Should you be on statins?


Dr. Anders Tengblad

Should you be on a cholesterol-lowering medication, a so called statin? This is much debated and this will likely be a controversial post.

Some claim that nobody should take such drugs, that they cause lots of side effects and no benefits, as heart disease “has nothing to do with cholesterol.”

Others claim that most people (even healthy people) should take statins daily to prevent heart disease, as they are “effective and almost free of side effects.” Many doctors prescribe statins to all their patients with a cholesterol level above a pre-set number. For example a total cholesterol above 200 mg/dl (5 mmol/l).

Pros and Cons

The truth is of course somewhere between these extreme alternatives. Statins have been showed to reduce the risk of heart disease, especially in people who already suffer from heart disease. However, they also carry a risk of side effects, such as an increased risk of diabetes, muscle aches, weakness and increased fatigue.

So who could benefit from this medication? Should you be on it? New guidelines – a step in the right direction – have been issued from the Swedish Medical Products Agency.

Here’s a sensible guest post on the subject by Dr. Anders Tengblad:

Guest Post

tengblad-pres2New guidelines on preventative treatment with drugs have been issued from the Swedish Medical Products Agency. The guidelines are also included in the new diabetes guidelines. If you’re 100% opposed to taking medication to prevent disease, you will of course not like these guidelines. Personally, I think the guidelines are good. Focus is moved from target levels to treating the total risk.

If you’ve had a routine check-up, you may have had a comment about your cholesterol level, high or low, good or bad. If the level was high you’ve probably been advised to change your diet or take medication in the form of a statin. Unfortunately in my opinion many have been told to take statins needlessly. At the same time, some who should have had it will not have been given preventative medication, because their risk has been misjudged.

Under the new guidelines, statins should be used only when the overall risk of a cardiovascular event within 10 years is higher than 5%, no matter what your cholesterol level is (except, however, for LDL levels above 190 mg/dl (5mmol/l) in which case the person may have a genetic cause for the elevated cholesterol levels).

Treating according to the total risk rather than an elevated level is a new way of looking at treatment. In addition, medications that only impact the cholesterol number, but haven’t been shown to be beneficial for cardiovascular disease are essentially dismissed. This applies to multiple drugs. But the fact is that this also applies to low-fat foods, for example margarines, which in some cases may lead to a slightly lower cholesterol number, but other than that haven’t produced any benefit at all.

Although many now believe that atherosclerosis develops due to inflammation and not because of too much fat in the blood, it’s nevertheless a fact that statins may reduce the risk of myocardial infarction in patients at high risk for heart attack and that’s where they can do some good. Statin drugs have side effects, such as muscle aches, but can also produce a slightly elevated blood sugar. If you administer the drug to a patient with a low risk for heart disease, the net effect may be negative, but if the patient has a high risk, the benefit may outweighs the risk.

The risk of future cardiovascular disease has been estimated based on previous population studies and has been compiled into a risk calculator called Score. An internet-based version is available at: European SCORE guidelines.

If you enter numbers for a non-smoking 55-year old man with normal blood pressure and a cholesterol level of 270 mg/dl (7 mmol/l) into the risk calculator, the risk is 3% and statins are therefore not indicated. Similarly, the risk of a non-smoking woman at 65 with a normal blood pressure and a cholesterol of 270 (7) is only 3%, while the risk of a man at the age of 65 is higher and statins may be appropriate.

There’s also a risk calculator for those who have diabetes. There are more parameters to enter here, for example HDL, but the feeling is that many over 45 years of age with diabetes have an indication for a statin.

Some think that these risk calculations are based on factors that are too restrictive. Heredity, obesity, psychosocial stress, eating habits, etc. are not included, but these factors may both increase and decrease the risk for an individual. However, overall I think that focus on the overall risk rather than individual target numbers is a major step towards a better use of drugs.

All doctors are of course not updated on the guidelines yet. If at a check-up you are recommended to start taking a statin I think you should ask if the recommendation is based on a target number or a risk level.

