I'm in my early 40s and my calcium score came back 200 with most of it in the LAD. How did this happen?

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S

Stoak

Active Member
My LDL has been relatively high for years creeping from 130-160 over the past 10 years. My natural HDL is 70-80 and when on TRT it's in the 50-60 level. My LDL basically stays flat on TRT or not. My triglycerides are always always always super low at 50 level. My ApoB recently came back at 119 which is high. I had a Lip(a) test done once and it was quite low at 8 which means I don't have this bad genetic marker.

Every year my PCP was never worried. Said I'm totally fine. This was literally happening for a decade. Then I did a consult with a bodybuilding doctor and he freaked the F out at my ApoB number and basically said I need to assume a diet of near zero saturated fat and get this number down ASAP.

This spooked me so I went to the cardiologist and told her my concerns. She dismissed the "bodybuilding doc" and said my numbers aren't really in the range to be treated but she ordered a calcium score and it would be zero she was certain. Well it came back near 200 and she started me on 10mg of Lipitor and said my LDL needs to be under 100 with this CAC risk.

I abused anabolics for 3 years about 15 years ago (best guess probably averaged 500mg weekly total androgen load for 3 years straight) then went on HRT 5 years ago. I also smoked half a pack a day for 7 years (she said that was basically nothing and wasn't a big contribution).

I'm just wondering if this sounds like any of you here bc I don't know how to continue other than listening to her. She said TRT most likely isn't contributing to my ASCVD based on the most current research but I can help but think running my free T at 30-35 for 5 years is somehow helping.

One forum guy say you'd be nuts to take statins, another guy says you would be nuts not to. I literally don't know what to believe but I'm considering just going back to low T as my best guess is my AAS use 15 years ago is the main cause (I could be wrong sure but that's what my heart of hearts tells me).

I've been fit my whole life. I resistance train 4+ days per week with multiple bouts of cardio for 25+ years straight. I do drink daily 3-4 drinks per day as measured (I can't find any real evidence that alcohol consumption causes ASCVD outside of one study done 20+ years ago.)

Just curious if any of you have a similar story. I just keep thinking I did all of this damage 15 years ago and it isn't progressing and I shouldn't start treating it but maybe I'm wrong.
 
Defy Medical TRT clinic doctor
I was 41 when I started getting pain when I bent over, which would resolve when I stood up after about a minute or so. I dismissed the doctor when he said it sounds like angina. I was fit, never smoked or drank, no steroids, no history in the family. But it didn't subside, so I had the angiogram. Afterward, the doctors came in and told me I needed an immediate bypass; my right descending artery was completely closed, and my all important left descending artery was 90% closed. They said I could die in the parking lot if I leave. I found that a little hard to believe, so I left.

For the next 15 years I had more angina than anybody could imagine. No heart attack. I took a small dose of beta blocker and nitro whenever I needed it. It was during that time that I made my fortune in life - I was busy ALL of the time.

I insisted I have the Lp(a) test, which was relatively unknown in 1997; it was very high. So at least I knew why. Statins made me feel crappy, and it made the Lp(a) worse (yep!). I found niacin around the late 90's and have been taking it since then; it addressed all my lipid concerns, and I'm certain it was a major factor in saving my life. That, and the bypass that I had at the end of the 15 year period in 2012.

Today I'm 68 and feeling good, heart disease is a worry of the past. I'm not suggesting what you should do, but if it were to happen to ME again, I wouldn't focus too much on why especially if I didn't have symptoms. I'd get the LDL down and go forward.
 
I would strongly suggest reading the book "The Clot Thickens" by Dr. Malcolm Kendrick. I'm going to post a formal book review here before too long but after reading it you will be vastly more fluent in the process of heart disease, (and LDL is a very minor player.) From what you've said, smoking and/or some sort of genetic predisposition are the most likely culprits. If TRT or AAS were the issue then we would have mechanisms and data to clearly see a signal. If the AAS or alcohol provoked prolonged high blood pressure or insulin resistance, then that could be a secondary cause. Nutrient deficiencies could also be an issue as could unresolved dental infections. Also, search for the thread here called something like "20 heart-healthy actions with better risk/reward than statins'. Bottom line is you will never know for sure and there likely are multiple causes, but you need to 1) become fluent in the topic, which the book will address, and 2) do all the little things right going forward since a lot of little things adds up to a big thing.
 
