I am on 88 mcg levothyroxine and 1 grain Natur thriod. If it were nor for the clot, I would be great. I am finally findind doctors whoseems interested in finding answers to my throat issues. The tonsils are very mildly inflamed, exp left one. She meant to biopsy it, but it was hard to see and she missed and hit the front arch, That is not all bad, I had had a sore there a month prior so that was ruled out. I just never recovered from being told I might have cancer twice in 2 months a few years back. Both apparently wrong. I was actually feeling btter on tests and just having more time between me an all that. Then my throat started hurting in may. We will see.
Can Testosterone Induce Blood Clots and Thrombosis? Interview with Dr Charles Glueck
- Thread starter Nelson Vergel
- Start date
what are ur thyroid bloods? how do they read? ive seen guys who went to a doc got put on the levo and to a different when they were felling like crap and that doc switched their meds and they felt better... just sayin... u might want to find a naturopath type doc, or even check with thyroid groups on fcebook if ur on there at all? might get better answers....
That was a naturopath. Regular MD insisted on T4 only. I feel better with some T3. My numbers are about perfect really. I have labs before they took my thyroid out and I am close. So tell me, when do you start to rebound after stopping testosterone
Dr Gleuck just emailed me and asked if I was completeing my tests. I told him I would, but would probably wait a few months. The chance that I may have no clotting factor issues would really make me focus on cancer. So, I am being a chicken for at least 6 months. Then I will test, most cancers would be found by then and I can move on
see if u feel better with some t3, id go to a doctor that balances YOU out and helps you to feel ur best by optomizing ur organs and hormones...
each person is different, if u can run a pct after comming off test that would be best, but if ur clotting doc g says not to hcg and everything such as that, so it could take months for ur hormones to normalize... it took me from october 2014 to april 2015.... and then i was put back onto trt because my numbers were still low... but i felt awesome... which is weird...
honestly if u already started with doc g's blood work, finish it, get a diagnoses and move on from there, too much anxiety and stressing about misdiagnoses (which it sounds like they did for cancer???) and being so stressed ur going to burn ur adrenals on top of everything else thats gone on and is still going on...
Nelson Vergel
Founder, ExcelMale.com
J Urol. 2015 Oct 30. pii: S0022-5347(15)05157-5. doi: 10.1016/j.juro.2015.10.134. [Epub ahead of print]
Association between use of exogenous testosterone therapy (eTT) and risk of venous-thrombotic-events among eTT-treated and untreated men with hypogonadism.
Li H1, Benoit K2, Wang W2, Motsko S2.
Abstract
PURPOSE:
Limited information exists about whether exogenous testosterone therapy (eTT) is associated with risk of venous thrombotic events (VTE). Here, we investigate via cohort and nested-case-control analyses whether eTT administration is associated with risk of VTE in men with hypogonadism.
MATERIALS AND METHODS:
Databases were reviewed to identify men prescribed eTT and/or men with a hypogonadism diagnosis. Propensity-score 1:1 matching was used to select patients for the cohort analysis. Cases (men with VTE) were matched 1:4 with controls (men without VTE) for the nested-case-control analysis. Primary outcome was defined as incident idiopathic VTE; Cox regression and conditional-logistic regression were used to assess hazard ratios (HRs) and odds ratios (ORs), respectively. Sensitivity analyses were also performed.
RESULTS:
102,650 eTT-treated patients and 102,650 untreated patients were included in the cohort analysis after matching; 2785 cases and 11,119 controls were included in the case-control analysis. Cohort analysis revealed an HR of 1.08 for all eTT-treated patients (95% CI: 0.91, 1.27; p=0.378). Case-control analysis resulted in OR=1.02 (95% CI: 0.92, 1.13; p=0.702) for current eTT exposure and 0.92 (95% CI: 0.82, 1.03; p=0.145) for past eTT exposure. These results remained non statistically significant after stratifying by eTT-administration-route and age category. Results from most of the sensitivity analyses yielded results that were consistent.
CONCLUSIONS:
No significant association was found between eTT and incidents of idiopathic VTE, as well as overall VTE in men with hypogonadism; however, some discrepant findings exist for the association between injectable formulations and overall VTE risk.
Association between use of exogenous testosterone therapy (eTT) and risk of venous-thrombotic-events among eTT-treated and untreated men with hypogonadism.
Li H1, Benoit K2, Wang W2, Motsko S2.
