Statin Wars?

[f35phixer]

Aside from the muscle pain what about the increase in diabetes and dementia? My uncle’s memory took a big dive when he went on them and improved when he got off.

This happened to me TOO. I got silly stupid, i have dementia in my family history, was worried, when through a battery of tests and scans... Nothing obvious, went off meds for 6months and wasn't stupid anymore.... I am now back on something and so far so good. The med i was on was Pravastain.

 

[Teacher Terry]

I don’t think we all will react the same way and he has been dead for 20 years. When that happened to him it made my mom determined not to take them. Interesting that I find my HBP medication will work for a number of years and then all of a sudden they stop. Luckily I get a headache when that happens. It used to happen to my mom also. In the 15 years I have been taking them I am on my 4th set of medications. I think our body chemistry is unique so difficult to know how a individual will react to a drug.

 

[youbet]

This happened to me TOO. I got silly stupid, i have dementia in my family history, was worried, when through a battery of tests and scans... Nothing obvious, went off meds for 6months and wasn't stupid anymore.... I am now back on something and so far so good. The med i was on was Pravastain.

I'm curious f35phixer, why did you go "back on something?" It sounds like there was some benefit to taking a statin you perceived and you worked with your doc to find one that minimized side effects. I don't want to put words in your mouth, but was that it?

 

[Scratchy]

Statins have a long list of potentially very serious side effects, as you probably know (including muscle tissue damage, diabetes, and even cancer). I just read the other day that almost half of all patients who start taking statins quit taking them within the first year or so, mainly due to muscle pain (that is one reason you don't see too many studies on the long-term effects of statins.......many statin users drop out of those studies early due to statin side effects). The only potentially serious side effect with aspirin is a small risk of GI bleeding. I don't want to minimize that risk, as it can be serious, but a relatively small number of people taking the low-dose aspirin experience any GI bleeding.


I would personally take a daily low-dose aspirin (which, by the way, has been shown to reduce the risk of colon cancer, also) before I ever took a statin drug. But again, that's my decision based on the research I have done........YMMV.

Anyone who is getting the impression that low dose aspirin is a better way to prevent CVD than statins should consider the following:

Studies released in 2018 have shown that older adults (whites 70 and older and blacks/hispanics 65 and older) do not have cardiovascular benefit from low dose aspirin, and in fact they have an increased risk of bleeding, not only in the GI tract, but also in the brain. For this reason, the current AHA/ACC Guidelines have significantly limited who they recommend aspirin for:

"For decades, low-dose aspirin (75-100 mg with US 81 mg/day) has been widely administered for ASCVD prevention. By irreversibly inhibiting platelet function, aspirin reduces risk of atherothrombosis but at the risk of bleeding, particularly in the gastrointestinal (GI) tract. Aspirin is well established for secondary prevention of ASCVD and is widely recommended for this indication, but recent studies have shown that in the modern era, aspirin should not be used in the routine primary prevention of ASCVD due to lack of net benefit. Most important is to avoid aspirin in persons with increased risk of bleeding including a history of GI bleeding or peptic ulcer disease, bleeding from other sites, age >70 years, thrombocytopenia, coagulopathy, chronic kidney disease, and concurrent use of nonsteroidal anti-inflammatory drugs, steroids, and anticoagulants. The following are recommendations based on meta-analysis and three recent trials:
Low-dose aspirin might be considered for primary prevention of ASCVD in select higher ASCVD adults aged 40-70 years who are not at increased bleeding risk.
Low-dose aspirin should not be administered on a routine basis for primary prevention of ASCVD among adults >70 years.
Low-dose aspirin should not be administered for primary prevention among adults at any age who are at increased bleeding risk."

The latest studies also have not shown a reduction in cancer deaths from low dose aspirin, in fact they have shown a surprising increase in cancer deaths.

Here is a link to the larger article:

https://www.acc.org/latest-in-cardi...guideline-on-primary-prevention-gl-prevention

Of note, AHA/ACC Guidelines recommend statins for prevention of CVD in much larger groups of patients than they recommend low dose aspirin.

I hope anyone considering whether or not to take aspirin (and statins) for CVD prevention makes their decision based on consultation with their doctor, making sure that the doctor is considering the current ACC/AHA Guidelines as unfortunately some doctors are slow to incorporate new information into their practice.