Anders Tengblad


Comment to the guest blog

I think this is a big step in the right direction. All doctors who prescribe statins – as well as their patients – should take away two things from the new guidelines:

  1. Under most circumstances, statins should not be taken just based on a certain cholesterol number.
  2. Instead, a high total risk of heart disease may make it worth medicating with a statin.

In practice this means – slightly simplified – that for people who already suffer from heart disease it’s often a good idea to take statins, and that it’s rarely worth risking the side effects from statins for people with a low risk of heart disease.

The problem with an LCHF diet

As Dr. Tengblad writes, the commonly used risk calculation is simplified. It only includes age, blood pressure, smoking and total cholesterol.

Simplifying to using only total cholesterol is a major problem for people who eat low-carb. The reason is that LCHF consistently – in repeated studies as well as in clinical practice – significantly raises the good cholesterol, HDL. A high number means a statistically much lower risk for heart disease. At the same time more HDL cholesterol means a higher total cholesterol and therefore very incorrectly that the simplified risk calculator will indicate a higher risk due to more HDL cholesterol despite the fact that the risk in reality is lower!

The error is not negligible. In practice if you have as an LCHF eater a high HDL number, for example above 58 mg/dl,  or even above 77 (1.5–2 mmol/l), then you likely have a lot lower risk of heart disease than what the risk calculator will show. If you’re on the border to be recommended a statin then it’s probably worth evaluating more deeply. Other calculators, such as one from the American College of Cardiology, are somewhat better as they factor in HDL and a diagnosis of diabetes.


The simplified model is still true in most cases:

  • People with heart disease often benefit from statins
  • People without heart disease are less likely to benefit from statins

Those who are prescribed statins without any known heart disease should ask their doctor whether this is based on older population-based cholesterol reference numbers or the newer risk calculations. And if it is the latter you should, as an LCHF eater, ask about having your risk adjusted to your HDL number before making a final decision. Otherwise the chance of benefit may be small compared to the risk of side effects.


Finally, of course we mustn’t forget that pills are only one way to impact your risk of heart disease. You can also significantly impact it with lifestyle changes.

Avoid smoking (of course) and try to maintain a good weight, a good blood pressure and blood sugar and a good cholesterol profile. A low-carbohydrate diet may help with all (except the smoking).

In the end, you may improve your health so much that statins would be completely unnecessary.

ADDENDUM- Since this post was written, the ACC/AHA has published newer guidelines that further help risk stratify patients. For patients at an intermediate risk of heart disease (defined as 7.5-20% 10-year risk of a cardiac event), the guidelines recommend further evaluation with a coronary calcium score prior to deciding on statin therapy. We see this as a definite step in the right direction as it can further help define those who are more or less likely to benefit from statin therapy. Of course we still wish there was more of an emphasis on lifestyle and reducing metabolic disease, but we hope those guidelines are coming soon!


Previously on cholesterol

LCHF for Beginners

Great Cholesterol Numbers After 4 Years on an Ultra-Strict LCHF Diet

Previously on heart disease


  1. Charles Grashow
    "for LDL levels above 193 mg/dl (5mmol/l) in which case the person probably has a genetic cause for the elevated cholesterol levels"

    Oh really - a good % of LCHF people have LDL above this - so what should they do??

    As to high HDL being cardio protective
    Now, a new study that makes use of powerful databases of genetic information has found that raising HDL levels may not make any difference to heart disease risk. People who inherit genes that give them naturally higher HDL levels throughout life have no less heart disease than those who inherit genes that give them slightly lower levels. If HDL were protective, those with genes causing higher levels should have had less heart disease.
    Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study

    Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.

    Replies: #6, #14, #19
  2. BobM
    Even for a genetic cause for "high" cholesterol levels, statins may do more damage than good. People with high cholesterol levels may die at slightly higher rates from heart disease but will die from lower rates of cancer. The overall death rate isn't much higher than the normal population.

    Furthermore, for those with heart disease, the benefits of statins are exceedingly small and the side effects are high. The number needed to treat is very high and the costs are substantial. The overall benefit is very low.

    See, for instance:

  3. tw
    What I find interesting about the risk charts is that risk is significantly elevated as you get older with almost any cholesterol level but especially a high total for non smokers.

