Can Testosterone Induce Blood Clots and Thrombosis? Interview with Dr Charles Glueck

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Nelson Vergel

Founder, ExcelMale.com
Yes, it is. But those numbers do not justify spending 800 dollars for testing every man who is about to start testosterone. Luckily, Dr Glueck can run those tests if you contact him at the email above.
 
Defy Medical TRT clinic doctor

Bass

New Member
Then to add more warning to the debate the recent FDA call for TRT and the relation to polycythemia , 2 days ago
http://www.foxnews.com/health/2014/...sterone-products-to-carry-blood-clot-warning/

its a known fact that testosterone will increase RBC, but there is a simple fix for this as you all know, donate! however I agree that this side needs to be added to the label as many doctors today have no clue how to treat it, some even refuse to give a script for blood letting. so I agree with FDA on adding this side effect to the label.
 

Nelson Vergel

Founder, ExcelMale.com
Both polycythemia or blot clots (in men with genetic predisposition) can happen with either testosterone gels or injections. Polycythemia is the most common side effect in testosterone replacement and it is easy to manage with blood donations. However, 2 percent of men may have genetic mutations that may make them more prone to blood clot formation on testosterone.
 

J2048b

Member
I agree, $800 is allot of money.

WOW AND THANK YOU IS ALL I CAN SAY! this interview is awesome and so is the doc that was interviewed,

let me tell everyone who cant afford these tests, the doc sent me a reply with paper work to fill out, and at the bottom of the last sheet, the questionnaire, and it states this:

#14. if you have not had clotting factors measured, we can arrange to have these measured. They are usually covered by insurance, but if not, WE WILL PICK UP THE COST THROUGH OUR RESEARCH FUND, AND THE CLOTTING TESTS WILL BE AT NO COST TO YOU, ONE WAY OR ANOTHER!!

they will interpret the results for FREE!! and advise you in regards to therapy!!


WOW i am speechless!!!
 

Nelson Vergel

Founder, ExcelMale.com
Here is a new study comparing blood thinners:

Clinical and Safety Outcomes Associated With Treatment of Acute Venous Thromboembolism
A Systematic Review and Meta-analysis

JAMA. 2014;312(11):1122-1135

Lana A. Castellucci, MD

Importance Many anticoagulant strategies are available for the treatment of acute venous thromboembolism, yet little guidance exists regarding which drug is most effective and safe.

Objective To summarize and compare the efficacy and safety outcomes associated with 8 anticoagulation options (unfractionated heparin [UFH], low-molecular-weight heparin [LMWH], or fondaparinux in combination with vitamin K antagonists); LMWH with dabigatran or edoxaban; rivaroxaban; apixaban; and LMWH alone) for treatment of venous thromboembolism.

Data Sources A systematic literature search was conducted using MEDLINE, EMBASE, and the evidence-based medicine reviews from inception through February 28, 2014.

Study Selection Eligible studies were randomized trials reporting rates of recurrent venous thromboembolism and major bleeding in patients with acute venous thromboembolism. Of the 1197 studies identified, 45 trials including 44 989 patients were included in the analyses.

Data Extraction and Synthesis Two reviewers independently extracted trial-level data including number of patients, duration of follow-up, and outcomes. The data were pooled using network meta-analysis.

Main Outcomes and Measures The primary clinical and safety outcomes were recurrent venous thromboembolism and major bleeding, respectively.

Results Compared with the LMWH–vitamin K antagonist combination, a treatment strategy using the UFH–vitamin K antagonist combination was associated with an increased risk of recurrent venous thromboembolism (hazard ratio
, 1.42; 95% credible interval [CrI], 1.15-1.79). The proportion of patients experiencing recurrent venous thromboembolism during 3 months of treatment were 1.84% (95% CrI, 1.33%-2.51%) for the UFH–vitamin K antagonist combination and 1.30% (95% CrI, 1.02%-1.62%) for the LMWH–vitamin K antagonist combination. Rivaroxaban (HR, 0.55; 95% CrI, 0.35-0.89) and apixaban (HR, 0.31; 95% CrI, 0.15-0.62) were associated with a lower risk of bleeding than was the LMWH–vitamin K antagonist combination, with a lower proportion of patients experiencing a major bleeding event during 3 months of anticoagulation: 0.49% (95% CrI, 0.29%-0.85%) for rivaroxaban, 0.28% (95% CrI, 0.14%-0.50%) for apixaban, and 0.89% (95% CrI, 0.66%-1.16%) for the LMWH–vitamin K antagonist combination.