Guided_by_Voices said:
I would strongly suggest reading the book "The Clot Thickens" by Dr. Malcolm Kendrick. I'm going to post a formal book review here before too long but after reading it you will be vastly more fluent in the process of heart disease, (and LDL is a very minor player.) From what you've said, smoking and/or some sort of genetic predisposition are the most likely culprits. If TRT or AAS were the issue then we would have mechanisms and data to clearly see a signal. If the AAS or alcohol provoked prolonged high blood pressure or insulin resistance, then that could be a secondary cause. Nutrient deficiencies could also be an issue as could unresolved dental infections. Also, search for the thread here called something like "20 heart-healthy actions with better risk/reward than statins'. Bottom line is you will never know for sure and there likely are multiple causes, but you need to 1) become fluent in the topic, which the book will address, and 2) do all the little things right going forward since a lot of little things adds up to a big thing.
Click to expand...

You need to paint the full picture here!

No f**king free lunch here when it comes to abusing T/AAS for the sole purpose of muscle/strength enhancement!

*Testosterone and other androgens, mainly at supraphysiological levels, affect every single body tissue or system, including the cardiovascular system




Some key points:

* Direct actions of testosterone in the cardiovascular system involves activation of proinflammatory and redox processes, decreased nitric oxide (NO) bioavailability, and stimulation of vasoconstrictor signaling pathways.

* Testosterone at supraphysiological levels increases cardiovascular disease risk, causes myocardial infarction, stroke, high blood pressure, blood clots, and heart failure

* Testosterone affects the cardiovascular system by changing lipid profile, insulin sensitivity, hemostatic mechanisms, sympathetic nervous system, and renin angiotensin-aldosterone system

* Testosterone activates proinflammatory and redox processes, decreases nitric oxide bioavailability, and stimulates vasoconstrictor signaling pathways

* Testosterone affects the vasculature by interfering with all mechanisms that control vascular function




www.excelmale.com

High Testosterone Levels: Impact on the Heart

Abstract Testosterone, the main endogenous active androgen, is used to treat many clinical conditions, such as hypogonadism, infertility, erectile dysfunction, osteoporosis, anemia, and in transgender therapy (female-to-male transsexuals). Androgens are also used by athletes to enhance...
www.excelmale.com www.excelmale.com

Testosterone and other androgens, mainly at supraphysiological levels, affect every single body tissue or system, including the cardiovascular system. Testosterone increases cardiovascular disease risk, causes myocardial infarction, stroke, high blood pressure, blood clots, and heart failure. Among the potential mechanisms whereby testosterone affects the cardiovascular system, both indirect and direct actions have been reported. Indirect actions of testosterone on the cardiovascular system include changes in the lipid profile, insulin sensitivity, and hemostatic mechanisms, modulation of the sympathetic nervous system and renin-angiotensin-aldosterone system. Direct actions of testosterone in the cardiovascular system involves activation of proinflammatory and redox processes, decreased nitric oxide (NO) bioavailability, and stimulation of vasoconstrictor signaling pathways.

This chapter focuses on the effects of androgens, mainly testosterone, on the vascular system. The effects of testosterone on endothelial and vascular smooth muscle cells, as well as mechanisms involved in the effects of testosterone will be reviewed. Effects of testosterone on the perivascular adipose tissue, the immune, sympathetic, and renin-angiotensin systems will also be mentioned.