    I was under the impression that higher total cholesterol after 50 was in fact more "protective" or rather, healthy seniors seem to have higher cholesterol.

    So are these risk tables accurate? Frankly it looks like everyone will be on statins based on this which begs the question: who designed the risk factor charts?

    Why don't we design a pill that keeps people from getting old. Wouldn't that be easier? Or is that what they are claiming to do?

  4. Johnny D.
    I can only state what my own personal experience has been. Seen I went off my cholesterol lowering drug and adopted a LCHF diet my LDL cholesterol has decreased from 151 to 116. My depression is almost non existent. I have eliminated my depression medication and I feel great and I'm less tried.
  5. Chris
    Basing a recommendation on % risk is much better than levels of cholesterol alone since it takes some of the pressure of cholesterol levels but.... If the risk is calculated using cholesterol levels at all, and cholesterol doesn't cause heart disease?.... That's a flaw that will cause a premature recommendation to take statins to lower it.

    Now for the big "but". Statins don't lower "risk of death" from heart disease, they lower cholesterol which is considered a "risk" of heart disease. And that was based on cholesterol being the bad guy. If cholesterol isn't the bad guy, why is it a risk factor? It's more of an indicator to the real problem, inflammation, than a risk. Not causal.

    This still doesn't add up. Am I missing something? Have I been Misinformed?

  6. Murray
    The main benefit of HDL, it seems from what I've seen, is to transfer cholesterol into LDL particles through cholesterol ester transfer protein (CETP). This keeps LDL particles larger and fluffier. The statin-pushing LDL-bots who view cholesterol in LDL as "bad" cholesterol thought a drug to block CETP activity would lower LDL cholesterol and be a sure winner. It worked to lower LDL, but of course it "counter-intuitively" increased incidence of heart disease. Just like the study that substituted saturated fat in the diet with vegetable oil and lowered LDL cholesterol, but increased the incidence of heart disease. Time for a new model.

    It seems the main driver of heart disease is elevated insulin and the resulting elevated C-peptide. Since C-peptide reduces HDL, higher HDL might not be all that directly significant but simply a sign that C-peptide and thus the average insulin level over time has been lower.

    "Association between Serum C-Peptide as a Risk Factor for Cardiovascular Disease and High-Density Lipoprotein Cholesterol Levels in Nondiabetic Individuals"

  7. Boundless
    re: ... statins should be used only when the overall risk of death from cardiovascular disease within 10 years is higher than 5% ...

    As other responders have pointed out, what really matters is all-cause mortality for the presentation, and not just CVD risk.

    Further, those advocating statins need to provide a credible explanation of WHY the statin has an alleged all-cause net benefit. If another type of intervention does the same thing, without the under-reported side effects of statins, that alternative needs to be tried first. Of course, that's apt to be a nutritional approach, and there's no money in that.

  8. corrie
    So between the guidelines as written in the article with the associated exceptions and variables, and the conflicting information raised in the comment section, there really is no helpful information here. Or must we all become doctors to understand what is best for our circumstances?
    Reply: #25
  9. Andrés
    Anyone without previous cardiovascular desease should take a look to a less naïve analysis: that of the Therapeutics Initiative.
  10. Boundless
    This just in from the BMJ:
    "Rosuvastatin: winner in the statin wars, patients’ health notwithstanding"
    Given the evidence of more serious risks and less clinical benefit than other statins how has the drug fared so well for so long?
  11. Judy Barnes Baker
    I seldom disagree with anything Dr. Eenfeldt puts on his blog, but I do on this issue. I fear that most of the studies on statins have been controlled by the drug companies. With billions of dollars at stake, they may be designing or interpreting the studies to get the desired results. For example, most of them only follow subjects for a few years so things like cancer, Parkinson's, and Alzheimer's are not likely to show up. Also, 5 to 20% of statin users have such bad reactions that they quit taking the drugs, which would certainly make the statistics regarding side effects for the remaining subjects look better.