Conclusions and Relevance Using meta-analytic pooling, there were no statistically significant differences for efficacy and safety associated with most treatment strategies used to treat acute venous thromboembolism compared with the LMWH–vitamin K antagonist combination. However, findings suggest that the UFH–vitamin K antagonist combination is associated with the least effective strategy and that rivaroxaban and apixaban may be associated with the lowest risk for bleeding.
 

Nelson Vergel

Founder, ExcelMale.com
DR Glueck paper on testosterone and thrombosis

Here is a copy of the original paper by Dr Glueck (attached for download)
 

Attachments

  • Glueck paper on Testosterone and Thrombosis.pdf
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stcrim

New Member
Rutin

This is a very interesting thread on Clots. You may want to look over this information out of Harvard: http://news.harvard.edu/gazette/story/2012/05/flavonoid-compound-can-prevent-blood-clots/ There are also numerous papers in PubMed on the subject of Rutin and clotting. There have been some minor human trials though the serious ones are just now recruiting. Rutin in cheap and seems like it would make a nice insurance policy against blood clots.

For the record in June I had a DVT caused by May Thurner Syndrome (a crossing of the iliac artery and vein causing the vein to be compressed). Had I stayed hydrated and not sat for extended periods at the office I would never have known I had MTS. Because I didn't know better I have a 100 percent blockage of the iliac vein and may be on Xarelto for life.

I have also been using T for years due to numbers well below 300. I prefer injection - the creams seem to increase my BPH for some reason. I would donate blood every two or three months to reduce my blood viscosity but for lack of time I went a year right before my DVT which also resulted in multiple, bilateral pulmonary embolisms.

All of that is a long story but here's my advice - stay hydrated (above all else). If you have to sit a lot get up every 30 minutes and move for a minute or two. Consider taking 500mgs or Rutin 3 times a day and become familiar with the symptoms of DVT. If you survive and that's a big if, the aftermath is no fun.

I use testosterone to this day and don't believe it had a thing to do with my DVT/PE.

Steve
 
This is a very interesting thread on Clots. You may want to look over this information out of Harvard: http://news.harvard.edu/gazette/story/2012/05/flavonoid-compound-can-prevent-blood-clots/ There are also numerous papers in PubMed on the subject of Rutin and clotting. There have been some minor human trials though the serious ones are just now recruiting. Rutin in cheap and seems like it would make a nice insurance policy against blood clots.

For the record in June I had a DVT caused by May Thurner Syndrome (a crossing of the iliac artery and vein causing the vein to be compressed). Had I stayed hydrated and not sat for extended periods at the office I would never have known I had MTS. Because I didn't know better I have a 100 percent blockage of the iliac vein and may be on Xarelto for life.

I have also been using T for years due to numbers well below 300. I prefer injection - the creams seem to increase my BPH for some reason. I would donate blood every two or three months to reduce my blood viscosity but for lack of time I went a year right before my DVT which also resulted in multiple, bilateral pulmonary embolisms.

All of that is a long story but here's my advice - stay hydrated (above all else). If you have to sit a lot get up every 30 minutes and move for a minute or two. Consider taking 500mgs or Rutin 3 times a day and become familiar with the symptoms of DVT. If you survive and that's a big if, the aftermath is no fun.

I use testosterone to this day and don't believe it had a thing to do with my DVT/PE.

