The cardiologists are now discussing a new set of guidelines about cholesterol.
I thought it worth posting since many readers are on treatment.
The idea is reducing heart disease risk, the leading cause of premature death and disability in America.
Commentary December 31, 2013
2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults
Peter Libby MD
The cardiovascular community has long-awaited new prevention guidelines. After many years of conscientious work, in June 2013 the National Heart, Lung and Blood Institute (NHLBI) announced that it would limit its participation to supporting and producing systematic reviews regarding prevention. In August of 2013, the NHLBI, American Heart Association (AHA), and American College of Cardiology (ACC) jointly announced that the ACC and AHA would jointly assume responsibility for the prevention guidelines. The community was, therefore, very gratified when four sets of guidelines were released in November of 2013.
With respect to the cholesterol guidelines, the previous Adult Treatment Panel III (ATP III), already some dozen years old, was based on then–emerging, large-scale randomized clinical trials and opinion of a seasoned and knowledgeable group of experts. The panel that produced the 2013 cholesterol guidelines hewed to an evidence-based approach, enriched by clinical trial results that have accumulated since ATP III.
On the basis of current evidence, the group defined four statin benefit groups.
1. All who have clinical atherosclerotic cardiovascular disease and thus fall into the “secondary prevention” category
2. Those with low-density lipoprotein (LDL) cholesterol ≥ 190 mg/dL without a secondary cause,
such as a high intake of saturated or trans fats or various drugs or diseases
3. Individuals with diabetes without established cardiovascular disease aged 40–75 years with LDL cholesterol between 70 and 189 mg/dL
4. Those without established ASCVD without diabetes aged 40–75 years with LDL cholesterol from 70–189 mg/dL with a calculated ASCVD ≥ 7.5%.
An online risk calculator was provided to aid clinicians and patients in calculating their risk. The panel recommended that clinicians and patients engage in a risk–benefit conversation before initiating statin therapy rather than relying solely on numbers emerging from a risk calculator or preordained categories—a patient-centered approach. The panel emphasized that medications do not replace a healthy lifestyle.
Summary of the Four Statin Benefit Groups Described in the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce ASCVD in Adults
Clinical ASCVD “secondary prevention”
LDL-C > 190 mg/dL without secondary cause (eg, high saturated/trans fats, drugs, certain diseases)
Primary prevention with Diabetes–Age 40-75 years–LDL-C, 70–189 mg/dL
Primary prevention without diabetes–Age 40-75 years–LDL-C, 70–189 mg/dL, estimated ASCVD risk ≥ 7.5%
Adapted from: Stone NJ, Robinson J, Lichtenstein AH, et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [published online ahead of print November 7, 2013]. J Am Coll Cardiol. doi: 10.1016/j.jacc.2013.11.002.
Perhaps the most surprising and difficult for many to comprehend was eliminating LDL targets for monitoring therapy. The panel noted that existing randomized controlled trials did not use designs that titrated therapy to a particular target. The guideline authors, therefore, judged that the current evidence does not support the practice of adjusting therapy to achieve a particular target level. This view contrasts strikingly with the former National Cholesterol Education Project and ATP III recommendations, which urged the public to “know their number” and the medical community to strive to reach a particular LDL level in patients in various risk categories.
Another important change in the new cholesterol guideline is the focus on statins rather than other categories of lipid-modulating drugs, including the fibrates, ezetimibe, and nicotinic acid. The panel pointed to the lack of evidence derived from well-conducted and sizable clinical trials that support improved cardiovascular outcomes in patients already treated with statins compared with other classes of drugs that modulate lipid levels.
The panel also provided some useful practical guidelines regarding management of perceived muscle toxicity attributed to statins, a major concern of many patients and practitioners.
The new guidelines have engendered considerable comment and discussion, and some controversy. Issues by commentators included the strength of the evidence supporting a net benefit for widespread statin use, particularly in primary prevention and in women. Others have questioned the calibration of the new risk instrument provided by the guidelines.
The new guidelines presented an enormous step forward as they include primarily evidence-based recommendations. Their implementation should improve cardiovascular health by promoting evidence-based practice. While many practitioners and the public may have initial discomfort with the abandoning of LDL target goals, the rationale presented by the panelists is quite compelling.
I think it is a refinement. Highlighted the important things.
If you are going ffor best contents like I do,
just pay a quick visit this web page every day because it presents quality
contents, thanks
Kidding aside, I wouldn’t turn my considerable nose up at any of the food you mentioned. Does that make me open minded or just a glutton?