Key Facts of Testosterone

• Testosterone regulates many processes in the male and in the female body

• Testosterone is used in clinical conditions (testosterone replacement therapy) and also in non medical conditions

• Testosterone can carry cardiovascular effects and risks

• Testosterone affects the vasculature by directly impacting endothelial and vascular smooth cells




Summary Points

• Testosterone, the main endogenous active androgen, is used to treat many clinical conditions

• Testosterone and other androgens are also used by athletes, non athlete weightlifters or bodybuilders to enhance muscle development, strength, and performance and endurance

• Testosterone at supraphysiological levels increases cardiovascular disease risk, causes myocardial infarction, stroke, high blood pressure, blood clots, and heart failure

• Testosterone affects the cardiovascular system by changing lipid profile, insulin sensitivity, hemostatic mechanisms, sympathetic nervous system, and renin angiotensin-aldosterone system

• Testosterone activates proinflammatory and redox processes, decreases nitric oxide bioavailability, and stimulates vasoconstrictor signaling pathways

• Testosterone affects the vasculature by interfering with all mechanisms that control vascular function

• In the endothelium, testosterone modulates NO, COX-derived metabolites and EDHF release and signaling

• In VSMCs, testosterone modulates ROS generation, expression, and activity of receptors and ion channels
 
Guided_by_Voices said:
I would strongly suggest reading the book "The Clot Thickens" by Dr. Malcolm Kendrick. I'm going to post a formal book review here before too long but after reading it you will be vastly more fluent in the process of heart disease, (and LDL is a very minor player.) From what you've said, smoking and/or some sort of genetic predisposition are the most likely culprits. If TRT or AAS were the issue then we would have mechanisms and data to clearly see a signal. If the AAS or alcohol provoked prolonged high blood pressure or insulin resistance, then that could be a secondary cause. Nutrient deficiencies could also be an issue as could unresolved dental infections. Also, search for the thread here called something like "20 heart-healthy actions with better risk/reward than statins'. Bottom line is you will never know for sure and there likely are multiple causes, but you need to 1) become fluent in the topic, which the book will address, and 2) do all the little things right going forward since a lot of little things adds up to a big thing.
Click to expand...

Everyone so caught up on CAC!

Non-calcified plaque in the coronary arteries.




This needs to be stressed!

*While CAC is a well-established prognostic tool, it is not a comprehensive measure of atherosclerotic burden. Focusing solely on CAC, without also considering non-calcified plaque (NCP) in the coronary arteries, may overlook changes in other categories of plaque relevant to CVD risk. Honing into CAC alone also ignores the timeline of atherosclerosis development; CAC typically manifests in the later stages of atherogenesis. Coronary atherosclerosis initiates as fatty streaks within the arterial wall, which then develop into noncalcified plaque — composed of lipids, inflammatory cells, and fibrous tissue. Over time, these plaques evolve and undergo calcification as calcium hydroxyapatite deposits within the fibrous cap, the stabilizing layer above the plaque’s lipid core. This process signifies plaque maturation, and calcified plaques typically develop in the later stages of atherosclerosis. These calcified deposits are associated with stable coronary artery disease (CAD), and they possess a lower risk of rupture.




www.excelmale.com

Testosterone Therapy and the Risk of Cardiovascular Disease

Abstract The debate over the cardiovascular (CV) implications of testosterone therapy (TT) have resulted in diverging safety recommendations and clinical guidelines worldwide. This narrative review synthesizes and critically evaluates long-term studies examining the effects of TT within the...
www.excelmale.com www.excelmale.com

Although observational studies suggest an association between low testosterone and increased risk of CVD, results from testosterone supplementation are inconsistent. RCTs indicate that short-term TT at standard replacement is not associated with increased CVD risk. Nevertheless, the cardiovascular sub-study of T Trials observed increases in NCP and CAC, signaling the need for further investigation into potential long-term implications of TT.

*CIMT, an ultrasound measure of thickness in the carotid artery lining, is a potential marker of early atherosclerosis. Compared to ultrasound assessment of carotid plaque presence, however, CIMT is less predictive. CAC scoring, in turn, has been directly compared to CIMT and carotid plaque scoring, within several observational and prospective studies. Initial hypotheses predicted that CAC would not predict stroke as effectively as CIMT. However, despite its anatomical distance from the carotid artery bed, coronary artery calcium presence and burden are strong predictors for CVD events (including stroke and transient ischemic attack). This well-established finding is likely rooted in atherosclerosis being a systemic process. CAC presence and CAC score, in fact, are both superior to CIMT for predicting CV events.


