Many of the skeptical cardiologist’s patients managed to quit cigarette smoking by using e-cigarettes . They often continue to vape, prolonging their addiction to nicotine but overall I felt they were probably better off than smoking cigarettes. However, a couple of recent articles have me very concerned about the overall effect of e-cigarettes on public health.
The first article came from the PR department at UCSF with the headline:
Smoking E-Cigarettes Daily, Doubles Risk Of Heart Attacks”
It focused on an abstract presented in Baltimore in February 2018 by Stanton Glantz, UCSF professor of medicine and director of the UCSF Center for Tobacco Control Research and Education. The abstract (paper yet to be published) was an observational study of about 70,000 individuals. Since it was observational the causality implied by the headline is not justified but the findings are still worrisome:
When adjusted for other risk factors, daily e-cigarette use was associated with significantly increased odds (Odds Ratio: 1.79) of having had a heart attack (myocardial infarction), as was daily conventional cigarette smoking (OR: 2.72). Former and occasional e-cigarette use were not associated with significant changes in the odds of having had a heart attack, while the same categories of cigarette smoking were associated with smaller increases in risk than for current smokers.
So e-cigarettes might be safer than real cigarettes but if you don’t quit smoking you are worse off:
“E-cigarettes are widely promoted as a smoking cessation aid, but for most people, they actually make it harder to quit smoking, so most people end up as so-called ‘dual users’ who keep smoking while using e-cigarettes,” said Glantz. “The new study shows that the risks compound. Someone who continues to smoke daily while using e-cigarettes daily has an increased risk of a heart attack by a factor of five.
Juul and The Rise In Teenage Vaping
The second article was from The New Yorker and is fascinating. Entitled “The Promise of Vaping and the Rise of Juul.” , it details an alarming rise in teenage vaping which often involves a particular brand of e-cigarette, Juul, which resembles a flash drive.
To Juul (the brand has become a verb) is to inhale nicotine free from the seductively disgusting accoutrements of a cigarette: the tar, the carbon monoxide, the garbage mouth, the smell. It’s an uncanny simulacrum of smoking. An analyst at Wells Fargo projects that this year the American vaporizer market will grow to five and a half billion dollars, an increase of more than twenty-five per cent from 2017. In the latest data, sixty per cent of that market belongs to Juul.
Scientists Warn of E-cigarette Health Risks
In March, a congressionally mandated report on the health effects of e-cigarettes from the National Academies of Sciences, Engineering, and Medicine concluded:
Evidence suggests that while e-cigarettes are not without health risks, they are likely to be far less harmful than conventional cigarettes, the report says. They contain fewer numbers and lower levels of toxic substances than conventional cigarettes, and using e-cigarettes may help adults who smoke conventional cigarettes quit smoking.
With respect to cardiovascular diseases, their conclusions were:
There is good evidence that in the short term the nicotine in e-cigarettes raises systolic and diastolic blood pressure and heart rate
There is limited evidence that e-cigarettes increase biomarkers of oxidative stress, increase endothelial dysfunction and arterial stiffness. All of these factors are known to contribute to the development of atherosclerosis.
Long term, it is anyone’s guess what the consequences of vaping on the cardiovascular system will be.
As the New Yorker article makes abundantly clear, however, the youth of America are taking up vaping and Juuling increasingly and the National Academies are appropriately worried:
However, their long-term health effects are not yet clear. Among youth — who use e-cigarettes at higher rates than adults do — there is substantial evidence that e-cigarette use increases the risk of transitioning to smoking conventional cigarettes
Are Your Kids Vaping?
In 2015 there was a 40% chance your middle school or high school child had used e-cigarettes. The chart below from the CDC shows how rapidly rates are climbing.
The surgeon general/CDC issued a warning in 2016, writing:
E-cigarette use among U.S. youth and young adults is now a major public health concern. E-cigarette use has increased considerably in recent years, growing an astounding 900% among high school students from 2011 to 2015. These products are now the most commonly used form of tobacco among youth in the United States, surpassing conventional tobacco products, including cigarettes, cigars, chewing tobacco, and hookahs. Most e-cigarettes contain nicotine, which can cause addiction and can harm the developing adolescent brain.