    Here are just some of the things that have been in the news about stain use:

    Some statin users will suffer Irreversible Muscle Damage and some will die. Many will suffer fatigue and muscle pain. Those taking statins exercise less and get less benefit from exercise. Statins increase the risk of diabetes--the increase in risk was 9% in just 4 years. How much would it be after 10 years? After 20 years? Trading a slight reduction on non-fatal heart events for a lifetime of diabetes, which is known to greatly increase the risk of heart disease, doesn't sound like a very good trade.

    It has been shown that statins do not prevent plaque buildup in the arteries, making it likely that any benefit they might provide is the result of an anti-inflammatory side effect. (Dr. Atkins pointed that out many years ago.) Surely there are better anti-inflammatory treatments that don't carry such severe risks.

  12. Judy Barnes Baker
    One more point: The instructions that come with statin prescriptions say to eat a low-fat/low-cholesterol diet while taking them. No doubt all the test subjects in all the studies of statins were told to follow that advice during the testing, which means all the results were collected from people eating the very diet that causes cholesterol problems in the first place. To my knowledge, there has never been a study done on those eating a low-carb/high-fat diet.
  13. Cheeta
    I agree with Judy Barnes Baker.
    I can recommend Malcolm Kendrick's book The Great Cholesterol Con:
    It was an eye opener for me...
  14. Paul the rat
    Hey Charlie,

    why don't you just stick around with your blog comedians buddies (I hope you are all comedians) who produce sentences like:
    "diabetes type 2 is caused by beta cells dysfunction" or

    "virtually all body fat comes from dietary fat in humans and humans can't synthesis PUFA".
    You see, my friends and I use this blog as an educational tool for our students. The game is: who will pick more in number and more hilarious statements from "all knowing experts in human biochemistry", which that blog seems to aggregate, gets top marks.
    That blog was brought to our attention by one of my students, and since than we have asocial gathering twice a month and we have a real ball !!!. Than you so much for the entertainment !!
    (we print in bold some of the statements posted on that blog and stick them on the walls around our lab)

    Reply: #15
  15. Paul the rat
    @ Charles Grashow
    By the way Charlie, I have noticed today that these 2 quotes I posted in #14 and one authoritatively stating: " ketone bodies are probably inert biochemically i humans" are framed and displayed in the corridor in our Department.
    Who needs Marx Brothers?.
  16. François Melançon
    I have to firmly disagree with the statement that statins are useful on a large scale. Though they do prevent a small fraction of MI's in a very small subgroup of patients, they do produce so many side effects (hidden and downplayed by the industry) - from heart failure to memory problems, from depression to severe myalgias , from diabetes to many, many other side effects- that in my humble opinion, side effects vastly outweigh any potential advantage.

    The question is the following: other than decreasing cholesterol, do statins work? Do they decrease death? Surprisingly, the answer is yes. But not like people think. And certainly not as much as people think they do. For example, 75% of statin prescriptions is done in primary prevention, which is that they are given to people before they have had a cardiovascular event. The only reason these people take statins is because their physician has told them they have “elevated cholesterol” that puts them at “high risk” of heart disease. This, by the way, is absolutely a fallacy. NO well done study has proven any efficacy of statins for reduction of cardiac risk in people with only elevated blood cholesterol. No study has also shown any benefit of statin therapy in women of any age… Statins even seem to increase type 2 diabetes risk in women and increase their risk of coronary calcifications.

    Statins have only been shown to “significantly” decrease cardiovascular events in men, age 50 to 65, who either already had had a coronary event or were at high risk of a coronary event through other risk factors (diabetes, high blood pressure). But though significant (which means not due to chance), even that effect is minimal! Let’s look into it.

    The Lipitor trials. The Lipitor trials (Sever PS et al., 2003) were conducted during 10 years on a group of men aged 50 to 65 at high risk of cardiovascular event through other risk factors or previous coronary event. After 10 years, the results were the following:
    In the LIPITOR group, 2 men out of 100 suffered an MI
    In the placebo group, 3,05 men out of 100 suufered an MI
    The ABSOLUTE difference is thus, for every 100 men taking Lipitor, 3.05 - 2.0 = 1.05. Lipitor “saved” one man from a cardiac death after 10 years of 100 men taking it with all its side effects. Not exactly an impressive result! But the Industry is ressourceful and has learned to use the RELATIVE risk. The technique is the following: you divide the small number by the large number and you substract the result from 1.
    In the case of the Lipitor trials, 2/3.05 = 0.64 (rounded) and 1 – 0.64 = 0.36 which enables the company to put adds everywhere stating that lipitor decreases the cardiac risk of death by 36%.