That was very enlightening. Thanks.
Didn’t know about yellow mustard and white mayo BBQ.
Kansas City deserved a mention, but i dont’ mind a little parochialism about the South. Otherwise we’d have to really go far afield and talk about chicago BBQ or Minneapolis or Billings . . . on and on.
The definitive authority.
Here’s what happened to you, contrarian extraordinaire.
You went into one of them NC BBQ places, smelled the vinegar and said–well that certainly doesn’t smell like BBQ, I think i’ll like it.
and you are one sick person. Nobody eats BBQ that is served with a ice cream scoop.
you eat your BBQ in big slabs of ribs, with properly built sausage, brisket and pork ribs and for a side you or for the ladies you serve chicken, and then you accessorize with potato salad and some pickles. and you serve the feast with the proper large Lone Star or Shiner Beer.
Only sick people eat vinegar tasting pulled pork BBQ. One time when i was driving to DC from NC i couldn’t help but notice all the road signs advertizing NC BBQ–i couldn’t believe it since i was getting away from it.
I would rather be choked by an Anaconda than eat NC BBQ. It ought to be a form of penance for really bad Catholics.
I knew you had a bad streak GHO5T and it’s plain bad taste and you will suffer an early demise for your commitment to NC BBQ, the worst BBQ in the UNIVERSE. Almost as bad as Schlitz Beer.
AHA! I knew there was something wrong with you. Anyone who doesn’t agree that NC has the best barbeque on the planet must have a truly corupted soul.
Thanks Dr. P and all the others, for taking the time to do the detail and get into the weeds for all my friends who love this stuff. Me, i don’t much care, but i do not like North Carolina BBQ and do not understand the people that do.
That’s my one food fetish, I think. Other than that I grew up in a big family and you ate what was on the table. I married a marvelous cook, so my problem is the usual–avoiding overeating, so recently i lost a bunch of weight by skipping lunch and cutting down on seconds at night. No more eating the whole meal at restaraunts–eat some, take some home is the best idea.
Thanks. I’m no doc. I was just curious due to the fact that testosterone is built out of cholesterol. It seemed reasonable, but reasonable associations and logical conclusions like that are similar in nature to “good intentions” with respect to where the road is taking you.
Thanks, Sandy.
Otvos and Cromwell at LipoScience have done the definitive work here. Lipoprotein Particle size drops out as a predicative risk factor when adjusted for particle number . We should assess and reduce particle number in those at risk. particle size gives us insight into the patient ‘s physiology (small particle size is most often associated with insulin Resistance ,etc.) but particle number is far more important..
These guidelines were most definitely a step backwards and moving medicine further away from any credible science and into nothing more than marketing. Statins are a huge money making industry and these new guidelines were primarily authored by those with ties to statin manufacturers. These new guidelines, according to Dr. John Abramson, would increase the number of Americans prescribed statins by 150% — in other words, put an additional 13.5 million more healthy Americans on statins. That’s quite a boon for the statin makers.
As was published in the BMJ (http://www.bmj.com/content/347/bmj.f6989), however, their algorithm overestimates cardiovascular risks by 75 to 150%. Worse, these recommendations fail to even consider the harms.
The most entertaining and rational overview of just how unscientific these guidelines are was by Dr. Malcolm Kendrick. (http://drmalcolmkendrick.org/2013/11/18/you-need-a-statin-now-what-was-the-question) “You can do absolutely everything ‘right’ be as healthy as healthy can be – according to the AHA and ACC.” Yet, by the age of 58 for men and 63 for women, according to these guidelines, you would need to take a statin – for the rest of your life.
Is there any decent research around about the benefits of statins as opposed to the costs? Quite a few people suffer unpleasant side effects from them, and it is a huge exercise in mass medication based on the myth that for most people, rising cholesterol levels as they age are a harbinger of heart disease. Could it be that rising cholesterol levels are about as relevant as greying hair?
In passing, the statements in the head post are full of self-congratulatory phrases such as “conscientious”, “seasoned and knowledgeable group of experts”, “enormous step forward” etc. Given all the backflips that have been performed over the last 30 years about cholesterol (eggs good/bad etc), it sounds as though they are just whistling in the dark to cheer themselves up.
What appears to be more important is the number and size range of lipoproteins anyway.
nope on correlation between low T replacement and statins. have read some stuff on effects of statins on T levels but the general consensus is that this is a clinically irrelevant effect.