Steve

This is the one I use. Probably more more effective than regular rutin:
https://www.pureformulas.com/betarutin-60-capsules-by-ecological-formulas.html
 

J2048b

Member
This is a very interesting thread on Clots. You may want to look over this information out of Harvard: http://news.harvard.edu/gazette/story/2012/05/flavonoid-compound-can-prevent-blood-clots/ There are also numerous papers in PubMed on the subject of Rutin and clotting. There have been some minor human trials though the serious ones are just now recruiting. Rutin in cheap and seems like it would make a nice insurance policy against blood clots.

For the record in June I had a DVT caused by May Thurner Syndrome (a crossing of the iliac artery and vein causing the vein to be compressed). Had I stayed hydrated and not sat for extended periods at the office I would never have known I had MTS. Because I didn't know better I have a 100 percent blockage of the iliac vein and may be on Xarelto for life.

I have also been using T for years due to numbers well below 300. I prefer injection - the creams seem to increase my BPH for some reason. I would donate blood every two or three months to reduce my blood viscosity but for lack of time I went a year right before my DVT which also resulted in multiple, bilateral pulmonary embolisms.

All of that is a long story but here's my advice - stay hydrated (above all else). If you have to sit a lot get up every 30 minutes and move for a minute or two. Consider taking 500mgs or Rutin 3 times a day and become familiar with the symptoms of DVT. If you survive and that's a big if, the aftermath is no fun.

I use testosterone to this day and don't believe it had a thing to do with my DVT/PE.

Steve

sooo if one where to take a rutin supp, which would be the best?

and

if one is on nattokinase would rutin be better? seems maybe perhaps?

very very interesting find...
 
what kind of effects do u see?

why did u start using this? did a doc recommend it or?

I started using it to help with venous insufficiency which was most likely caused by the clots I suffered from back in 2012. I did my own research. Don't know if it's helping or not. I also use the fibrin enzymes (nattokinase, lumbrokinase, serrapeptase, etc.). Thus far, there is no solid confirmation that I have a familial thrombophilia, just two episodes of unknown cause which I detailed in my original post of this thread. The only markers out of the myriad of tests I have done since 2012 showed an elevation in Factor VIII and von Willebrand, both of which can be from inflammation and are not necessarily of genetic origin since they are both acute phase reactants. Interestingly, since stopping synthetic T3, my levels have been in in normal range. Too much thyroid hormone can cause blood clots by activation of the coagulation cascade. I started T3 monotherapy in 2010. I had my first clot in 2012. There is no family history of any clotting disorders on either side of my family. For Factor VIII to considered a familial clotting disorder, the elevation has to be consistent. It will take more time and repeat testing and second and third opinions from expert hematologists to feel more confident that the increases in these markers that may have been the cause of my clots and were acute phase and not genetic. If so, then TRT would not be contraindicated. That is what I hope for.
 

J2048b

Member
I started using it to help with venous insufficiency which was most likely caused by the clots I suffered from back in 2012. I did my own research. Don't know if it's helping or not. I also use the fibrin enzymes (nattokinase, lumbrokinase, serrapeptase, etc.). Thus far, there is no solid confirmation that I have a familial thrombophilia, just two episodes of unknown cause which I detailed in my original post of this thread. The only markers out of the myriad of tests I have done since 2012 showed an elevation in Factor VIII and von Willebrand, both of which can be from inflammation and are not necessarily of genetic origin since they are both acute phase reactants. Interestingly, since stopping synthetic T3, my levels have been in in normal range. Too much thyroid hormone can cause blood clots by activation of the coagulation cascade. I started T3 monotherapy in 2010. I had my first clot in 2012. There is no family history of any clotting disorders on either side of my family. For Factor VIII to considered a familial clotting disorder, the elevation has to be consistent. It will take more time and repeat testing and second and third opinions from expert hematologists to feel more confident that the increases in these markers that may have been the cause of my clots and were acute phase and not genetic. If so, then TRT would not be contraindicated. That is what I hope for.

oh wow sorry to hear this! did u happen to get ahold of the doc in the interview DR GLUECK? he sends u a script to get everything checked, it is very indepth! ive yet to get it done as ive been taken off trt and wont know for sure if im ever going back on until after january sometime...
 

stcrim

New Member
Nattokinase as mentioned above appears to break down existing fibrin (sort of) but does no appear to prevent it. There are a lot of N=1 examples of people re-clotting on it. Based strictly on the publically available information, Rutin appears to prevent clots in both arteries and veins.