Compared with older adults, the brain of youth and young adults is more vulnerable to the nega- tive consequences of nicotine exposure. The effects include addiction, priming for use of other addic- tive substances, reduced impulse control, deficits in attention and cognition, and mood disorders. Furthermore, fetal exposure to nicotine during pregnancy can result in multiple adverse consequences, including sudden infant death syndrome, altered corpus callosum, auditory processing deficits, effects on behaviors and obesity, and deficits in attention and cognition. Ingestion of e-cigarette liquids con- taining nicotine can also cause acute toxicity and possibly death if the contents of refill cartridges or bottles containing nicotine are consumed.
Stealth Vaping Devices
Vaping devices no longer clearly look like cigarettes. Here are some examples from the CDC report.
Note, however, that the Juul is not depicted.
It doesn’t look like a cigarette or a device that would be facilitating your child’s addiction to nicotine. And it has a USB port so it can be recharged from a laptop.
This wasn’t an issue as far as I can tell when my children were teens but I’m pretty sure if I had teenagers I would ban vaping and would confiscate anything that resembled an e-cigarette including flash or thumb drives that aren’t flash or thumb drives.
If you have had a heart attack at an early age or one of your parents did but your standard risk factors for coronary heart disease are normal you should consider getting tested for Lipoprotein(a) or Lp(a).
The standard lipid profile that most patients get checks LDL (bad) HDL (good) and total cholesterol along with triglycerides. While these are useful, I have many patients who have normal standard values but have developed advanced coronary heart disease at an early age despite following a perfect lifestyle (not smoking, regular aerobic exercise, healthy diet.)
The skeptical cardiologist tests such patients for Lp(a) (pronounced LP little a) and it is quite frequently elevated.
For patients, these are the facts to know about Lp(a)
It is the strongest single inherited (monogenetic) risk factor for the early development of coronary artery disease, heart attacks and strokes.
In addition to increasing risk of atherosclerosis, high Lp(a) is strongly associated with the development of calcific aortic valve disease which can result in narrowing of the aortic valve and aortic stenosis.
Depending on the cut-off used up to one in five individuals may have elevated Lp(a)
Levels of Lp(a) can be measured with a simple blood test that should cost no more than 50 to 100$. This is not included in standard lipid or cholesterol testing.
Risk for heart attack starts to rise with levels above 30 mg/dl and Canadian guidelines from 2016 (see here)) consider >30 mg/dl to be a risk factor and they recommend measuring Lp(a) in those with a family history of premature CAD or those at intermediate risk.
The European Atherosclerosis Society (EAS, 2010), suggested levels of <50 mg/dl as optimal. The EAS advised measuring Lp(a) once in all patients with premature CVD.
As levels get even higher risk also rises as these graphs show
Treatment For High Lp(a)
The lifestyle changes (both exercise and diet) that improve bad and good cholesterol levels have no effect on Lp(a). Our best drugs, the statins, for reducing risk of heart attack and stroke also don’t lower Lp(a) levels.
Only niacin has been shown to reduce Lp(a) across broad populations but there is no evidence that Lp(a) lowering by niacin lowers cardiovascular risk so it cannot be recommended for treatment.(In the AIM-HIGH study niacin did not reduce cardiovascular events in patients with Lp(a) with levels>50 mg/dl, despite achieving a mean Lp(a) reduction of 39%.)
Cholesteryl ester transfer protein inhibitors which raise HDL levels also reduce lipoprotein(a) concentrations, but three such inhibitors have not shown a clinical benefit.
In fact, currently there are no studies showing that lowering Lp(a) with any drug will effectively lower the associated risk of heart attack, stroke and aortic stenosis.
In the not too distant future, effective therapies may emerge. There are promising newer agents (antisense oligonucleotides or ASOs) currently in clinical trials and in limited populations the PCSK9 inhbitors, mipomersen and estrogen have lowered Lp(a) levels.
Why Test For Lp(a)?
If we have no effective therapies that work by lowering Lp(a) why recommend testing for it?
I test Lp(a) for two reasons.
First, since it is inherited, patients with high levels should consider having first degree relatives tested for Lp(a) to identify those who are going to be at high risk. This provides an early warning of who in the family is most at risk for cardiovascular complications early in life. Such patients should be considered for early screening for subclinical atherosclerosis. In addition, they should be additionally motivated to do everything possible to reduce their elevated risk by lifestyle changes.