The sad fact is that 90% of so-called “preventive health” research is just underhanded food marketing. Why advertise the truth about genetic predispositions when you can convince millions that the next new “super food”, supplement, or prescription is the only way to feel safe? With your $530 scan every ten years after 40 that’s only $2650 per person (assuming you stop having them after 80).
Compare that to statins which range from $314 to $1428 per year. If they get you started at 40 they’re getting between $12,560 and $57,120 over the same 40 year period. I’ve read about 33% of Americans are on statins. Even taking the low generic price, that’s $3.1 Billion a year. How much of that money would the pharmaceuticals lose if scanning were recommended? And we haven’t even gotten to the fad diet and supplement markets.
With all that in mind, the $53 a year scan doesn’t sound too expensive at all. Especially considering that you can never actually know what statins are doing for/to you otherwise. Cholesterol was never anything more than a proxy measure based on questionable statistics anyway. My only problem with the full-body scanning concept was the potential to gin up even more hypochondria and increase the number of unnecessary surgeries rather than unnecessary medication, but that’s the sort of decision making best left to the individual.
Here’s an interesting question to all the doctors in the house; is the new focus on low testosterone in any way related to the mass prescription of cholesterol lowering drugs and therapies? It seems to me like more and more modern drugs are actually just prescribed to deal with side-effects of other drugs.
Smokey, I’m with you. As an avid reader of the now idle Junkfoodscience.com blog, I have STILL not seen a single study that suggests statins do anything other than lower cholesterol and cause liver failure with no measureable impact on ASCVD rates. I’m having my coffee and eggs right now. (I do love sawmill gravy though)
Cliff’s Notes:
“The relationship between heart disease and the various levels & types of cholesterol is more complex than the new guidelines might lead one to believe. Also, some meta-studies showed a slightly increased risk of CD &/or CVD when people had higher triglycerides.
“Therefore, we don’t like the new guidelines.”
Fin
As someone who understands that dietary cholesterol has almost no impact on blood cholesterol and, further, puts more faith in the “heart disease is a response to inflammation/infection” concept than the “the next thing you put in your mouth could kill you” paradigm, I’ll just have another scoop of that sawmill gravy on my biscuits and wait for the next set of guidelines to come out, thanks.
(For bwanajohn, et al: there’s always room for one more at our table; grab a plate, throw what you like on it and enjoy the morning for a minute, why don’t you?)
Dr. P I am a lowly emergency physician–and actually don’t get involved much in these preventive activities.
Your scholarship and expertise clearly deserves attention. Do the cliff’w notes version for the lay people reading. I am not qualified.
The new guidelines are a step BACKWARD, and not endorsed by ANY true Clinical Lipidologists I know, nor the National Lipid Assn. nor the American Assn of Clinical Endocrinologists. here’s a nice summary of some reason why and another link to more. We recommend clinicians either continue ATP III, IAS guidelines or EAS guidelines.
———————————————-
From the “Ivory Tower” to the trenches: A practical approach to the 2013 ACC/AHA Cholesterol and Risk Assessment Guidelines
DOI: 10.1016/j.jacl.2013.12.010 (Seth Baum MD, Journal of Clinical Lipidology)
—————————————————————————-
R3i EDITORIAL http://www.r3i.org/pg/1/editorial.asp?id=47 (Residual Risk Education Initiative)
Long-overdue US guidelines for lipid management oversimplify the evidence
Prof. Jean Charles Fruchart, Prof. Jean Davignon, Prof. Michel Hermans
An Editorial from the R3i Trustees
Prof. Jean Charles Fruchart, Prof. Jean Davignon, Prof. Michel HermansMuch has been made of the new guidelines for the management of cholesterol, from the American College of Cardiology (ACC) and American Heart Association (AHA).(1) Long-overdue since Adult Treatment Panel III, the guidelines sought to simplify lipid management for the clinician. Gone are recommendations for low-density lipoprotein (LDL) cholesterol, non-high-density lipoprotein (non-HDL) cholesterol and apolipoprotein B as performance targets, integral to other international guidelines.(2,3)
Instead, the guidelines present a statin-centric approach, supported by evidence-from randomised controlled trials (which predominantly relate to statins) with the exclusion of lower levels of evidence. Four main groups who would benefit from statin therapy were identified (Table 1).