Marco - if you have markers for 2 genetic coagulation issues you should really be speaking with a qualified hematologist who can also check your T3 and RT3. If a blood clot becomes a pulmonary embolism there is only a 2 in 10 chance of surviving. The odds of surviving a heart attack are far better at 5 in 10.

I had not heard that about T3 - any chance you have a link or two that explains it? I am on NP thyroid which is the same thing as armour thyroid.

For the past 6 months I have been on Xarelto (an anti-coagulant) and may be for some time to come. Again, I don't think T had anything to do with my clot and neither do my doctors (though they really aren't qualified to make that call).
 
oh wow sorry to hear this! did u happen to get ahold of the doc in the interview DR GLUECK? he sends u a script to get everything checked, it is very indepth! ive yet to get it done as ive been taken off trt and wont know for sure if im ever going back on until after january sometime...

I communicated via email with Dr. G. extensively for several months. I already had all the tests done well before this. He believed my aforementioned markers are familial. I think the jury's still out on that, IMO. Therefore, TRT is still an option. I just need more confirmatory testing and possibly to stay on my 15mg Xarelto as a prophylactic, get regular phlebs, monitor all estrogen levels, CBC, etc.
 
Nattokinase as mentioned above appears to break down existing fibrin (sort of) but does no appear to prevent it. There are a lot of N=1 examples of people re-clotting on it. Based strictly on the publically available information, Rutin appears to prevent clots in both arteries and veins.

Marco - if you have markers for 2 genetic coagulation issues you should really be speaking with a qualified hematologist who can also check your T3 and RT3. If a blood clot becomes a pulmonary embolism there is only a 2 in 10 chance of surviving. The odds of surviving a heart attack are far better at 5 in 10.

I had not heard that about T3 - any chance you have a link or two that explains it? I am on NP thyroid which is the same thing as armour thyroid.

For the past 6 months I have been on Xarelto (an anti-coagulant) and may be for some time to come. Again, I don't think T had anything to do with my clot and neither do my doctors (though they really aren't qualified to make that call).


The FVIII (and vWF - which is essentially the same thing) that were elevated can be familial or can be acute phase reactants or both. That is why more repeat testing must be done.

Here is how dangerous elevated FVIII is (in terms of thrombosis) and too little is (in terms of hemophilia):
http://atvb.ahajournals.org/content....fullhttp://en.wikipedia.org/wiki/Factor_VIII
http://www.ncbi.nlm.nih.gov/pubmed/10669145
http://www.ncbi.nlm.nih.gov/pubmed/12567199
http://en.wikipedia.org/wiki/Factor_VIII
http://www.ncbi.nlm.nih.gov/pubmed/9184386
http://www.wisegeek.com/what-is-factor-viii.htm
http://www.jaoa.osteopathic.org/content/112/3/140.full.pdf

Although few, if any, physicians' knowledge base encompasses even a slight understanding of this link (most likely because it is limited to a minority of prone individuals), there are nonetheless several papers showing such between an excess of exogenous thyroid hormone and thrombosis. Here are most of the links to my research on how excess thyroid hormone (T3 or T4) induces a hypercoagulable state, making one prone to thrombotic events:
http://www.bloodjournal.org/content/115/22/4344.full?sso-checked=true
http://www.ncbi.nlm.nih.gov/pubmed/3659809
http://www.ncbi.nlm.nih.gov/pubmed/21249601
http://press.endocrine.org/doi/full/10.1210/jc.2007-0199
http://www.ncbi.nlm.nih.gov/pubmed/6814317
http://www.ncbi.nlm.nih.gov/pubmed/6411844
http://www.ncbi.nlm.nih.gov/pubmed/5304832
http://www.ncbi.nlm.nih.gov/pubmed/11288984
http://www.ncbi.nlm.nih.gov/pubmed/21257724
http://annals.org/article.aspx?articleid=696027
http://www.researchgate.net/publica...helium-associated_proteins_in_thyroid_disease
http://press.endocrine.org/doi/full/10.1210/jc.2007-0199