Second, I tend to recommend more aggressive cholesterol lowering in patients who have evidence for early plaque build up for atherosclerotic events early in life than I otherwise would be. I tend to agree with the approach diagrammed below:
With this approach for patients who have had events related to atherosclerosis or advanced CAC for age we work super aggressively on optimizing all risk factors. I try to lower LDL to <70 with statins and with the addition of ezetimibe or PCSK9 inhbitors if needed.
If the patient has more problems with atherosclerotic events despite optimizing risk factors and Lp(a) >60 mg/dl, some experts recommend using apheresis a technique which runs the patient’s blood through a filter which removes LDL and Lp(a). Personally, I have not sent any patients for apheresis and await better studies proving its benefit.
For those patients seeking more detailed information and references I recommend Dr. Siggurdson’s excellent post on Lp(a)
I was hurriedly shaving the other day and felt a sharp stinging sensation in my philtrum. Shortly thereafter, blood began pouring forth from the area and dribbling into my mouth.
I don’t typically name-check the area between the nose and the margin of the upper lip, but if one cuts the area (and wants to write about the experience), it is useful to have a single noun that describes it precisely.
The human philtrum is apparently vestigial; per Wikipedia
Although lacking function, it does cause a protrusion in the otherwise smooth facade of the face, and as a consequence, is at an increased risk for cuts.
Despite holding pressure on the cut for many minutes and daubing it with toilet paper, it continued to bleed. The bleeding continued on for much longer than I am use to, and after a while I realized that my bleeding was prolonged due to the aspirin I have been taking.
I’ve been following my own advice to those with documented significant atherosclerotic plaque, and have been taking 81mg aspirin daily. I began chewing daily my chewable aspirin after writing my post on the best form of baby aspirin to take. Prior to that it was only intermittently.
BARCing Up the Willow Tree
As a cardiologist I commonly hear patients complain about the nuisance of bruising and bleeding caused by the aspirin and other blood thinners I have prescribed them. Now I had joined their ranks.
Doctors mostly worry about major bleeding caused by aspirin; things like bleeding from the gastrointestinal (GI) tract, or into the head. A recent review found that baby aspirin doubles the risk of bleeding from the upper GI tract, and increases the risk of intracranial hemorrhage by a factor of 1.4.
There is relatively little concern about the type of minor bleeding I experienced. However, beginning in 2010, the Bleeding Academic Research Consortium (BARC) investigators came up with a more precise way of categorizing bleeding events, the BARC bleeding types.
By far, the most common bleeding on aspirin is the kind I had: Type 1 BARC.
Type 1: bleeding that is not actionable and does not cause the patient to seek unscheduled performance of studies, hospitalization, or treatment by a healthcare professional. Examples include, but are not limited to, bruising, hematoma, nosebleeds, or hemorrhoidal bleeding for which the patient does not seek medical attention. Type 1 bleeding may include episodes that lead to discontinuation of medications by the patient because of bleeding without visiting a healthcare provider.
Indeed, my Type 1 bleeding prompted me to skip my aspirin doses for the next few days.
Many patients do the same thing. Just this morning a patient told she had stopped taking her aspirin because she thought it was causing “little red spots” on her arms.
Does Prolonged Bleeding Mean You Are Taking Too Much Aspirin?
My philtrum persisted in bleeding, and as I felt the need to use my hands for something other than holding pressure, I put a band-aid on the area (actually a Nexcare), which temporarily stemmed the bleeding tide: I began pondering if I was taking too much aspirin.
Since aspirin is so widely used to prevent heart attacks and strokes caused by sticky platelets, why isn’t there a way to see how effective it is at making sticky platelets less sticky? We have such methods for blood pressure meds (blood pressure levels) and cholesterol lowering drugs (cholesterol levels).
And for the older blood thinner warfarin, we have a blood test which helps us make sure the dosage of medication is keeping the blood thinning in a range that maximizes effectiveness and minimizes bleeding risk.
It turns out there are lots of ways to measure how effective aspirin is in an individual, but no consensus on which particular method should be used, and authorities don’t recommend we make such measurements.
This article on platelet function tests lists 13 different platelet function tests, ranging from the mostly historical “bleeding time” to sophisticated tests of platelet aggregation.
The Verify Now test (not available in the US) of platelet reactivity predicted in one study which patients would have BARC type I bleeding like mine. The test did not predict major bleeding complications, things like GI bleeding and intracranial hemorrhage.
Those patients who had minor bleeding problems were more likely to be noncompliant, stopping their aspirin therapy.
