90:678-88.

3. Savas Ü, Wei S, et al. 20-Hydroxyeicosatetraenoic Acid (HETE)-dependent hypertension in human cytochrome P450 (CYP) 4A11 transgenic mice: normalization of blood pressure by sodium restriction, hydrochlorothiazide, or blockade of the type 1 angiotensin ii receptor. J Biol Chem 2016;291:16904-19.

4. Wu CC, Gupta T, et al. 20-HETE and blood pressure regulation: clinical implications. Cardiol Rev 2014;22:1-12.

5. Harmon SD, Fang X, et al. Oxygenation of omega-3 fatty acids by human cytochrome P450 4F3B: effect on 20-hydroxyeicosatetraenoic acid production. Prostaglandins Leukot Essent Fatty Acids 2006;75:169-77.

6. Rojas-Vega L, Gamba G. Mini-review: regulation of the renal NaCl cotransporter by hormones. Am J Physiol Renal Physiol 2016;310:F10-4.

7. Singh H, Schwartzman ML. Renal vascular cytochrome P450-derived eicosanoids in androgen-induced hypertension. Pharmacol Rep 2008;60:29-37.

8. Borst SE, Shuster JJ, et al. Cardiovascular risks and elevation of serum DHT vary by route of testosterone administration: a systematic review and meta-analysis. BMC Med 2014 Nov 27;12:211(16 pp).

9. Liu X, Wu J, et al. Disturbed ratio of renal 20-HETE/EETs is involved in androgen-induced hypertension in cytochrome P450 4F2 transgenic mice. Gene 2012;505:352–359.

10. Jiang Y, Hou J, et al. T8590C polymorphism of CYP4A11 is a risk factor for hypertension: a meta-analysis. Chin Med J 2014;127:2382-5.
 
Beyond Testosterone Book by Nelson Vergel
I really wish the bloat issue could get figured out in regards to a long term solution. I've read that article as well and appears to be pointing to diuretics/ARB's/ACE Inhibitors, but not sure on the actual longterm ramifications of a diuretic, etc. Feel pretty good except for the constant bloat that goes away a bit with Telmisartan and a lot with a diuretic, but comes back when discontinuing.

The diuretic may simply be making up for the sodium retention issue so may not be harmful long term but if a drug can be avoided that would be awesome but also cannot stand the bloat face that I get.
 
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