Abstract
PURPOSE:
Limited information exists about whether exogenous testosterone therapy (eTT) is associated with risk of venous thrombotic events (VTE). Here, we investigate via cohort and nested-case-control analyses whether eTT administration is associated with risk of VTE in men with hypogonadism.
MATERIALS AND METHODS:
Databases were reviewed to identify men prescribed eTT and/or men with a hypogonadism diagnosis. Propensity-score 1:1 matching was used to select patients for the cohort analysis. Cases (men with VTE) were matched 1:4 with controls (men without VTE) for the nested-case-control analysis. Primary outcome was defined as incident idiopathic VTE; Cox regression and conditional-logistic regression were used to assess hazard ratios (HRs) and odds ratios (ORs), respectively. Sensitivity analyses were also performed.
RESULTS:
102,650 eTT-treated patients and 102,650 untreated patients were included in the cohort analysis after matching; 2785 cases and 11,119 controls were included in the case-control analysis. Cohort analysis revealed an HR of 1.08 for all eTT-treated patients (95% CI: 0.91, 1.27; p=0.378). Case-control analysis resulted in OR=1.02 (95% CI: 0.92, 1.13; p=0.702) for current eTT exposure and 0.92 (95% CI: 0.82, 1.03; p=0.145) for past eTT exposure. These results remained non statistically significant after stratifying by eTT-administration-route and age category. Results from most of the sensitivity analyses yielded results that were consistent.
CONCLUSIONS:
No significant association was found between eTT and incidents of idiopathic VTE, as well as overall VTE in men with hypogonadism; however, some discrepant findings exist for the association between injectable formulations and overall VTE risk.
Concerned wife
New Member
Because of my own's husband susceptibility to hypercoagulability, polycythemia and need for TRT, I have been vigilant in trying to find the best ways to prevent blood clots. This article was informative to me, regarding the different types of clots formed (what the clots are made of) in arteries versus veins. Scroll to the bottom to see what compounds work on what kind of clots. Interestingly, fish oil isn't listed, but we will continue using it.
http://www.med.unc.edu/htcenter/pat...s/blood-clot-education-1/what-is-a-blood-clot
http://www.med.unc.edu/htcenter/pat...s/blood-clot-education-1/what-is-a-blood-clot
Marco N Cognito
Member
For his TRT, is he on injections, pellets, or a gel? What's his dosing protocol? Also, you mention susceptibility to hypercoagulability. Has he experienced any thrombotic events? I'm assuming he hasn't been formally tested nor diagnosed with any familial or acquired clotting disorder, otherwise, he'd likely be on an anticoagulant. Polycythemia can be managed with routine CBCs and periodic therapeutic phlebotomy. Fish oil is in the same class as aspirin and other OTC agents that work to inhibit platelet aggregation only. They are completely ineffective against the more serious clots that form DVTs; only prescription anticoagulants (i.e. warfarin) address this. The article is way behind the times. In the last 3-4 years, there are a few newer anticoagulants that have been FDA-approved (i.e. Xarelto, Pradaxa, Eliquis) that have replaced the old standby warfarin (Coumadin) which was originally used as rat poison. I am not knocking OTC natural thinners, as I take them all myself, however, if one is at risk for any type of thrombophilia, I wouldn't rely on them exclusively, but it's great you have a basic understanding of the risk potential and are trying to act preventatively which is where mainstream medicine has largely failed us.
Last edited:
Marco N Cognito
Member
Much appreciated again, Nelson, for posting this & keeping us abreast of these forthcoming studies that refute prior research in this area. It would be interesting to see what Glueck would have to say now that more research continues to oppose his. Since the above is only an abstract of the actual study, it would be interesting to see exactly what types of VTE those men had, or, if they were only idiopathic (of unknown origin). I think I fall into this category, as to this day, we still have not been able to determine what the exact etiology of my thrombotic events were back in 2012. There are only intermittent indications in certain clotting factors and the fact I have a MTHFR defect that may at best contribute to or be possible causal factors, but nothing solid.
Concerned wife
New Member
Hi Marco! He's been on all three but is currently using compounded bio-identical cream. My husband is pretty private about his medical info being online so I can't share a lot of personal detail, but I will tell you the TRT replacements does not get his numbers to ideal levels. He has been diagnosed with a disorder that makes him susceptible to hypercoagulability, but again, for privacy's sake, I won't mention what it is. It's true that mainstream physicians and even some functional medicine doctors would recommend an anticoagulant but the long-term side effects of those, at least in our opinion, are worse than the relative risk we are taking by "only" using natural products. Long-term warfarin will cause problems, especially osteoporosis and hardening of the arteries, and can put a person at risk for other types of stroke. At this point, it's just not worth it for us to "go there." Also, Warfarin doesn't dissolve clots that have already formed, whereas nattokinase, serrapeptase and lumbrokinase have the potential to do so. Regarding the newer medicines, same thing, except they haven't been on the market long enough to really know what the long-term effects might be.