    Nearly all people (including physicians) think in absolute numbers and will therefore conclude that Lipitor has saved more than 1 man out of 3 from cardiac death. But it is not the case! Lipitor has saved 1 man from cardiac death for every 100 men taking it for 10 years…
     IF the patients were men,
     IF they were already at high risk of cardiac events through a multitude of other risk factors and
     IF they were between 50 and 65 years of age.
    The “relative risk” trick is so misleading that it is used regularly by the pharmaceutical industry. Take for example the Crestor JUPITER study. A 54% reduction in cardiac events and a 27% reduction in strokes... Why on earth do we not put statins in drinking water? Simply because those numbers are relative. The true numbers are far, far less impressive. In the placebo group, 0,76% of people had an MI. In the treated group, it was 0,35%. So in absolute numbers, the true difference is 0,75% - 0,35% = 0,41%, thus less than half of one percent of people. In the JUPITER study, less than one half of one percent of people were “saved” from a cardiac event. Not glorious. But let's change this into a relative risk! 0,35/0,76 is 0,46. 1 - 0,46 is 0,54 and voilà! You can now state – and this is what was done - that the medication in primary prevention decreased the risk of heart disease by 54%. Reviewers at the Cochrane Systematic Review Group (Taylor F et al., 2011) looked at this data and concluded that the actual benefit of statins in primary prevention was overstated, as patients having already had a cardiac event were included in the “primary prevention” group, thus artificially improving a very poor result .
    People's brains think in absolute numbers and will thus conclude that more than half of people were saved from heart disease. But this is not true! Less than one half of one percent were saved from cardiovascular disease. And since in absolute numbers, around 20% of people (highly under-reported by physicians) suffer important side effects of statins, hopefully, no one will ever put statins in the drinking water. (No healthy baby would ever be born again if this did happen - it takes a lot of cholesterol to make a healthy baby).
    In the end, statins should be prescribed to a very small subgroup of patients: males, 50 to 65, with many coronary artery risk factors, who are unwilling to make any change in their lifestyle. And to nobody else.

    Reply: #27
  17. Arlene S
    I am a 68 year old female, T @ diabetic, 5'11 tall, weight 326 lbs. I have fantastic cholesterol numbers LDL 63, HDL 54 risk ratio 3. I was placed on a statin because of 15 % risk of 10 year MI. Is this correct? I have gotten a second opinion as I am also of the way of thinking that this study could be a push of the Pharm Co. I do have brady/tachy and a pacemaker for Afib.
  18. François
    @ Arlene,

    May I respectfully suggest that the statins you are taking increase your diabetes risk? It seems to be something well known and quite common. My next door neighbor told me that she became a diabetic when she was prescribed a statin because of "high cholesterol". May I also suggest to seriously look into LCHF as a way to start burning all that extra fat you carry? As far as whether or not you should take statins, it may not be wise to ask this question on a blog. But I do encourage you to discuss the following information with your physician and then, make an informed decision. The articles I am referencing are easy to find on the internet. The Sultan and Hynes article can be found in full and is worth reading completely.
    “One question involves disagreement about whether the statin side effects are merely uncomfortable or actually pose significant heath risks… Like most medications, statins can have side effects. These include muscle pain or muscle weakness; nausea, constipation, or diarrhea; liver damage; and kidney damage. Recently, researchers have found that for a small number of people, statins are associated with an increased risk of type 2 diabetes.” (Sugerman DT et al., Statins, 2013)
    “Statin therapy has been associated with a wide range of adverse events including liver dysfunction, acute renal failure, and cataracts; cognitive symptoms, neuropathy, and sexual dysfunction; decreased energy and exertional fatigue; and psychiatric symptoms, including depression, memory loss, confusion, and aggressive reactions. On the positive side, statins have been associated with a decreased risk of oesophageal cancer.” (Abramson JD et al., 2013)