The question therefore is: what is considered excess exogenous thyroid replacement? Just because one's thyroid labs are within range doesn't mean they aren't getting too much replacement, as there could be issues such as pooling, thyroid hormone resistance, etc. Everyone is unique. When the body doesn't need something that is being forced upon it in amounts over what it produces naturally, it will react in various way. One is inflammation. FVIII is an acute phase reactant that will elevate when the individual is stressed or inflamed. Overtraining will increase FVIII levels transiently, for example. This tells us that there isn't always a genetic cause to an abnormal level.

Anecdotally, since I've reduced my overall thyroid replacement, my FVIII and vWF markers have dropped as I suspected.

Again, in my case, I have none of the other markers that are strictly familial other than MTHFR c677T +/+, but that is considered only weakly thrombogenic according to Glueck and beyond keeping one's methylation balance and homocysteine in check, there is no evidence to suggest it has any further effects on thrombosis. BTW, I check my thyroid markers every month, so I'm on top of it! Hematologists know very little about this research. Also, hyperparathyroidism can induce hypercoagulation. In July, I had a parathyroid tumor removed, so this is yet another facet of what could contribute to non-familial thrombophilia. It is unlikely that there is just one factor that contributes to this pathology, let alone any. Time will tell all. As with any pharmaceutical intervention, there is ALWAYS a risk, even with Xarelto prophylaxis, as it is so new AND there is still no commercially-available anecdote for it if you start to hemorrhage. So, unless one has documented proof of a life-threatening familial coagulation disorder (i.e. Factor 5 Leiden, etc.), to ban those of us who are full-blown hypogonadal or borderline hypogonadal from the benefits of TRT is depriving us of a quality of life.

Did your clot occur while toy were on Xarelto? What dose are you on now?
 

stcrim

New Member
Marco - I am on 20mg. Started out on 15 twice a day. Now I would very much like to move to 15 for a few months and then down to 10mg.

Am I reading correctly that Dr. G only sees testosterone as an issue for those with a genetic factor that tilts towards clotting?

If one is dehydrated that alone can predispose an individual to high clotting risk. There is at least one study that shows that staying hydrated can cut the risk of a heart attack in half. In a nutshell low blood viscosity (thinner blood) is extremely protective for both arteries and veins.

One additional risk factor I may have the fact I have been low-carb for years. There are quite a few studies that show low-carb increase the blood viscosity where true wheat free vegetarians enjoy very low viscosity.
Short history - This June on Father's Day (Sunday) I was doing sprints on steps midday with the temperature around 90 degrees. On the sixth set I passed out briefly; probably because of not eating first and dehydration. I was at a resort hotel on the Gulf Coast so plenty of people responded. Within 10 or 15 minutes of that event I was fine and went home. Spent the next few days working and sitting for long hours, something I normally do. By Wednesday my left leg started swelling quickly and was painful. I also developed a mild cough which may have been about the time the pulmonary embolism happened. By Thursday I was in the hospital. I would never have known I had a pulmonary embolism if not for the CT in the hospital.

Five days later I was discharged on Coumadin with an INR of 1.3 and self administered Lovenox. The doctor raised my Coumadin to 15mg at which point my INR jumped to 4.2. His nurse called and told me to get off Coumadin and Lovenox for the next 3 or 4 days. Within 24 hours I was in unbelievable pain.

Found a new doctor that let me start Xarelto. The pain was gone within 2 days.
 
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