I could easily visualize the following scenario as the blood began pooling underneath my band-aid and progressing down my philtrum.
Let’s say I’ve just had a heart attack and had a drug-eluting stent placed in one of my coronary arteries. I’ve been started on aspirin and another anti-platelet drug. I cut myself and bleed excessively and prolongedly. I decide that the aspirin is the reason, and start skipping doses. The lower aspirin levels subsequently allow my platelets to become sticky again. As a result a clot forms in my coronary stent and a heart attack ensues.
Thus, prolonged bleeding from a cut, considered a minor side effect of aspirin therapy, could increase heart attack risk.
There is a clinically available test for aspirin effect called AspirinWorks.
The AspirinWorks Test Kit is an enzyme-linked immunoassay (ELISA) to determine levels of 11-dehydrothromboxane B2 (11dhTxB2) in human urine, which aids in the qualitative detection of aspirin effect in apparently healthy individuals post ingestion. Unlike platelet aggregation tests, which require freshly drawn blood that must be evaluated within at least four hours, the AspirinWorks Test is performed on a random urine sample that can easily be obtained in any doctor’s office.
AspirinWorks points out the putative benefits of testing for aspirin effect:
An increasing body of evidence in the medical literature overwhelmingly supports clinically significant variability in aspirin effect, which has been well-established in findings from trials, including the Heart Outcomes Prevention Evaluation (HOPE) Study and the CHARISMA trial published in Circulation (Journal) (2002 and 2008). These trials have demonstrated that:
Increased levels of urinary 11dhTxB2 are associated with as much as a four fold increased risk for adverse cardiovascular events or death.
Statin treatment is associated with lower concentrations of 11dhTxB2
11dhTxB2 is an independent, modifiable predictor of risk for stroke, heart attack and cardiac death (CHARISMA).
I have never ordered this test and am unaware of any other physicians ordering it on their patients.
Dealing With Minor Bleeding
Doctors don’t test for aspirin effect in individual patients because it is expensive and it won’t change our approach in most cases.
Taking 81 mg aspirin daily might be too high a dose to optimize the balance between bleeding and clotting in me. If I took it every other day I might have less Type I BARC episodes. However, we don’t have any good evidence that adjusting the dosage based on aspirin effectiveness testing will improve my outcomes.
Thus, we bleeders on baby aspirin (the BOBA) of the world must find better ways of dealing with minor bleeding.
When I changed the band-aid on my philtrum several hours after the initial cut, I began actively bleeding again. This time I decided to apply ice to the area to vasoconstrict the arteries. This, plus more pressure and time, almost completely stopped the bleeding.
Another Nexcare was applied to the area, and when it was removed the next morning, the bleeding did not resume.
There are a variety of other measures that can be tried with varying degrees of success, as described here (deodorant, lip balm, listerine, Visine) and here (styptic pencils and powders, cayenne pepper, tea bag, sugar, alum-ironically this article mentions making a paste out of aspirin and applying it to the cut).
There also appears to be a thriving industry devoted to commercial products for stopping bleeding from minor cuts outlined here.
Should We Worry About Minor Bleeding?
Ultimately, the seemingly excessive bleeding one experiences upon incidentally cutting oneself while taking aspirin is best viewed as a reassuring sign that the drug is doing its job: Your platelets are less sticky, less likely to cause bad clots that cause strokes and heart attacks.
Platelets don’t know bad from good clots, they just react indiscriminately.
The small amount of blood that exudes from superficial cuts can be scary but it can be controlled with fairly simple measures.
The little red dots my patient experiences, although unattractive, are benign.
The skeptical cardiologist watched a little bit of the Judd Apatow HBO Documentary on Garry Shandling last night. For fans of the comedian like me, it is fascinating. As I watched I was reminded of two posts I had written about the cause of his death and the physician detective in me searched for clues to his ultimate demise.
Right after his sudden death at the age of 66, media sources reported that he had died of a massive heart attack “according to insiders.”
At the time, TMZ reported that “Sources familiar with the situation tell TMZ Shandling died from a massive heart attack, with no prior warning whatsoever”
Although a heart attack resulting in ventricular fibrillation is the most common cause of a sudden, unexpected death in individuals over the age of 40, it is not the only one.