Although observational studies suggest an association between low testosterone and increased risk of CVD, results from testosterone supplementation are inconsistent. RCTs indicate that short-term TT at standard replacement is not associated with increased CVD risk. Nevertheless, the cardiovascular sub-study of T Trials observed increases in NCP and CAC, signaling the need for further investigation into potential long-term implications of TT.

*CIMT, an ultrasound measure of thickness in the carotid artery lining, is a potential marker of early atherosclerosis. Compared to ultrasound assessment of carotid plaque presence, however, CIMT is less predictive. CAC scoring, in turn, has been directly compared to CIMT and carotid plaque scoring, within several observational and prospective studies. Initial hypotheses predicted that CAC would not predict stroke as effectively as CIMT. However, despite its anatomical distance from the carotid artery bed, coronary artery calcium presence and burden are strong predictors for CVD events (including stroke and transient ischemic attack). This well-established finding is likely rooted in atherosclerosis being a systemic process. CAC presence and CAC score, in fact, are both superior to CIMT for predicting CV events.

*While CAC is a well-established prognostic tool, it is not a comprehensive measure of atherosclerotic burden. Focusing solely on CAC, without also considering non-calcified plaque (NCP) in the coronary arteries, may overlook changes in other categories of plaque relevant to CVD risk. Honing into CAC alone also ignores the timeline of atherosclerosis development; CAC typically manifests in the later stages of atherogenesis. Coronary atherosclerosis initiates as fatty streaks within the arterial wall, which then develop into noncalcified plaque — composed of lipids, inflammatory cells, and fibrous tissue. Over time, these plaques evolve and undergo calcification as calcium hydroxyapatite deposits within the fibrous cap, the stabilizing layer above the plaque’s lipid core. This process signifies plaque maturation, and calcified plaques typically develop in the later stages of atherosclerosis. These calcified deposits are associated with stable coronary artery disease (CAD), and they possess a lower risk of rupture.
 
Stoak said:
My LDL has been relatively high for years creeping from 130-160 over the past 10 years. My natural HDL is 70-80 and when on TRT it's in the 50-60 level. My LDL basically stays flat on TRT or not. My triglycerides are always always always super low at 50 level. My ApoB recently came back at 119 which is high. I had a Lip(a) test done once and it was quite low at 8 which means I don't have this bad genetic marker.

Every year my PCP was never worried. Said I'm totally fine. This was literally happening for a decade. Then I did a consult with a bodybuilding doctor and he freaked the F out at my ApoB number and basically said I need to assume a diet of near zero saturated fat and get this number down ASAP.

This spooked me so I went to the cardiologist and told her my concerns. She dismissed the "bodybuilding doc" and said my numbers aren't really in the range to be treated but she ordered a calcium score and it would be zero she was certain. Well it came back near 200 and she started me on 10mg of Lipitor and said my LDL needs to be under 100 with this CAC risk.

I abused anabolics for 3 years about 15 years ago (best guess probably averaged 500mg weekly total androgen load for 3 years straight) then went on HRT 5 years ago. I also smoked half a pack a day for 7 years (she said that was basically nothing and wasn't a big contribution).

I'm just wondering if this sounds like any of you here bc I don't know how to continue other than listening to her. She said TRT most likely isn't contributing to my ASCVD based on the most current research but I can help but think running my free T at 30-35 for 5 years is somehow helping.

One forum guy say you'd be nuts to take statins, another guy says you would be nuts not to. I literally don't know what to believe but I'm considering just going back to low T as my best guess is my AAS use 15 years ago is the main cause (I could be wrong sure but that's what my heart of hearts tells me).

I've been fit my whole life. I resistance train 4+ days per week with multiple bouts of cardio for 25+ years straight. I do drink daily 3-4 drinks per day as measured (I can't find any real evidence that alcohol consumption causes ASCVD outside of one study done 20+ years ago.)

Just curious if any of you have a similar story. I just keep thinking I did all of this damage 15 years ago and it isn't progressing and I shouldn't start treating it but maybe I'm wrong.
Click to expand...
First thing you have to do is just relax. That score is actually last year's score. It takes one year for soft plaque to calcify. And you must have calcified plaque to measure it. Now you must slow your score down to 10% or less a year. So you never have a stroke or heart attack. Your arteries will adjust and open up if you slow down your growth. I wonder what your APO-E is.
 