I understand that fish oil inhibits platelet aggregation only but don't understand why you would say that the clots that form DVTs are "more serious." I think heart attacks and strokes (caused from blood clots blocking arteries) are as bad or worse than pulmonary embolisms and DVTs. It's ALL bad! This is why he also uses lumbrokinase, nattokinase and serrapeptase. Those DO break down fibrin, which is what the DVT type clots are made of.
Thanks for the phlebotomy info. I replied previously to another post on that, if you're interested in seeing my thoughts.
https://www.excelmale.com/forum/sho...ing-low-ferritin-levels-and-frequent-donation
I appreciate your kind warning about only using natural blood thinners. Mainstream medicine HAS largely failed us and my husband is a case study in that...wish I could share more, but we have had to become extremely proactive to keep him from further problems and more medicine due to his underlying condition.
If you're interested, here are more links I found helpful...you may already know it all, but perhaps someone else will run across this thread and glean some benefit.
http://healthiertalk.com/natural-alternative-coumadin-2230
http://nutritionandhealing.com/2012/06/06/a-guide-to-using-fish-oil-to-reduce-clotting/
http://www.ncbi.nlm.nih.gov/pubmed/19783511
http://www.ncbi.nlm.nih.gov/pubmed/9253809
http://www.ncbi.nlm.nih.gov/pubmed/8268550
http://www.ncbi.nlm.nih.gov/pubmed/18597751
http://www.ncbi.nlm.nih.gov/pubmed/19358933
http://www.health.harvard.edu/famil...od-like-your-waistline-the-thinner-the-better
https://www.astenzymes.com/nattokinase-literature-review
I understand that fish oil inhibits platelet aggregation only but don't understand why you would say that the clots that form DVTs are "more serious." I think heart attacks and strokes (caused from blood clots blocking arteries) are as bad or worse than pulmonary embolisms and DVTs. It's ALL bad! This is why he also uses lumbrokinase, nattokinase and serrapeptase. Those DO break down fibrin, which is what the DVT type clots are made of.
Thanks for the phlebotomy info. I replied previously to another post on that, if you're interested in seeing my thoughts.
https://www.excelmale.com/forum/sho...ing-low-ferritin-levels-and-frequent-donation
I appreciate your kind warning about only using natural blood thinners. Mainstream medicine HAS largely failed us and my husband is a case study in that...wish I could share more, but we have had to become extremely proactive to keep him from further problems and more medicine due to his underlying condition.
If you're interested, here are more links I found helpful...you may already know it all, but perhaps someone else will run across this thread and glean some benefit.
http://healthiertalk.com/natural-alternative-coumadin-2230
http://nutritionandhealing.com/2012/06/06/a-guide-to-using-fish-oil-to-reduce-clotting/
http://www.ncbi.nlm.nih.gov/pubmed/19783511
http://www.ncbi.nlm.nih.gov/pubmed/9253809
http://www.ncbi.nlm.nih.gov/pubmed/8268550
http://www.ncbi.nlm.nih.gov/pubmed/18597751
http://www.ncbi.nlm.nih.gov/pubmed/19358933
http://www.health.harvard.edu/famil...od-like-your-waistline-the-thinner-the-better
https://www.astenzymes.com/nattokinase-literature-review
Marco N Cognito
Member
Wow, I am impressed at the research you have done. Few besides myself take the time to delve into the dark waters of research as I do! Your husband is a very fortunate man to have you in his life.
In addition to using high-dose omega 3s and 7, I also use all those natural fibrinolytics you mention, my favorite being Boluoke lumbrokinase, as it is the only lumbrokinase to have had at least some research which is continuing. It comes at a much higher cost per cap than the competition, but the others just don't measure up. I also use Arthur Andrew Serratia (very high dose serrapeptase), nattokinase, and a great product from them called Neprinol AFD. These are all great, but the problem with familial or acquired thrombophilia is that, although effective in dissolving fibrin, these agents do not inhibit thrombin from forming, hence, the necessity for some of the newer Rx protocols (i.e. Pradaxa) which are direct thrombin inhibitors. I, myself, am on a lower dose of Xarelto for DVT/PE prophylaxis for the last year and have noticed no side effects and all markers are within range (I run extensive labs monthly).