Table 1. Patient groups who would benefit from statin therapy
1. Clinical atherosclerotic cardiovascular disease (ASCVD)*
2. Primary elevated LDL cholesterol >190 mg/dL or 4.9 mmol/L (likely to be of genetic origin)
3. Aged 40 to 75 years with diabetes, LDL cholesterol 70-189 mg/dL (1.8 to <4.9 mmol/L) and without clinical ASCVD
4. Without clinical ASCVD or diabetes and with LDL cholesterol 70-189 mg/dL (1.8 to 7.5%.
* Defined by the inclusion criteria for the secondary prevention statin randomised controlled trials (i.e. acute coronary syndromes, or a history of myocardial infarction [MI], stable or unstable angina, coronary or other arterial revascularisation, stroke, transient ischaemic attack, or peripheral arterial disease of atherosclerotic origin)
The guidelines recommend either “high-intensity” or “moderate-intensity” statins, categorised on the basis of the average expected reduction in LDL cholesterol levels (i.e. ≥50% and 30% to <50%, respectively). The former is recommended for the first two patient groups, and for diabetes patients with an estimated 10 year risk for ASCVD ≥7.5% based on the recently developed Pooled Cohort Equations.(4) Where high-intensity statin therapy is contraindicated or there are statin-associated adverse events, a moderate-intensity statin strategy is proposed. Moderate to high-intensity statin therapy is recommended for primary prevention patients without diabetes taking into account estimated 10 year ASCVD risk, contraindications and the potential for statin adverse effects and interactions.
No case for omitting non-LDL lipids and residual CV risk.
With this narrow focus, management of lipoproteins beyond LDL has been disregarded. Notably, the guidelines do not offer any recommendations for managing atherogenic dyslipidaemia, the combination of elevated triglycerides and low HDL cholesterol, which is justifiably considered an important driver of atherogenic risk, as well as a contributor to residual CV risk, even when LDL cholesterol is controlled on statin therapy.(2,5,6) The guidelines argue that outcomes evidence from randomised controlled trials do not support a strategy for secondary lowering of non-HDL cholesterol in patients with controlled LDL cholesterol levels. This expert group bases this conclusion on findings from two recent randomised controlled studies with niacin: AIM-HIGH and HPS2-THRIVE which showed that niacin failed to significantly impact CV outcomes.7,8) However, both trials had shortcomings. AIM-HIGH, which was specifically designed to evaluate the merits of targeting residual atherogenic dyslipidaemia (median HDL cholesterol 0.91 mmol/L [35 mg/dL] and median triglycerides 1.82 mmol/L [161 mg/dL]) in statin-treated patients with optimal LDL cholesterol levels, lacked statistical power for a number of reasons including funding constraints, and was further flawed by the inclusion of a low dose of niacin in the placebo comparator. The trial was prematurely terminated due to futility.(7) HPS2-THRIVE, although appropriately powered, was not a test for targeting atherogenic dyslipidaemia, as patients had baseline levels of HDL cholesterol (1.14 mmol/L or 44 mg/dL) and triglycerides (1.43 mmol/L or 125 mg/dL) which would not normally have merited initiation of niacin treatment in routine practice.(8)
The expert group disregarded post hoc analyses from the fibrate trials. While acknowledging the limitations inherent to such post hoc analyses, the R3i and other expert groups,6 do recognise that there is consistent evidence of a clinical benefit in targeting atherogenic dyslipidaemia to reduce residual CV risk. Indeed, a meta-analysis of subgroups with similar lipid criteria for atherogenic dyslipidaemia from the major fibrate trials, conducted by the R3i, showed that fibrate treatment was associated with a 35% relative reduction in CV risk in individuals with atherogenic dyslipidaemia versus 6% in individuals without this dyslipidaemia.(9) Furthermore, while there is ongoing controversy about the role of low HDL cholesterol as a direct contributor to residual CV risk,(10) there is accumulating evidence implicating a causal role for triglyceride-rich lipoproteins (TRLs) and their remnants (for which triglycerides are a marker), whose presence is often comorbid with low HDL cholesterol. Indeed, recent studies highlighted by the R3i strengthen this causal link. Data from the CARDIoGRAM collaborative group(11) showed that common genetic variants that influence plasma triglycerides levels are associated with increased coronary artery disease risk. A Mendelian randomisation study(12) showed a causal association between remnant cholesterol, contained in TRL, and ischaemic heart disease risk which was independent of HDL