 

[youbet]

I don’t think we all will react the same way and he has been dead for 20 years. When that happened to him it made my mom determined not to take them. Interesting that I find my HBP medication will work for a number of years and then all of a sudden they stop. Luckily I get a headache when that happens. It used to happen to my mom also. In the 15 years I have been taking them I am on my 4th set of medications. I think our body chemistry is unique so difficult to know how a individual will react to a drug.

Sorry for your loss. Given his distant passing, I guess we won't know (and it wouldn't mean much even if we did I guess) how much of what statin he was taking and for how long and why.

Regarding your HBP....... I've lost 70 lbs over the past couple of years and also began a mild exercise regime. The benefit has been a significant reduction in my BP and my doc has taken me off all my HBP meds. If your current personal situation might call for some weight loss and exercise increase, I highly recommend it (with your doc's approval of course).

 

[razztazz]

Originally Posted by RAE View Post
Statins have a long list of potentially very serious side effects, as you probably know

RAE, where are you reading that?

I got my list from reading the package insert, although it did not list the one about dementia at the time.

And real-life. Many of them happened to me. The assertion: "The chances of an adverse reaction is very small" means the following:

1) Those small chances are 100% for somebody. That's how those stats actually work.

2) The dr is willing to roll the dice and wants you to do the same.

3) The probability of something happening is not as important as it's effects in the event is does happen. And this is no Black Swan. It's a "Known unkown."

Think about it. They want you to take chemicals every day for the last 20-50 yrs of your life for a potential disease or event which , in your case, they cannot predict. It's all aggregate data and you are literally being downgraded from life form to statistic so you'll fit in.

And they tell you that taking this chemical for 50 yrs is safe! But eggs cause heart attacks. Safer than possibly some day 10-20-30-40 yrs from having a heart attack . Muscle pain, dizziness, brown urine... Hey man it's safe. You have to keep taking it for 50 yrs

So then they say go to Walmart and eat coQ10 pills for the muscle pain. Tell the dr you're curing your other ailments
at the Walmart pill aisle and see what he/she says

They seem to want to prevent everything and eliminate all possible risk. Not possible no matter how clever you are at measuring these things. Except the risk of unfortunate sequelae. That's a risk we've got to accept at all costs.

 

[Teacher Terry]

All I remember is that his cholesterol was high and my mom lowered hers with diet. Most everyone on my mom’s side of the family get HBP by 31 despite being fit and active. At 50 I developed HBP and a extremely fast erratic heart rate despite walking 6-8 miles daily, not being overweight and hiking in the mountains on the weekends. After many tests they have no clue why the issue with my heart rate. He said it was a miracle I hadn’t had a stroke and I also had asthma.

 

[Scratchy]

Aside from the muscle pain what about the increase in diabetes and dementia? My uncle’s memory took a big dive when he went on them and improved when he got off.

TT, I have noticed quite a number of posts where you report a friend, relative, etc that had harmful side effects from a medication. I am assuming that you report these events with the purpose of influencing the decision process of readers here considering whether to take these medications, but please correct me if I'm wrong about that.

At the risk of stating the obvious, the safety and efficacy of a drug is best evaluated in a controlled study preferably with thousands of data points. It is these types of studies that are conducted before a drug is approved and that bodies like the AHA, ACC and US Preventative Services Task Force evaluate before writing Guidelines/recommendations. This is not to say all approved drugs are safe, or that some may be removed from the market due to newly evident side effects.
But an anecdotal report in a forum about someone's uncle's memory is not a data point that should be considered, in my opinion.

 

[Scratchy]

Statins have a long list of potentially very serious side effects, as you probably know (including muscle tissue damage, diabetes, and even cancer). I just read the other day that almost half of all patients who start taking statins quit taking them within the first year or so, mainly due to muscle pain

RAE, where are you reading that?

I got my list from reading the package insert, although it did not list the one about dementia at the time.

My question "where are you reading that" related to the statement

"I just read the other day that almost half of all patients who start taking statins quit taking them within the first year or so, mainly due to muscle pain"

I was not asking about the list of side effects.

 

[Teacher Terry]

Scratchy, I have a PHD so know how studies are conducted. I Never try to influence anyone. I do discuss personal stories as they are important to me. Seeing things happen to people I know are something I take into consideration for myself. My very best friend is on a statin and I would never try to influence her not to take it. I firmly believe that we all should make our own decisions on our health because we are the only ones that have to live with the consequences.

 

[Scratchy]

I Never try to influence anyone.

TT, I do appreciate many of your heartfelt and interesting posts but I'd like to say also that in my opinion there is a strong possibility that your anecdotes about friends and relatives harmed by statins may indeed influence other readers, due to their sheer number, even if that was not your intention.