    In a 2013 review of the literature, two vascular surgeons in Ireland, Drs Sherif Sultan and Niamh Hynes wrote the following in their abstact: “… statins actually augment cardiovascular risk in women, patients with Diabetes Mellitus and in the young. Furthermore statins are associated with triple the risk of coronary artery and aortic artery calcification”…
    In their conclusion, they state: “There is increased risk of Diabetes Mellitus, Cataract formation, and Erectile Dysfunction in young statin users, all of which are alarming. Furthermore there is a significant increase in the risk of cancer and neurodegenerative disorders in the elderly plus an enhanced risk of a myriad of infectious diseases. All side effects are dose dependant and persist during treatment”…
    Knowing how cholesterol is synthetized in the body and its numerous essential actions, one can understand that any drug that cuts off its production so high up in the biochemical series of events that end up in cholesterol will have major side effects.
    Unfortunately, most physicians have long forgotten biochemical pathways (and they simply do not believe the patients that tell them they have side effects, from dry skin and wicked itchiness (abnormal cell walls due to insufficient cholesterol and saturated fats) to painful muscles and heart failure (low coQ10), depression and memory trouble (low Tau proteins and prenylated proteins), to digestive problems (not enough bile) to sexual dysfunction (not enough testosterone and estrogens) and osteoporisis (lack of vitamin D). Despite the fact there is no evidence of any positive effect, 75% of all the prescriptions of statins are done in primary prevention, a totally useless “non-indication”.
    And there is unfortunately more! In their review of the litterature, cardiovascular surgeons Sultan and Hynes have found that “For normal healthy individuals who are eager to achieve primary prevention, we discovered that for every 10,000 people taking a statin, there were 307 extra patients with cataracts, 23 additional patients with acute kidney failure and 74 extra patients with liver dysfunction. Furthermore, statin therapy increased muscle fatigabilty by 30% with 11.3% incidence of rhabdomyolysis at high doses. What’s more, it induces inflammatory myopathy, including necrotizing autoimmune myopathy with immunosuppression and the statin-related myopathy can last for 12 months”.
    It is unfortunate that physicians rather believe the pharmaceutical companies that tell them that there is almost nothing published on side effects because there are very few and those that do exist are minimal as the Industry hides them and physicians simply do not believe their patients, thinking that it’s all in the patient’s head ! “What is even more disparaging is that not only has there been a failure to report on these negative side-effects of statins, there has actually been active discouragement to publish any negative studies on statins.” (Sultan & Hynes, 2013)

    So please do not take anybody's advice (mine included) at face value but rather, do your research and discuss it with your physician. Bring him the articles I referred to and do discuss them. Then make your decision. And please consider LCHF: I fear you will soon be offered bariatric mutilation. Good luck to you.

  19. Jim
    @Charles: You did not really read the study you cited, right?

    They found a 1.54 fold increase in myocardial infarction risk per 1 SD increase in LDL levels ("in the wild"). The real interesting thing is: An HDL level increase by 1 SD was associated with only a 0.62 fold risk. So HDL *is* protective.

    What strikes me is that 0.62 almost equals 1/1.54. Meaning HDL seems to directly compensate for LDL! Sounds familiar, doesn't it? LDL:HDL ratio and such...

    However: Genetic anomalies probably break cholesterol regulation. Unnecessarily high HDL does not help anything, if LDL is just normal anyway! Unnecessarily high LDL *without* an associated increase in HDL obviously is risky.

    This actually means HDL *is* protective. Whether you're genetically impaired or not. But if your infarction risk is just normal... then against what could HDL protect you?! That's like the old joke about set theory: If there are 7 persons in a room and then 10 leave... Then obviously 3 persons have to enter the room for it to be empty.

    And now... just go and take your statins. The more the better, right? ;-)

  20. Murray
    Regarding side effects of statins, the diabetes risk is more than just for a small number. There is also doubled risk of Parkinson's disease. And the damage to muscles that many experience, seems to include damage to the heart muscle. All factors to consider.