cholesterol plasma concentration. Most recently, this month’s Focus on article(13) highlights a meta-analysis of 61 studies in general populations from America, Asia, Australia and Europe, which provided robust evidence of an association between elevated triglycerides and increased risk for CVD and all-cause mortality. In this analysis, each 1 mmol/L increase in triglycerides was associated with 13% increase in CVD mortality and 12% increase in all-cause mortality. The US guidelines also run counter to a consistent body of expert opinion, including the European Atherosclerosis Society6 and International Atherosclerosis Society,(14) which support a strategy targeting atherogenic dyslipidaemia, especially for insulin-resistant individuals, to manage residual CV risk that remains despite appropriate LDL cholesterol management. It is also notable that both the US National Lipid Association and American Association of Clinical Endocrinologists have declined to endorse these new US guidelines due to concerns relating to the scientific basis for their recommendations and lack of consideration of strategies for patients at risk from cardiovascular disease with a statin-centric approach.(15,16)
Thus, the R3i believes that the paradigm shift in lipid management recommended by the new US guidelines is an oversimplification of the current evidence-base and risks confusion. The underlying aim of all guidelines should be to help clinicians in their routine practice select the best management strategies for an individual patient, taking into account not only outcomes data but also expert consensus on emerging evidence, as well as benefit versus risk considerations. As well as strength of the evidence, congruence of the evidence from mechanistic studies at large is as important to consider when drafting new guidelines. This is sadly lacking from the “new” approach taken.
In particular, the R3i believes that the failure to acknowledge the relevance of other atherogenic lipoproteins, notably TRLs, to lipid-related CV risk is one of several important omissions in this guideline. Clearly definitive outcomes data are needed, but the accumulating evidence from animal, genetic and clinical studies, as well as consistent expert consensus, implies a role for managing persistently elevated TRLs in patients who remain at high CV risk despite optimal statin therapy. Against the background of escalating rates of obesity, metabolic syndrome and type 2 diabetes, residual hypertriglyceridaemia is an increasingly relevant issue facing clinicians in their routine practice and should not be ignored.
References
1. Stone NJ, Robinson J, Lichtenstein AH et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. J Am Coll Cardiol 2013; doi:10.1016/j.jacc.2013.11.002 [Epub ahead of print].
2. Reiner Z, Catapano AL, De Backer G et al. ESC/EAS Guidelines for the management of dyslipidaemias. Eur Heart J 2011;32:1769–818.
3. Anderson TJ, Grégoire J, Hegele RA et al. 2012 update of the Canadian Cardiovascular Society guidelines for the diagnosis and treatment of dyslipidemia for the prevention of cardiovascular disease in the adult. Can J Cardiol 2013;29:151-67.
4. The Pooled Cohort Equations, downloadable spreadsheet and a web-based calculator are available from http://my.americanheart.org/cvriskcalculator and http://www.cardiosource.org/science-andquality/practice-guidelines-and-quality-standards/2013-prevention-guideline-tools.aspx.
5. Fruchart JC, Sacks FM, Hermans MP et al; Residual Risk Reduction Initiative (R3I). The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in dyslipidaemic patients. Diab Vasc Dis Res 2008,5:319-35.
6. Chapman MJ, Ginsberg HN, Amarenco P et al; European Atherosclerosis Society Consensus Panel. Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. Eur Heart J 2011;32:1345-61.
7. The AIM-HIGH Investigators; Boden WE, Probstfield JL, Anderson T et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. New Engl J Med 2011;365:2255-67.
8. HPS2-THRIVE Collaborative Group. HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment. Eur Heart J 2013;34:1279-91.
9. Sacks FM, Carey VJ, Fruchart JC. Combination lipid therapy in type 2 diabetes. N Engl J Med 2010,363:682-4.
10. Genest J. High-Density Lipoprotein and Residual Cardiovascular Risk, De Minimis Non Curat Medicus or the COURAGE to be SMART?∗ J Am Coll Cardiol 2013;62:1842-4.
11. Do R, Willer CJ, Schmidt EM et al. Common variants associated with plasma triglycerides and risk for coronary artery disease. Nat Genet 2013 Oct 6. doi: 10.1038/ng.2795.
12. Varbo A, Benn M, Tybjærg-Hansen A, Jørgensen AB, Frikke-Schmidt R, Nordestgaard BG. Remnant cholesterol as a causal risk factor for ischemic heart disease. J Am Coll Cardiol 2013;61:427–36.