Guided_by_Voices said:
I would strongly suggest reading the book "The Clot Thickens" by Dr. Malcolm Kendrick. I'm going to post a formal book review here before too long but after reading it you will be vastly more fluent in the process of heart disease, (and LDL is a very minor player.) From what you've said, smoking and/or some sort of genetic predisposition are the most likely culprits. If TRT or AAS were the issue then we would have mechanisms and data to clearly see a signal. If the AAS or alcohol provoked prolonged high blood pressure or insulin resistance, then that could be a secondary cause. Nutrient deficiencies could also be an issue as could unresolved dental infections. Also, search for the thread here called something like "20 heart-healthy actions with better risk/reward than statins'. Bottom line is you will never know for sure and there likely are multiple causes, but you need to 1) become fluent in the topic, which the book will address, and 2) do all the little things right going forward since a lot of little things adds up to a big thing.
Click to expand...

I simply don't understand how LDL can be a very minor cause when the entire goal of mainstream cardiology is to lower LDL when evidence of ASCVD is present. I don't believe everything is some sort of conspiracy theory.
 
Stoak said:
I simply don't understand how LDL can be a very minor cause when the entire goal of mainstream cardiology is to lower LDL when evidence of ASCVD is present. I don't believe everything is some sort of conspiracy theory.
Click to expand...
Then read the book!!!! There is no substitute for becoming literate on the details. CVD is a combination of 1) damage to the glycocalyx and endothelium, 2) excess blood clotting to repair the damage, and 3) inadequate removal/reabsorption of the repair (plaques). If lowering LDL reduced these risks then we would see dramatically improved outcomes from the use of statins, however the observed outcomes are barely detectable as measured by all-cause mortality, and any benefits may be due to other mechanisms beyond LDL such as anti-inflammatory properties. Further, the damage from statins has never been well-quantified since most adverse events are never attributed to the statin or reported. You need to be focused on the things that will really move the needle. For example, do you avoid fried foods? If not, then that has to be fixed immediately and will give nothing but benefit.
 
madman said:
You need to paint the full picture here!

No f**king free lunch here when it comes to abusing T/AAS for the sole purpose of muscle/strength enhancement!

*Testosterone and other androgens, mainly at supraphysiological levels, affect every single body tissue or system, including the cardiovascular system




Some key points:

* Direct actions of testosterone in the cardiovascular system involves activation of proinflammatory and redox processes, decreased nitric oxide (NO) bioavailability, and stimulation of vasoconstrictor signaling pathways.

* Testosterone at supraphysiological levels increases cardiovascular disease risk, causes myocardial infarction, stroke, high blood pressure, blood clots, and heart failure

* Testosterone affects the cardiovascular system by changing lipid profile, insulin sensitivity, hemostatic mechanisms, sympathetic nervous system, and renin angiotensin-aldosterone system

* Testosterone activates proinflammatory and redox processes, decreases nitric oxide bioavailability, and stimulates vasoconstrictor signaling pathways

* Testosterone affects the vasculature by interfering with all mechanisms that control vascular function




www.excelmale.com

High Testosterone Levels: Impact on the Heart

Abstract Testosterone, the main endogenous active androgen, is used to treat many clinical conditions, such as hypogonadism, infertility, erectile dysfunction, osteoporosis, anemia, and in transgender therapy (female-to-male transsexuals). Androgens are also used by athletes to enhance...
www.excelmale.com www.excelmale.com

Testosterone and other androgens, mainly at supraphysiological levels, affect every single body tissue or system, including the cardiovascular system. Testosterone increases cardiovascular disease risk, causes myocardial infarction, stroke, high blood pressure, blood clots, and heart failure. Among the potential mechanisms whereby testosterone affects the cardiovascular system, both indirect and direct actions have been reported. Indirect actions of testosterone on the cardiovascular system include changes in the lipid profile, insulin sensitivity, and hemostatic mechanisms, modulation of the sympathetic nervous system and renin-angiotensin-aldosterone system. Direct actions of testosterone in the cardiovascular system involves activation of proinflammatory and redox processes, decreased nitric oxide (NO) bioavailability, and stimulation of vasoconstrictor signaling pathways.