    "Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms."
    Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99. doi: 10.1586/17512433.2015.1011125. Epub 2015 Feb 6.

  21. robert lipp
    Comment 5 by Chris refers
    He asks a critical question which has not been answered.

    "Now for the big "but". Statins don't lower "risk of death" from heart disease, they lower cholesterol which is considered a "risk" of heart disease. And that was based on cholesterol being the bad guy. If cholesterol isn't the bad guy, why is it a risk factor? It's more of an indicator to the real problem, inflammation, than a risk. Not causal.

    This still doesn't add up. Am I missing something? Have I been Misinformed?"

    Perhaps our DietDoctor or someone else can propose an answer

    Reply: #22
  22. Zepp
    You are right.. high cholesterole manly high LDL-P and/or APOb is indications!

    One can put those indications in several ways.. LDL-C/HDL-C= riskfactor, LDL-p/HDL-p= riskfactor, or APOb/APOA1= riskfactor!

    Its altso indicates that if HDL is high.. you probably have a healty metabolism.. and if HDL is high the risk from LDL-p, LDL-c and APOb is lesser!

    And Statins do lower LDL a bit.. by ading mycotoxins, that lower intra cellular cholesterole production.

    Glucagon altso lower LDL in blood by downregulate intra cellular cholesterole production.. whitout adding any toxins!

    Wich do you prefer?

    Recently I had been to hospital for regular DM T2 Check up. I am a layman and not from medical fraternity. So please excuse me for wrong words. My HB1Ac is 5.4 fbs: 124 PPBS 174. LDL-184; HDL:35. triglycerides 251. I was advised to continue with metformin 250mg (twice a day) and rosuvastatin f (5 ng +fenofibrate) . Yet I have not started rosuvastatin f . I want get better cholesterol & triglyceride numbers by next visit after 60 days . I do not suspect bonafides of reverred physician
  24. dannythetrucker
    I don't know what to do. I'm on a keto diet and was feeling good. My doc prescribed lipitor because my cholesterol was 240.

    I've been feeling crappy, weak, fatigued, since I started taking it. (Granted, the feeling crappy could be caused by something else) I'd just really like to stop taking the lipitor and see if I start feeling better, BUT...

    I think if a person is not going to trust their doctor, and follow their orders, there's no point in going to the doctor. Hopefully we can arrive at some sort of compromise. I figure if the lipitor brings down my cholesterol in a few months, doc should let me off it. If it doesn't bring down the cholesterol in a few months, doc should probably let me off it too. Why take something if it doesn't produce results? lol.

    Unfortunately, I think doc will see this the opposite. If it helps that will be proof I should keep taking it, and if it doesn't help then I must keep taking it because my cholesterol is too high!

  25. Travis Lefevre
    We do not need to become doctors. But to become guinea pigs of ourselves to see what works for ourselves
  26. Chris Wunsch
    I was disabled in 2002, due to unpublished effects of Lipitor, in me they caused a 28 day, end stage Alzheimer's like hospital stay, I did not know my wife. My 2 year old son, my parents, nor siblings. I could not walk, nor speak coherently, could not feed myself, I was incontinent of both bowel and bladder. Brain MRI revealed "innumerable lesions scattered throughout the white matter of my brain, biopsy revealed lesions to be apoptosis. Electron Microscopy revealed mitochondrial DNA mutations that resembling MELAS, lysosomal and autophagic vacuoles, with thickened disarrayed cristae. I was to transfer to a nursing home pending bed placement, I was 34 years old, high functioning Critical care RN of 12 years. When a visiting professor from Johns Hopkins was asked to evaluate me, he started on a mitochondrial cocktail and improved somewhat within 24 hours, and 4 days later discharged home, with aggressive rehab. To this day, I have constant relentless muscle pain in my legs, unbelievable fatigue, peripheral neuropathy. BRAIN MRI is unchanged. I enrolled in the UCSD statin effect study which concluded my use of lipitor was the cause of the holes in my brain and the mitochondrial DNA mutations and neuropathy.
  27. Diane
    Thank you for your very straightforward assessment (cutting through the BS). I am preparing for a discussion with my Dr.

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