In fact, People magazine reported that Sanders experienced shortness of breath and pain in his legs just a day before his death, and that he spoke to a doctor friend about his symptoms, who stopped by that night to check on him,
Shortness of breath and pain in the legs raise the possibility of a clot or DVT in the leg, which can break loose and embolize into the pulmonary arteries. Such a pulmonary embolism, if massive, can result in swift and sudden death.
I wrote another post on this after his autopsy was released.
His autopsy revealed that he died from a pulmonary embolism, the disease I had raised as a likely alternative cause of his sudden death in my post in April, 2016. The actual death certificate can be viewed here.
The medical report on his death reveals that Shandling had a prior history of clots in the leg (s) (DVT) and that previously he had had an IVC filter implanted.
An IVC filter is an umbrella shaped device that is inserted into the major vein draining blood from the the lower half of the body (the inferior vena cava) to physically obstruct the vein and thereby prevent clots from reaching the pulmonary artery. These are used in cases where the normal medical treatment for blood clots (anticoagulants or blood thinners) can’t be utilized due to bleeding risk or have proven ineffective.
Although effective 95% of the time in preventing legs clots from migrating to the pulmonary artery there are reported failures and Shandling was clearly one.
Risk factors for DVT and PE include cancer, surgery and immobility. Shandling, it appears, was recently in Hawaii and long plane flights like the one he must have taken back to LA are notorious causes of immobility that can lead to DVT.
What Can We Learn From Shandling’s Death
Some take home points
-When some one dies suddenly and unexpectedly it is not automatically due to a massive heart attack. Do not assume your family member or spouse who was found dead in bed suffered a myocardial infarction.
-Unless the victim was quite old or had advanced cancer consider asking for an autopsy to find out the true cause of death. Whatever disease caused the death could be inherited by the victim’s offspring.
-Pulmonary embolism can be a rapidly lethal disease. Consider a medical evaluation for it if you are experiencing leg pain/swelling, sudden, unexplained shortness of breath or chest pain which worsens upon taking a breath. If you have risk factors for leg clots or prior leg clots be even more vigilant.
Watching the Zen Diaries of Garry Shandling gave me no further insights into his death. Sudden death typically happens without warning to the victim and even those who are closest to him/her.
N.B. In the second post I talked about Carrie Fisher’s death (also widely reported falsely as due to a “massive heart attack”) and speculated that we might never know the cause of her death because I anticipated that her autopsy (with toxicology) would not be released.
I was right about her not dying of a “massive heart attack” .
Her cause of death was listed as sleep apnea with other factors.
The other factors appear to be LOTS of drugs:
“Fisher’s toxicology review found evidence of cocaine, methadone, MDMA (better known as ecstasy), alcohol and opiates when she was rushed to Ronald Reagan UCLA Hospital on Dec. 23, a toxicology report showed.”
No autopsy was done per family request but CT scanning was performed.
Avid readers of the skeptical cardiologist know that he is not an advocate of fish oil supplements.
One of my first posts (1/2013) was devoted to taking down the mammoth OTC fish oil industry because recent scientific evidence was clearly showing no benefit for fish oil pills.
", the bottom line on fish oil supplements is that the most
recent scientific evidence does not support any role for them inpreventing heart attack, stroke, or death. There are potential
down sides to taking them, including contaminants and the impact on the marine ecosystem. I don’t take them and I advise my
patients to avoid them (unless they have triglyceride levels
Despite a lack of evidence supporting taking them, the fish oil business continues to grow, buttressed by multiple internet sites promoting various types of fish oil (and more recently krill oil) for any and all ailments and a belief in the power of “omega-3 fatty acids”.
Another Meta-Analysis Concludes No Benefit To Fish Oil Supplements
A publication this month evaluated the 10 randomized controlled trials involving 77 917 thousand individuals that have studied fish oil supplements in preventing heart disease. The writers concluded that fish oil supplements do not significantly prevent any cardiovascular outcomes under any scenario.
It was written by a group with the ominous title of “The Omega-3 Treatment Trialists’ Collaboration.”
The Omega-3 Treatment Trialists’ Collaboration was established to conduct a collaborative meta-analysis based on aggregated study-level data obtained from the principal investigators of all large randomized clinical trials of omega-3 FA supplements for the prevention of cardiovascular disease, using a prespecified protocol and analysis plan. The aims of this meta-analysis were to assess the associations of supplementation with omega-3 FAs on (1) fatal CHD, nonfatal MI, stroke, major vascular events, and all-cause mortality and (2) major vascular events in prespecified subgroups.