This chapter focuses on the effects of androgens, mainly testosterone, on the vascular system. The effects of testosterone on endothelial and vascular smooth muscle cells, as well as mechanisms involved in the effects of testosterone will be reviewed. Effects of testosterone on the perivascular adipose tissue, the immune, sympathetic, and renin-angiotensin systems will also be mentioned.




Key Facts of Testosterone

• Testosterone regulates many processes in the male and in the female body

• Testosterone is used in clinical conditions (testosterone replacement therapy) and also in non medical conditions

• Testosterone can carry cardiovascular effects and risks

• Testosterone affects the vasculature by directly impacting endothelial and vascular smooth cells




Summary Points

• Testosterone, the main endogenous active androgen, is used to treat many clinical conditions

• Testosterone and other androgens are also used by athletes, non athlete weightlifters or bodybuilders to enhance muscle development, strength, and performance and endurance

• Testosterone at supraphysiological levels increases cardiovascular disease risk, causes myocardial infarction, stroke, high blood pressure, blood clots, and heart failure

• Testosterone affects the cardiovascular system by changing lipid profile, insulin sensitivity, hemostatic mechanisms, sympathetic nervous system, and renin angiotensin-aldosterone system

• Testosterone activates proinflammatory and redox processes, decreases nitric oxide bioavailability, and stimulates vasoconstrictor signaling pathways

• Testosterone affects the vasculature by interfering with all mechanisms that control vascular function

• In the endothelium, testosterone modulates NO, COX-derived metabolites and EDHF release and signaling

• In VSMCs, testosterone modulates ROS generation, expression, and activity of receptors and ion channels
Click to expand...
I agree that 500mg of androgens per week is likely a net negative (although how much an active lifestyle counters this is worthy of discussion.) However, singling out that one thing does not seem valid in comparison to other potential contributors. Further, it's not really relevant now and could distract from acting on all the things which can be done to improve OP's health trajectory (which is yet another problem with statins since they give a false sense of comfort and distract from much more impactful interventions.)
 
Guided_by_Voices said:
I agree that 500mg of androgens per week is likely a net negative (although how much an active lifestyle counters this is worthy of discussion.) However, singling out that one thing does not seem valid in comparison to other potential contributors. Further, it's not really relevant now and could distract from acting on all the things which can be done to improve OP's health trajectory (which is yet another problem with statins since they give a false sense of comfort and distract from much more impactful interventions.)
Click to expand...

Yes but it still needs to be stressed here!
 
Two additional thoughts...

Dr. Gundry mentioned in one of his books/podcasts that there are actually long-lived, healthy people who smoke, however they also live in areas where their diet is very high in Vitamin C. The mechanism is apparently that smoking causes very high oxidative stress which in turn depletes Vitamin C, so most people who smoke are very low in Vitamin C which causes other problems such as poor blood vessel integrity. My point is that Vitamin C is way more important than most people give it credit for.

Also, while I don't agree with the recent attacks on alcohol (see Chris Masterjohn's discussion on the topic), 3-4 drinks per day sounds like a lot. If that was causing poor sleep architecture and/or reduced thyroid function for example, those could cause CVD issues. That much would absolutely damage my conditioning and workouts.
 
If you go down the Heart Disease Rabbit Hole, it may be a long time before you come out, and chances are you won't emerge any smarter than when you went in. Books? I've read more than my share in the last 30 years on heart disease, and most made very good arguments that the layperson couldn't dispute one way or another (so then what do you do?).

You should be grateful that you don't have any heart symptoms. If it was me, I'd focus more on where I'm going vs. where I've been. I'd clean up my act, take a small dose of statin (as insurance and as directed by your cardiologist) and move on . . .
 
Melody68 said:
If you go down the Heart Disease Rabbit Hole, it may be a long time before you come out, and chances are you won't emerge any smarter than when you went in. Books? I've read more than my share in the last 30 years on heart disease, and most made very good arguments that the layperson couldn't dispute one way or another (so then what do you do?).