 

[Teacher Terry]

I actually convinced my husband to go on a statin when his cholesterol was 260. It didn’t go well. I had a neurologist tell me I should be on one yet my primary is fine with my numbers and ratio. When I retired and went back to visit people told me there were 3 things they missed about me: my laugh, positive attitude and my stories about different things. So don’t know that I could stop now). Even if I was a doctor I wouldn’t try to convince others on a message board to do anything. Even a doctor doesn’t live with the consequences of his patients and there’s a reason it’s
called a practice because it’s constantly changing. My primary spends much of her free time keeping up on advances in the field.

 

[RAE]

This study you quote is from 2003! In evaluating cost effectiveness, the benefit and cost of each therapy is compared. There is an enormous amount of new data on the benefits of these drugs, and the costs are also different (statins are now much cheaper). So this study's findings are completely outdated.

Well, Scratchy, we could go back and forth for a long time, each citing studies to support what we believe. I'm not sure that is going to very useful at this point. I will say, that, if you want to talk about what is "outdated", we can talk about the diet/heart hypothesis, which was actually first proposed (as a cause for CHD) decades ago, using data from the 1950s/60s (Ancel Keys, past head of the Dept. of Hygiene at Minnesota University, conducted many of these early studies). The current treatment guidelines (for statin use) may have been slightly revised over the years, but ultimately they are still based on that hypothesis - which in the view of many cardiologists and medical researchers, is fatally flawed.

Here is a link to a paper from 2014, which is lengthy, but worth reading if you want to understand the history of how the diet/heart hypothesis came to be, and why it likely to be all wrong.

https://pdfs.semanticscholar.org/21f1/b42a2504ce77b8df9176097a719abe3e8c99.pdf

Here is the abstract from the paper:

Abstract
The lipid hypothesis of coronary heart disease proposes that a high total cholesterol level has a causative role in coronary heart disease (CHD), specifically in the development of atherosclerosis. It forms the basis for formulating target levels of serum cholesterol and hence the widespread use of statins for lowering cholesterol. An extension of the lipid hypothesis is the diet/heart hypothesis of coronary heart disease. This theory combines two ideas—that saturated fat raises cholesterol levels, and that a reduced saturated fat intake will lower cholesterol levels, thereby inhibiting the development of atherosclerosis and manifestations of CHD. Those who make diet recommenda- tions or prescribe medication to reduce cholesterol may be unaware of the underpinning science. The original research behind these recommendations has given us “healthy heart” guidelines and preventive measures we assume to be true. While the lipid and diet/heart hypotheses are often presented as fact, they remain inadequately proven theories that have little agreement from ex- perts. Historical perspectives can help us understand the basis of current-day beliefs. In the lipid hypothesis case, research from the 1950s and 60s was instrumental in its formation. This early work should not be considered irrelevant, outdated or obsolete because current recommenda- tions from national heart associations in many countries continue to be shaped by these studies.This paper examines evidence used to formulate the lipid hypothesis and, subsequently, the diet/heart hypothesis. By critically evaluating steps in the formation of the theory, inconsistencies,mistakes and alternate explanations become apparent and cast doubt on its validity.


And here is one particularly interesting quote from the paper, talking about the Framingham Study, another old study from the 1940s/50s, on the supposed link between total cholesterol and CHD:


"In an overview of the history of the Framingham study, G. Oppenheimer comments, “The language of risk, specifically, the probability of developing CHD...permeated early Framingham publications” [79]. “In their 1957 report, Dawber and co-authors used the term ‘risk’ at least 18 times, generally to mean ‘probability’, as in ‘there is an increased risk of [CHD] in persons with elevated cholesterol’.” According to Oppenheimer, over the next couple of years Framingham authors referred to hypercholesterolemia as a “factor” possibly associated with the development of CHD and in a 1961 publication as a “factor of risk”, contracted in the same article to “risk factor”. This was apparently done without much thought. “Kannel, the lead author, claims to have soon forgot- ten that they had coined the term, or at least first applied it to epidemiology.” However, the legacy of this word choice may have had important consequences in influencing perception of the role of TC in the aetiology of CHD. As Oppenheimer states, “the very ambiguity of ‘risk factor’, resonating ‘cause’ while denoting ‘correlation’, gave it added imaginative power.” He adds that even though the cause of CHD was unknown and that epidemiological “links” were correlations only, “This did not prevent ‘risk factors’ from being known as causal agents” [79]. In 1962, not long after the associations were first reported and one year after the term “risk factor” was intro- duced by Framingham authors, these same researchers were suggesting therapeutic interventions to reduce blood pressure, weight and dietary fats [80]. Likewise, in 1964 a committee of the Surgeon General’s Office in the US J. Elliott1899“...called for action against CHD risk factors despite the lack of demonstrated causal association” [81]. It is a pity that instead of following an early path of supposed causation, researchers at Framingham and elsewhere did not ask the simple question, “What else may explain the association between higher TC and CHD?” One possi- bility is that a higher TC level may be a marker for a metabolic abnormality or a disease state that is causative."