The authors conclusions:
. Randomization to omega-3 fatty acid supplementation (eicosapentaenoic acid dose range, 226-1800 mg/d) had no significant associations with coronary heart disease death (rate ratio [RR], 0.93; 99% CI, 0.83-1.03; P = .05), nonfatal myocardial infarction (RR, 0.97; 99% CI, 0.87-1.08; P = .43) or any coronary heart disease events (RR, 0.96; 95% CI, 0.90-1.01; P = .12). Neither did randomization to omega-3 fatty acid supplementation have any significant associations with major vascular events (RR, 0.97; 95% CI, 0.93-1.01; P = .10), overall or in any subgroups, including subgroups composed of persons with prior coronary heart disease, diabetes, lipid levels greater than a given cutoff level, or statin use.
Nothing. Nada. No benefit.
There is clearly no reason to take fish oil supplements to prevent cardiovascular disease!
American Heart Association Sheepishly Recommends Fish Oil Supplements
If the science was conclusive on this in 2013 why did the American Heart Association (AHA) issue an “advisory” in 2017 suggesting that the use of omega-3 FAs for prevention of coronary heart disease (CHD) is probably justified in individuals with prior CHD and those with heart failure and reduced ejection fractions?
Oddly, this is the study that prompted me to write my first fish oil post in 2013
The AHA advisory totally distorts the completely negative conclusions of the Rizos meta-analysis, writing:
A meta-analysis published in 2012 examined the effects of omega-3 PUFA supplementation and dietary intake in 20 RCTs that enrolled patients at high CVD risk or prevalent CHD and patients with an implantable cardioverter-defibrillator (total n=68 680). That meta-analysis demonstrated a reduction in CHD death (RR, 0.91; 95% CI, 0.85–0.98), possibly as the result of a lower risk of SCD (RR, 0.87; 95% CI, 0.75–1.01).11
Strangely enough, if you look at the conclusions of Rizos, et al. they are
No statistically significant association was observed with all-cause mortality (RR, 0.96; 95% CI, 0.91 to 1.02; risk reduction [RD] -0.004, 95% CI, -0.01 to 0.02), cardiac death (RR, 0.91; 95% CI, 0.85 to 0.98; RD, -0.01; 95% CI, -0.02 to 0.00), sudden death (RR, 0.87; 95% CI, 0.75 to 1.01; RD, -0.003; 95% CI, -0.012 to 0.006), myocardial infarction (RR, 0.89; 95% CI, 0.76 to 1.04; RD, -0.002; 95% CI, -0.007 to 0.002), and stroke (RR, 1.05; 95% CI, 0.93 to 1.18; RD, 0.001; 95% CI, -0.002 to 0.004) when all supplement studies were considered.
Nothing. Nada. No significant benefit!
The AHA was so confused by their own advisory that in the AHA news release on the article they quote Dr. Robert Eckel, a past AHA president as saying he remains “underwhelmed” by the current clinical trials.
“In the present environment of evidence-based risk reduction, I don’t think the data really indicate that fish oil supplementation is needed under most circumstances.”
The end of the AHA news article goes on to quote Eckel as indicating he doesn’t prescribe fish oil supplements and the science advisory won’t change his practice:
Eckel said he doesn’t prescribe fish oil supplements to people who have had coronary events, and the new science advisory won’t change that. “It’s reasonable, but reasonable isn’t a solid take-home message that you should do it,” he said.
AHA: Wrong On Coconut Oil and Fish Oil
It’s hard for me to understand why the AHA gets so many things wrong in their scientific advisories. In the case of the recent misguided attack on coconut oil , their ongoing vilification of all saturated fats, and their support for fish oil supplements I don’t see evidence for industry influence. The authors of the fish oil supplement advisory do not report any financial conflicts of interest.
There is, however, one bias that is very hard to measure which could be playing a role: that is the bias to agree with what one has previously recommended. The AHA issued an advisory in 2002 recommending that people take fish oil. Changing that recommendation would mean admitting that they were wrong and that they had contributed to the growth of a 12 billion dollar industry serving no purpose.
Personally, I am aware of this kind of bias in my own writing and strive to be open to new data and publications that challenge what I personally believe or have publicly recommended.
In the case of fish oil supplements for preventing cardiovascular disease, however, the most recent data supports strongly what I wrote in 2013:
Don’t take fish oil supplements to prevent heart disease.