You should be grateful that you don't have any heart symptoms. If it was me, I'd focus more on where I'm going vs. where I've been. I'd clean up my act, take a small dose of statin (as insurance and as directed by your cardiologist) and move on . . .
Click to expand...

Agreed. If it was as simple as just reading a book every would be solved and it isn't. Modern cutting edge steroid abusers are now crushing their LDLs and ApoB to sub 50 with low dose crestor and Zetia. Perhaps they are correct that it enables them to abuse much more safely. Nobody can really tell me why we need an LDL or ApoB of 50+ other than weird tik tok interviews where vagaries like "the brain" or "the body creates it so how can it hurt us?" ...that's a great one lol. If sub 50 ApoB literally crushes your risk to near zero I cannot understand why everyone isn't doing this if they can tolerate the medicines needed.

I am going to get a second opinion as I sometimes feel like the doctors look AT me instead of listening TO me. I have heard stories of former AAS abusers needing stents prior to 40. I walk in at 43 looking like I'm in my late 20s and incredibly fit and they just assume I'm "fine" and don't listen to my history of AAS abuse, large amounts of historical animal protein consumption etc. It's very difficult IMO to get a doctor to see that problems can be inside of they don't appear outside.
 
@Stoak

Diagnosis:
What was your diet 15 years ago in terms of carbs, sugars, and junk food? Smoking half a pack a day for 7 years is not "nothing". Nicotine is well known to damage blood vessels.

Treatment:
Why is your current LDL high? Are you on a meat heavy diet?
 
Stoak said:
I am going to get a second opinion as I sometimes feel like the doctors look AT me instead of listening TO me.
Click to expand...
If your medical problem isn't in your doctors top ten greatest hits, common medical diagnosis, your experience will be a negative one. He hears you but doesn't know what's causing your issues and you'll know it when he has nothing to say about it.
 
Guided_by_Voices said:
I would strongly suggest reading the book "The Clot Thickens" by Dr. Malcolm Kendrick.
Click to expand...
Wow this is a good book so far! I'm about one third through. Thank you for the recommendation.

I'm in kind of a similar boat as Stoak, with an 18.9 calcium score at age 44, which puts me in the 78th percentile. Of course, my PCP says that's great and didn't recommend I do anything about it.

I had a calcium score done at age 40 and my score was a 3 then, which I thought was great, because it was so close to zero. Now I understand that it should have been zero, and there is a big difference between a little and none. My score then also put me around the 75-80th percentile, so my lifestyle over the intervening years has apparently not done anything positive or negative to influence progression beyond what is typical.

This has led me to start intensely researching CVD. I think regardless of what camp you end up in with regard to your beliefs around cholesterol, you should measure the impact of your interventions with everything available, including carotid IMT, calcium scans, coronary angiograms, etc. Year over year changes in markers of actual plaque will be the most useful way to determine whether you are on the right path.

P.S. don't inhibit aromatase
 
Beyond Testosterone Book by Nelson Vergel
Guided_by_Voices said:
If lowering LDL reduced these risks then we would see dramatically improved outcomes from the use of statins, however the observed outcomes are barely detectable as measured by all-cause mortality, and any benefits may be due to other mechanisms beyond LDL such as anti-inflammatory properties.
Click to expand...
Yes, I think this is the clearest evidence that there is more to the story than cholesterol. On the same theme, with the PSCK9 inhibitors, researchers are debating whether there is a small reduction or an increase in mortality associated with these drugs which obliterate LDL levels. There would be obvious, massive reductions in mortality rates using PSCK9 drugs if the cholesterol hypothesis was entirely accurate.

www.tctmd.com

Study Alleges Mortality Miscount in FOURIER Trial; TIMI Group Disagrees

Clinical trialists, including Marc Sabatine, as well as evolocumab’s manufacturer reject the reanalysis as flawed and sensationalistic.
www.tctmd.com www.tctmd.com

Also, tadalafil. Tadalafil is being found to reduce CVD events and mortality far better than statins, despite having no effect on cholesterol: Long-term effects of phosphodiesterase-5 inhibitors on cardiovascular outcomes and death: a systematic review and meta-analysis - PubMed
 
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