What are your thoughts on Dr. Glueck's work that I and many others posted upthread? As you can see, he vehemently opposes the use of TRT/HRT of any kind in cases of familial or acquired thrombophilia which does not resolve the issue for those that who are hypogonadal AND have a clotting disorder. I am fortunate that, at age 55, my T levels are still somewhat adequate, so I have not yet embarked on a TRT protocol. Sure, I could use more for that extra edge in the gym, but it's a risk/reward issue, and would rather find a way to facilitate endogenous production as opposed to using exogenous T. Thus, I am more interested in finding agents to stimulate LH and FSH (i.e. clomiphene) into producing T, however, these drugs have their own sets of side effects. I believe that there will be a better alternatives soon. Until then, we have what we have.
Last edited:
Concerned wife
New Member
Marco, thanks so much for your kind words. I ADORE my precious husband and he has been through A LOT. I guess I feel it's my mission to do all I can to spare him from anything -- at least anything that might be within our control.
I am going to have to look into the Omega 7s. I don't think I am familiar with those. I have looked at Arthur Andrew stuff, and Neprinol, but haven't bought any as of yet.
I understand what you are saying about the natural agents not inhibiting thrombin forming directly and would always advise people to make their own, careful decisions, based on their particular condition and the best medical and holistic advice possible. Regarding Dr. Glueck's work, I'm sure his numbers don't lie. I also know, though, that there are many people who have recurrent thromboembolism, despite "adequate" medical treatment with pharmaceutical drugs.
I would never recommend someone go on TRT if they do not truly NEED it. I would exhaust all other avenues first, including diet change, natural supplements and other approaches to raise testosterone (as you mentioned with your own case). I do believe that a lot of men who are generally healthy would be able to see improvements with these other approaches. However, for men who are truly hypogonadal and whose health precludes these lesser measures working, I would advocate the same approach that is taken for any therapy -- weigh the benefits versus risks. Life can seem unlivable if you are suffering severe symptoms from low hormone levels and in those patients, maybe the risk is worth taking. I wouldn't do it without a lot of vigilance and caution, but everyone has to decide for themselves, based on their own quality of life, or lack thereof.
I am going to have to look into the Omega 7s. I don't think I am familiar with those. I have looked at Arthur Andrew stuff, and Neprinol, but haven't bought any as of yet.
I understand what you are saying about the natural agents not inhibiting thrombin forming directly and would always advise people to make their own, careful decisions, based on their particular condition and the best medical and holistic advice possible. Regarding Dr. Glueck's work, I'm sure his numbers don't lie. I also know, though, that there are many people who have recurrent thromboembolism, despite "adequate" medical treatment with pharmaceutical drugs.
I would never recommend someone go on TRT if they do not truly NEED it. I would exhaust all other avenues first, including diet change, natural supplements and other approaches to raise testosterone (as you mentioned with your own case). I do believe that a lot of men who are generally healthy would be able to see improvements with these other approaches. However, for men who are truly hypogonadal and whose health precludes these lesser measures working, I would advocate the same approach that is taken for any therapy -- weigh the benefits versus risks. Life can seem unlivable if you are suffering severe symptoms from low hormone levels and in those patients, maybe the risk is worth taking. I wouldn't do it without a lot of vigilance and caution, but everyone has to decide for themselves, based on their own quality of life, or lack thereof.
Concerned wife
New Member
This is a little off the subject, but I wonder if doctors of women having issues are refusing them hormone therapy because of the risks? I have a female friend with Factor V Leiden and she has resisted pharmaceutical blood thinners.
This is an excerpt of the benefit versus risk ratio for these patients. I am sure some suffering women are willing to take their chances for a better quality of life:
What Are the Special Considerations for Women With Factor V Leiden?
Hormone Use
The use of hormones, such as oral contraceptive pills (OCPs) and hormone replacement therapy (HRT, including estrogen and estrogen-like drugs) taken after menopause, increases the risk of developing DVT and PE. Healthy women taking OCPs have a 3- to 4-fold increased risk of developing a DVT or PE compared with women who do not take OCP. Women with factor V Leiden who take OCPs have about a 35-fold increased risk of developing a DVT or PE compared with women without factor V Leiden and those who do not take OCPs. This would translate to an about 35 per 10 000 chance per year of use on average for women in their twenties with factor V Leiden. Likewise, postmenopausal women taking HRT have a 2- to 3-fold higher risk of developing a DVT or PE than women who do not take HRT, and women with factor V Leiden who take HRT have a 15-fold higher risk. This is about a 15 to 40 per 1000 chance per year of use, on average, for women in their fifties with factor V Leiden. Women with heterozygous factor V Leiden who are making decisions about OCP or HRT use should take these statistics into consideration when weighing the risks and benefits of treatment.