Americans want a “magic-bullet” type pill to take to ward off aging and the diseases associated with it. There isn’t one. Instead of buying pills and foods manipulated and processed by the food industry which promise better health, eat real food (including fish) eat a lot of plants and don’t eat too much.
N.B. I have no patients on the two prescription fish oil supplements available, Lovaza and Vascepa. I wrote about Vascepa here
Below is an excerpt:
Like the first prescription fish oil available in the US, Lovaza, VASCEPA is only approved by the FDA for treatment of very high triglycerides (>500 mg/dl).
This is a very small market compared to the millions of individuals taking fish oil thinking that it is preventing heart disease.
The company that makes Vascepa (Amrin;$AMRN)would also like to have physicians prescribe it to their patients who have mildly or moderatelyelevated triglycerides between 200 and 500 which some estimate as up to 1/3 of the population.
Given the huge numbers of patients with trigs slightly above normal, before approving an expensive new drug, the FDA thought, it would be nice to know that the drug is actually helping prevent heart attacks and strokes or prolonging life.
After all, we don’t really care about high triglycerides unless they are causing problems and we don’t care about lowering them unless we can show we are reducing the frequency of those problems.
Data do not exist to say that lowering triglycerides in the mild to moderate range by any drug lowers heart attack risk.
In the past if a company promoted their drug for off-label usage they could be fined by the FDA but Amarin went to court and obtained the right to promote Vascepa to physicians for triglycerides between 200 and 500.
Consequently, you may find your doctor prescribing this drug to you. If you do, I suggest you ask him if he recently had a free lunch or dinner provided by Amarin, has stock in the company (Vascepa is the sole drug made by Amrin and its stock price fluctuates wildly depending on sales and news about Vascepa) or gives talks for Amarin.
If he answers no to all of the above then, hopefully, your triglycerides are over 500.
The skeptical cardiologist recently asked his Eternal Fiancée to grab a bottle of baby aspirin while she was at the local Walgreen’s. Aspirin or acetyl salicylic acid (ASA) comes in either a 325 mg dose or in a low dose which can be between 75 to 100 mg and is often called “baby” aspirin.
However, since a link between aspirin use and a potentially lethal disease called Reye’s syndrome was identified in the 1980s, no authorities recommend aspirin in children or babies, and the low dose ASA (LDASA) is primarily marketed and used for prevention of cardiovascular disease.
Although Bayer and Dr. Oz would have us believe that all individuals over the age of 55 should be taking LDASA, as I pointed out here in 2014, the FDA no longer recommends it for prevention of cardiovascular disease.
The USPSTF recommends initiating low-dose aspirin use for the primary prevention of cardiovascular disease (CVD) and colorectal cancer (CRC) in adults aged 50 to 59 years who have a 10% or greater 10-year CVD risk, are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years.
I’m 63 years old, so the USPTF recommendation for me to take LDASA is a little less enthusiastic:
The decision to initiate low-dose aspirin use for the primary prevention of CVD and CRC in adults aged 60 to 69 years who have a 10% or greater 10-year CVD risk should be an individual one. Persons who are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years are more likely to benefit. Persons who place a higher value on the potential benefits than the potential harms may choose to initiate low-dose aspirin.
Following my own advice (see here), I have started taking 81mg of aspirin regularly (well, when I remember) in order to prevent stroke and heart attack. I do have subclinical atherosclerosis with a plaque in my LAD, and I think the aspirin will make my platelets less sticky and less likely to form clots if my plaque ruptures, thereby reducing my chances of an acute heart attack.
I am willing to accept the increased risk of bleeding from the gastrointestinal tract and hemorrhagic stroke associated with LDASA use.
Previous to this I had been taking ASA from little sample bottles that Bayer sends to my office. These bottles are quite annoying as they are stuffed with cotton and contain very few pills making extrication of the tiny pills an exercise in futility (I am using this as an excuse for my lack of regularity in taking them).
There’s no reason to pay the premium for Bayer ASA despite the company’s advertising attempts to link inextricably their name with ASA. Aspirin is aspirin, whether Bayer made it or Walgreens. In Bayer’s defense, their website has reasonable information on heart attacks and they appear to be giving aspirin away to people named Smith.
But what type of aspirin should you get? Enteric-coated, safety-coated, delayed release, chewable?
I asked the Eternal Fiancée to buy the cheapest baby aspirin possible.