If you read and understand the history, you will begin to understand why the whole diet/heart hypothesis is flawed, and why we really need to start thinking about CHD in very different terms. As I mentioned in an earlier post, CHD may actually have its roots in insulin resistance and inflammation, as supported by many recent studies.

 

[RAE]

My question "where are you reading that" related to the statement

"I just read the other day that almost half of all patients who start taking statins quit taking them within the first year or so, mainly due to muscle pain"

In this paper: (the whole paper is worth reading, but here is the pertinent quote):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4513492/

"In the largest statin survey ever conducted, the National Lipid Association observed that roughly 30% of statin patients reported experiencing muscle pain and weakness and 57% of surveyed patients reported stopping the drug due to side effects[37]"

 

[Scratchy]

Well, Scratchy, we could go back and forth for a long time, each citing studies to support what we believe. I'm not sure that is going to very useful at this point. I will say, that, if you want to talk about what is "outdated", we can talk about the diet/heart hypothesis, which was actually first proposed (as a cause for CHD) decades ago, using data from the 1950s/60s (Ancel Keys, past head of the Dept. of Hygiene at Minnesota University, conducted many of these early studies). The current treatment guidelines (for statin use) may have been slightly revised over the years, but ultimately they are still based on that hypothesis - which in the view of many cardiologists and medical researchers, is fatally flawed.

Here is a link to a paper from 2014, which is lengthy, but worth reading if you want to understand the history of how the diet/heart hypothesis came to be, and why it likely to be all wrong.

https://pdfs.semanticscholar.org/21f1/b42a2504ce77b8df9176097a719abe3e8c99.pdf

Here is the abstract from the paper:

Abstract
The lipid hypothesis of coronary heart disease proposes that a high total cholesterol level has a causative role in coronary heart disease (CHD), specifically in the development of atherosclerosis. It forms the basis for formulating target levels of serum cholesterol and hence the widespread use of statins for lowering cholesterol. An extension of the lipid hypothesis is the diet/heart hypothesis of coronary heart disease. This theory combines two ideas—that saturated fat raises cholesterol levels, and that a reduced saturated fat intake will lower cholesterol levels, thereby inhibiting the development of atherosclerosis and manifestations of CHD. Those who make diet recommenda- tions or prescribe medication to reduce cholesterol may be unaware of the underpinning science. The original research behind these recommendations has given us “healthy heart” guidelines and preventive measures we assume to be true. While the lipid and diet/heart hypotheses are often presented as fact, they remain inadequately proven theories that have little agreement from ex- perts. Historical perspectives can help us understand the basis of current-day beliefs. In the lipid hypothesis case, research from the 1950s and 60s was instrumental in its formation. This early work should not be considered irrelevant, outdated or obsolete because current recommenda- tions from national heart associations in many countries continue to be shaped by these studies.This paper examines evidence used to formulate the lipid hypothesis and, subsequently, the diet/heart hypothesis. By critically evaluating steps in the formation of the theory, inconsistencies,mistakes and alternate explanations become apparent and cast doubt on its validity.


And here is one particularly interesting quote from the paper, talking about the Framingham Study, another old study from the 1940s/50s, on the supposed link between total cholesterol and CHD:


"In an overview of the history of the Framingham study, G. Oppenheimer comments, “The language of risk, specifically, the probability of developing CHD...permeated early Framingham publications” [79]. “In their 1957 report, Dawber and co-authors used the term ‘risk’ at least 18 times, generally to mean ‘probability’, as in ‘there is an increased risk of [CHD] in persons with elevated cholesterol’.” According to Oppenheimer, over the next couple of years Framingham authors referred to hypercholesterolemia as a “factor” possibly associated with the development of CHD and in a 1961 publication as a “factor of risk”, contracted in the same article to “risk factor”. This was apparently done without much thought. “Kannel, the lead author, claims to have soon forgot- ten that they had coined the term, or at least first applied it to epidemiology.” However, the legacy of this word choice may have had important consequences in influencing perception of the role of TC in the aetiology of CHD. As Oppenheimer states, “the very ambiguity of ‘risk factor’, resonating ‘cause’ while denoting ‘correlation’, gave it added imaginative power.” He adds that even though the cause of CHD was unknown and that epidemiological “links” were correlations only, “This did not prevent ‘risk factors’ from being known as causal agents” [79]. In 1962, not long after the associations were first reported and one year after the term “risk factor” was intro- duced by Framingham authors, these same researchers were suggesting therapeutic interventions to reduce blood pressure, weight and dietary fats [80]. Likewise, in 1964 a committee of the Surgeon General’s Office in the US J. Elliott1899“...called for action against CHD risk factors despite the lack of demonstrated causal association” [81]. It is a pity that instead of following an early path of supposed causation, researchers at Framingham and elsewhere did not ask the simple question, “What else may explain the association between higher TC and CHD?” One possi- bility is that a higher TC level may be a marker for a metabolic abnormality or a disease state that is causative."


If you read and understand the history, you will begin to understand why the whole diet/heart hypothesis is flawed, and why we really need to start thinking about CHD in very different terms. As I mentioned in an earlier post, CHD may actually have its roots in insulin resistance and inflammation, as supported by many recent studies.

RAE, the diet/heart hypothesis, whether flawed or not, does not appear particularly relevant to whether statins are efficacious for primary prevention of CVD.

 

[Scratchy]

In this paper: (the whole paper is worth reading, but here is the pertinent quote):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4513492/

"In the largest statin survey ever conducted, the National Lipid Association observed that roughly 30% of statin patients reported experiencing muscle pain and weakness and 57% of surveyed patients reported stopping the drug due to side effects[37]"

This article is from the World Journal of Cardiology, established less than 10 years ago by Baishideng Publishing Group. Editor in Chief is an associate professor at University of Bari.

I am unconvinced and believe the figure of 5 % to 10 % experiencing symptoms with a subset of those needing to discontinure statins is more realistic.

 

[Scratchy]

When I retired and went back to visit people told me there were 3 things they missed about me: my laugh, positive attitude and my stories about different things. So don’t know that I could stop now).

TT I do see those good qualities in many of your posts.

Even if I was a doctor I wouldn’t try to convince others on a message board to do anything.

Honestly, this has sparked an "AHA" moment for me. I am a physician, and I have tried to be careful to limit what I write here to directing people to sources of information that I consider more reliable and making medical decisions under the guidance of their physician. But if I am honest with myself, the purpose of my posts on this topic of statins is to convince people of something-i.e. not to believe the large amount of information written here which I consider to be outdated or erroneous on the topic of statin use.

It's clearly time for me to reconsider the wisdom of doing so, as I think all the other health care practitioners who from time to time jump into this fray have done. First, it is low yield. The anti-statin posts will continue and perhaps even be invigorated by any response. Second, if I say that forums are not the place to obtain medical advice it is hypocritical of me to participate in any way. I recognize it is not my job to correct medical information I believe to be wrong that is written here. (Probably a little later than was wise!)

One more time: the best guidance, in my opinion, you can get on statins is from a doctor who has incorporated the current AHA/ACC Guidelines into his/her practice. I have nothing, and will not, say any more on this here.

I have meant no disrespect in my posts on this topic to any other forum members. I want to specifically mention RAE who I have debated with a few times this morning but who I respect as someone very intelligent and admirably committed to diligently researching this and other medical topics of interest.

I still look forward to continuing to participate in this forum on non-statin threads.

 

[aja8888]

Sounds like from reading above, I should get off 81 mg/day aspirin that I have been taking for a decade or so (I'm 75). Next year, when I have my annual doctor visit, I'll see what she says.

I think I got told to take one daily when I was put on BP meds years ago. I'm off BP meds (cardiologist told me I probably never needed them in the first place in 2018) so maybe I don't need the aspirin too.

 

[bmcgonig]

When do you think we should take social security?

[emoji48][emoji48][emoji16][emoji16]

 

[Scratchy]

When do you think we should take social security?

[emoji48][emoji48][emoji16][emoji16]

OK I have to admit, this post is better than anything I have written here!!!

 

[Rianne]

When do you think we should take social security?

[emoji48][emoji48][emoji16][emoji16]

Why is that a good question? Here's a thought. My DH refuses to take statins. Cholesterol in a dangerous zone. PCP strongly encouraged him to take them. I feel if he doesn't want to take them, ok. It is his body.