13. Liu J, Zeng FF, Liu ZM, Zhang CX, Ling WH, Chen YM. . Effects of blood triglycerides on cardiovascular and all-cause mortality: a systematic review and meta-analysis of 61 prospective studies. Lipids Health Dis 2013 Oct 29;12(1):159. [Epub ahead of print].
14. The International Atherosclerosis Society. An International Atherosclerosis Society Position Paper: Global recommendations for the management of dyslipidemia. Full report [http://www.athero.org/download/IASPPGuidelines_FullReport_2.pdf].
15. National Lipid Association. NLA Statement on the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Available at https://www.lipid.org/nla/2013-accaha-guideline-treatment-blood-cholesterol-reduce-atherosclerotic-cardiovascular-risk.
16. American Association of Clinical Endocrinologists. Member alert re. guidelines. Available at https://www.aace.com/membership/member_alerts.
I meant to say the first scan at 40, then every 10 years if nothing discovered. I know 40 seems young, but think of the people between 40 and 50 that have heart attacks. Odds are against them having one, but that’s cold comfort when you are one of the lucky winners of that lottery.
Really? For your life? You invest in a scan and discover you have one or more 80% occlusions and can immediately get treated for the predictable heart attack and $530 is too much? You find out that you have no noticeable occlusions and you’re 62 years old, so that your cholesterol count is essentially irrelevant? $530 is still too much? Well, different strokes.
What surprises me is that health insurance companies don’t offer the first one as free preventative medicine and able to be repeated every 10 years thereafter (assuming no problems found). Seems like finding and preventing 10% of the heart attacks that would have happened otherwise would be cheaper than getting the scans. I’d expect a pretty big discount for guaranteeing that many scans.
well some would say that’s a little too much, or too expensive.
Here’s a thought, how about forgetting about risk factors and go down to your local imaging facility and get a Cardiac CTA with at least a 128 slice machine. That way you’ll know exactly what the state of your arteries are, with the side benefit of great images of your heart to tell about whether there is any thickening or valve problems, portions of your lungs to see what condition they are in and, sometimes, a peek at your upper abdomen. Isn’t better to actually know than to play around with risk factors that may or may not even apply to your genetic predispositions? Mine cost me $530. Plus you get really cool pictures and videos you can bore people with.
Doc, Tom may have entered his total cholesterol number, not LDL. If so, then his LDL is probably way lower, therefore not a candidate for statins. However, this continued fascination with numbers in the guidelines is puzzling. I would recommend Tom ask his pysician for a cholesterol density test.
why do you think i don’t even know what my cholesterol is, and i am an old man.
these reducing risk games really bother me.
you put the numbers to it, mr. g. I like your style.
Here’s the things about statins. I’m 55 with normal BP, weight and Chol of 230. No heart disease hx. An online calculator gives me a risk of event of 7% in the next 10 years. If i plug 180 in, I get a risk of 4%. So if i take a statin my risk goes down 50%, but only 3% of people like me are going to benefit from statins. I have a 1:30 chance of that statin preventing an event. Yet, there is a risk of diabetes from maybe 4-10%, likely higher risks of muscle problems and mental dysfunction. So although the statin might?? help prevent a serious ht attack, the chance that the pill regime will hurt is much higher. Although the hurt is likely to be less serious than a ht attack.
glad to.
On the basis of current evidence, the group defined four statin benefit groups. (Dunn note: that means those who should take statins.)
1. All who have clinical atherosclerotic cardiovascular disease and thus fall into the “secondary prevention” category ( Dunn note: if you haven’t had any events or proof of disease, you go into cat 4 below)
2. Those with low-density lipoprotein (LDL) cholesterol ≥ 190 mg/dL without a secondary cause,
such as a high intake of saturated or trans fats or various drugs or diseases
3. Individuals with diabetes without established cardiovascular disease aged 40–75 years with LDL cholesterol between 70 and 189 mg/dL
4. Those without established ASCVD without diabetes aged 40–75 years with LDL cholesterol from 70–189 mg/dL with a calculated ASCVD ≥ 7.5%.
(Dunn: looks like with a chol of 220 in cat 4 you would be recommended for a statin.) That’s how i read the recommendations, but I am an emergency physician, haven’t written for a statin in my whole life except maybe for somebody who ran out and needed to get a refill until they saw their doc.
This report is apparently authored by and for the benefit of medical professionals and specialists. Please translate this to language I can understand. I am a healthy active 65 year old guy with a cholesterol level of 220 or so with no apparent heart disease. What the hell does this mean to me?