This is an excerpt of the benefit versus risk ratio for these patients. I am sure some suffering women are willing to take their chances for a better quality of life:
What Are the Special Considerations for Women With Factor V Leiden?
Hormone Use
The use of hormones, such as oral contraceptive pills (OCPs) and hormone replacement therapy (HRT, including estrogen and estrogen-like drugs) taken after menopause, increases the risk of developing DVT and PE. Healthy women taking OCPs have a 3- to 4-fold increased risk of developing a DVT or PE compared with women who do not take OCP. Women with factor V Leiden who take OCPs have about a 35-fold increased risk of developing a DVT or PE compared with women without factor V Leiden and those who do not take OCPs. This would translate to an about 35 per 10 000 chance per year of use on average for women in their twenties with factor V Leiden. Likewise, postmenopausal women taking HRT have a 2- to 3-fold higher risk of developing a DVT or PE than women who do not take HRT, and women with factor V Leiden who take HRT have a 15-fold higher risk. This is about a 15 to 40 per 1000 chance per year of use, on average, for women in their fifties with factor V Leiden. Women with heterozygous factor V Leiden who are making decisions about OCP or HRT use should take these statistics into consideration when weighing the risks and benefits of treatment.
Nelson Vergel
Founder, ExcelMale.com
Thanks Marco. This thread is the best on the subject in the entire Internet. And also thanks to concerned wife. I will let Marco answer your question since he is our in-house expert on this subject.
I wonder if the estradiol levels were better controlled here . Mine was definateley high at the time of my DVT. Of coarse my Doc was pushing high levels of testosterone. Also Glueck only estimates 1.2 percent. I am no mathematician, but would that rise to significance statistically.
Last edited:
Nelson Vergel
Founder, ExcelMale.com
Glueck CJ, Prince M, Patel N, et al.
Thrombophilia in 67 Patients With Thrombotic Events After Starting Testosterone Therapy.
Clin Appl Thromb Hemost.
http://cat.sagepub.com/content/early/2015/11/27/1076029615619486.abstract
We compared thrombophilia in 67 cases (59 men and 8 women) with thrombotic events after starting testosterone therapy (TT) versus 111 patient controls having unprovoked venous thrombotic events without TT. In the 67 patients, thrombosis (47 deep venous thrombosis-pulmonary embolism, 16 osteonecrosis, and 4 ocular thrombosis) occurred 6 months (median) after starting TT. Cases differed from controls for factor V Leiden heterozygosity (16 of the 67 [24%] vs 13 [12%] of the 111, P = .038) and for lupus anticoagulant (9 [14%] of the 64 vs 4 [4%] of the 106, P = .019). After a first thrombotic event and continuing TT, 11 cases had a second thrombotic event, despite adequate anticoagulation, 6 of whom, still anticoagulated, had a third thrombosis. Screening for thrombophilia before starting TT should identify men and women at high risk for thrombotic events with an adverse risk-benefit ratio for TT. When TT is given to patients with familial and acquired thrombophilia, thrombosis may occur and recur in thrombophilic men despite anticoagulation.
Thrombophilia in 67 Patients With Thrombotic Events After Starting Testosterone Therapy.
Clin Appl Thromb Hemost.
http://cat.sagepub.com/content/early/2015/11/27/1076029615619486.abstract
We compared thrombophilia in 67 cases (59 men and 8 women) with thrombotic events after starting testosterone therapy (TT) versus 111 patient controls having unprovoked venous thrombotic events without TT. In the 67 patients, thrombosis (47 deep venous thrombosis-pulmonary embolism, 16 osteonecrosis, and 4 ocular thrombosis) occurred 6 months (median) after starting TT. Cases differed from controls for factor V Leiden heterozygosity (16 of the 67 [24%] vs 13 [12%] of the 111, P = .038) and for lupus anticoagulant (9 [14%] of the 64 vs 4 [4%] of the 106, P = .019). After a first thrombotic event and continuing TT, 11 cases had a second thrombotic event, despite adequate anticoagulation, 6 of whom, still anticoagulated, had a third thrombosis. Screening for thrombophilia before starting TT should identify men and women at high risk for thrombotic events with an adverse risk-benefit ratio for TT. When TT is given to patients with familial and acquired thrombophilia, thrombosis may occur and recur in thrombophilic men despite anticoagulation.