If he dies before he takes SS or his pension, sayonara to those income streams. I'll be fine, but just saying, that's a good question.

 

[Amethyst]

If statins didn't have obnoxious side effects for many people, would patients get so wrapped up in whether or not to believe their doctors about statins? Just wondering.

 

[f35phixer]

I'm curious f35phixer, why did you go "back on something?" It sounds like there was some benefit to taking a statin you perceived and you worked with your doc to find one that minimized side effects. I don't want to put words in your mouth, but was that it?

Dr. Put me on Ezetimibe - YES IT IS A STATIN ALSO!!! We decided to take me off for >6 months, see how my head felt, it felt much less stupid! We had cognitive tests, CAT or MRI SCANS on head all come back as normal for a 58yr old... During that time, my cholesterol when back up to >250 from ~ 155. We eat health, not a lot a meat, no beef really and lots of veggies and salads with minimal oils. not a lot of exercise for me, but get my >10000 step a day weight about 175.... So i reluctantly when back on knowing first sign of getting stupid, off i came.... Been feeling fine, will continue to watch.....

 

[beowulf]

"So, I decided to donate blood to get my ferritin level down and see if that helped any (after going to a different doctor, who also had no clue what was causing my symptoms). Result: after a couple of blood donations, the symptoms improved markedly. After about the 3rd or 4th donation, they disappeared completely, and have been gone since."

Maybe the use of leeches on an occasional basis would help . If someone has an elevated level of something that's not good for you, wouldn't it be a better idea to find out why those levels were so high? It just didn't happen randomly. And, without knowing what caused it, what would prevent it from happening again?

Doctors are not all knowing and aren't always right. But would you rather have a car mechanic performing surgery on you than a real surgeon? How about prescribing drugs? Maybe follow the advice on Twitter rather than a real medical professional. My life has been save more than once by MDs. And if I see a Dr who doesn't seem to understand my problem, I see another. I do plenty of research, but my knowledge doesn't include medical school, an internship and regular professional updates.

 

[RAE]

"So, I decided to donate blood to get my ferritin level down and see if that helped any (after going to a different doctor, who also had no clue what was causing my symptoms). Result: after a couple of blood donations, the symptoms improved markedly. After about the 3rd or 4th donation, they disappeared completely, and have been gone since."

Maybe the use of leeches on an occasional basis would help . If someone has an elevated level of something that's not good for you, wouldn't it be a better idea to find out why those levels were so high? It just didn't happen randomly. And, without knowing what caused it, what would prevent it from happening again?

Beowulf, I did a LOT of reading about iron and ferritin when I had my issue. If you had done any reading on iron overload yourself, you would know that it's not uncommon for older males (in particular) to have elevated serum ferritin levels, as I did. 16 million Americans probably have some degree of iron overload, although many of them don't know it, as they are not (yet) symptomatic. The reason for high iron/ferritin levels is that we all ingest foods containing iron on a regular basis (particularly if you eat a fair amount of meat, as I do), and humans don't have a good mechanism to rid the body of excess iron. That is probably because, in our evolutionary history, iron was a precious commodity to be held onto by the body when acquired, as meat was not often available. Females lose iron through menstruation up until menopause, then many women begin to slowly accumulate more iron also. But iron/ferritin levels in women tend to be lower than men, since men accumulate iron throughout their lives (and never really get rid of it), as I probably did. My ferritin level finally reached 400, which is when I finally started having troubling symptoms (irregular heartbeat, for one). I wish I had known that my ferritin was elevated some years before my symptoms appeared, but I didn't, as the serum ferritin test is not a test routinely ordered by doctors when you get your blood test package (in my view, it should be).

So, I do have a good idea what caused my ferritin to be too high.....it likely gradually got higher over the years (decades), as it does in a lot of males, due to ingestion of iron in the diet (meat, foods fortified with iron), and the inability of my body to get rid of the excess iron. And I now know what to do to keep it from getting too high ever again.........donate blood on a regular basis. My ferritin level is now about 60, and I keep it at that level by donating blood at least 2-3 times each year.

I know that you will probably still not believe any of what I stated above (since it did not come out of the mouth of an MD that I saw), and that is your prerogative. But please don't assume that people like me are somehow incapable of doing research to help figure out what is wrong with them, when the doctors are not helping much. You'd be surprised at the information that is out there on things like iron overload (much of it written by doctors and medical researchers, by the way), if you just do a little searching of your own.