Nelson Vergel
Founder, ExcelMale.com
Is taurine supplementation the answer?
[h=2]Influence of chronic administration of anabolic androgenic steroids and taurine on haemostasis profile in rats: a thrombelastographic study[/b]
Anabolic androgenic steroids (AAS) are synthetic derivatives of testosterone with thrombogenic potential in high doses and long-term administration. Taurine, a widely distributed amino-sulfonic acid, is known for its beneficial effects in hypercoagulable states. In order to assess the impact of chronic administration of high doses of AAS and taurine upon haemostasis process in rats, 40 male Wistar rats were divided into four equal groups: control group (group C) – no treatment; androgen group (group A) – received 10 mg/kg per week of nandrolone decanoate (DECA); taurine (group T) – received oral supplementation of 2% taurine in drinking water; androgen and taurine group (group AT) – concomitant administration of DECA and taurine. After 12 weeks, blood samples were collected and haemostasis parameters were assessed with the thrombelastographic (TEG) analysis system: reaction time, clot kinetics (K, α
, final clot strength, coagulation index and the clot lysis (Ly30). Nandrolone significantly decreased reaction time in group A compared with control (P < 0.001), whereas taurine significantly increase reaction time (P = 0.01), and this effect was maintained in group AT compared with group A (P = 0.009). Similar differences between groups have been recorded for the clot kinetics parameters K, α. The final clot strength and coagulation index were significantly increased in group A versus group C (P = 0.04, respectively P < 0.001), but not in group AT versus group C (P > 0.05). There were no differences in clot lysis, as shown by Ly30. Nandrolone produces an accelerated clot development and an increased clot firmness in Wistar rats. Taurine association ensures a protective effect against this hypercoagulable state, partially restoring the altered parameters of the coagulation profile.
http://mobile.journals.lww.com/bloo...ewer.aspx?year=2013&issue=04000&article=00007
[h=2]Influence of chronic administration of anabolic androgenic steroids and taurine on haemostasis profile in rats: a thrombelastographic study[/b]
Anabolic androgenic steroids (AAS) are synthetic derivatives of testosterone with thrombogenic potential in high doses and long-term administration. Taurine, a widely distributed amino-sulfonic acid, is known for its beneficial effects in hypercoagulable states. In order to assess the impact of chronic administration of high doses of AAS and taurine upon haemostasis process in rats, 40 male Wistar rats were divided into four equal groups: control group (group C) – no treatment; androgen group (group A) – received 10 mg/kg per week of nandrolone decanoate (DECA); taurine (group T) – received oral supplementation of 2% taurine in drinking water; androgen and taurine group (group AT) – concomitant administration of DECA and taurine. After 12 weeks, blood samples were collected and haemostasis parameters were assessed with the thrombelastographic (TEG) analysis system: reaction time, clot kinetics (K, α
, final clot strength, coagulation index and the clot lysis (Ly30). Nandrolone significantly decreased reaction time in group A compared with control (P < 0.001), whereas taurine significantly increase reaction time (P = 0.01), and this effect was maintained in group AT compared with group A (P = 0.009). Similar differences between groups have been recorded for the clot kinetics parameters K, α. The final clot strength and coagulation index were significantly increased in group A versus group C (P = 0.04, respectively P < 0.001), but not in group AT versus group C (P > 0.05). There were no differences in clot lysis, as shown by Ly30. Nandrolone produces an accelerated clot development and an increased clot firmness in Wistar rats. Taurine association ensures a protective effect against this hypercoagulable state, partially restoring the altered parameters of the coagulation profile.http://mobile.journals.lww.com/bloo...ewer.aspx?year=2013&issue=04000&article=00007
ok so how does one increase theirs naturally then? im so tired of pinning, and worrying about this crap im ready to be done with all this!
Nelson Vergel
Founder, ExcelMale.com
These may or may not work on some men. When you stop TRT your T will be suppressed for a while
How to Increase Testosterone Naturally
How to Increase Testosterone Naturally
Share this page
Sponsors
Online statistics
- Members online
- 3
- Guests online
- 112
- Total visitors
- 115
Latest posts
-
Can an older man still build muscle while taking statins?- Latest: Mountain Man
-
-
-
Erection Supplements- Do They Work to Improve ED?- Latest: Nelson Vergel
-
-