She ended up buying a chewable formulation with orange flavoring, presumably aimed at children:
When I put one of these in my mouth I tasted the sickly sweet taste of an artificial sweetener. The ingredients are listed as: Dextrates, Ethyl Cellulose, FD&C Yellow 6 Aluminum Lake, Orange Flavor, Sodium Saccharin, Starch. Saccharine! Yikes!
The only reason to chew ASA is if you are having an acute heart attack.
In this situation, chew 4 of the LDASA or one regular 325 mg aspirin. Chewing the aspirin makes the levels rise faster in your blood stream and can help dissolve the clot causing your heart attack more rapidly.
How do you know if you are having a heart attack? This is actually a very difficult question to answer with certainty. See here for a reasonable discussion.
Low Dose Aspirin: Enteric-Coated versus Non-coated
It is very difficult (perhaps impossible) to find low dose, non-chewable ASA that has not been “safety-coated” or “enteric-coated.” These formulations have become popular by promoting the idea that they are less likely to cause stomach pain or bleeding.
The concept is that the coating leads to delaying the aborption of the ASA until it reaches the small intestines where, presumably, it will do less damage. However, there is no good evidence to support lower bleeding risk with enteric-coasted (EC) ASA.
There is, on the other hand, very good evidence that therapeutic levels of aspirin in the bloodstream, and therefore the speed and efficacy of ASA in preventing heart attacks, is reduced by these “safety” formulations.
Volunteers were given either 325mg regular ASA or 325mg EC ASA and researchers looked at how each formulation effected platelet activity. The onset of antiplatelet activity was determined by the rate and extent of inhibition of serum thromboxane B2(TXB2) generation.
The EC ASA took longer and was less effective at blocking platelet activity than plain ASA. Presumably, this translates into lower efficacy in preventing heart attacks and strokes.
Therefore, if you feel like you are having a heart attack, chew ASA which is not enteric or safety-coated. Yes, you can chew a regular 325 mg ASA pill. Or you can chew 4 of the LDASA, preferably uncoated but still helpful if coated.
If it turns out you weren’t having a heart attack there is no down side to having chewed 325 mg ASA.
I just spent a fair amount of time trying to find non EC, non-chewable LDASA online and failed.
For the time being I will be swallowing daily the orange chewable LDASA and I will carry a bottle around in my satchel for emergency use.
N.B. Aspirin is generally recommended in secondary prevention of cardiovascular disease, ie. for those who have had heart attacks, stents or bypass surgery . For a good review of the evidence for this see here.
In October, 2016 the skeptical cardiologist predicted that Donald Trump’s coronary calcium score, if remeasured, would be >100 . At that time I pointed out that this score is consistent with moderate coronary plaque build up and implies a moderate risk of heart attack and stroke.
Trumps’ score gave him a seven-fold increase risk of a cardiovascular event in comparison to Hilary Clinton (who had a zero coronary calcium score) .
I was able to predict this score because we knew that Trump’s coronary calcium was 98 in 2013 and that on average calcium scores increase by about 10% per year.
I pointed out that his previous score was average for white men his age and his repeat score is also similar to the average white male of 71 years.
Entering Trump’s numbers into the MESA coronary calculator shows us he is at the 46th percentile, meaning that 46% of white men his age have less calcium.We can also calculate Trump’s 10 year risk of heart attack and stroke using the app from the ACC (the ASCVD calculator) and entering in the following information obtained from the White House press briefing:
Total Cholesterol 223
LDL Cholesterol 143
HDL Cholesterol 67
Systolic Blood Pressure 122
Never Smoked Cigarettes
Taking aspirin 81 mg and rosuvastatin (Crestor) 10 mg.
His 10 year risk of heart attack or stroke is 16.7%.
Given that his calcium score is average it doesn’t change his predicted risk and the conclusion is that his risk is identical to the average 71 year old white man-moderate.
We also know that Trump had an exercise stress echocardiogram which was totally normal and therefore can be reasonably certain that the moderate plaque build up in his arteries is not restricting the blood flow to his heart.
Here is what Dr. Jackson said about the stress echo:
He had an exercise stress echocardiogram done, which demonstrated above-average exercise capacity based on age and sex, and a normal heart rate, blood pressure, and cardiac output response to exercise. He had no evidence of ischemia, and his wall motion was normal in all images. the stress echo:
The New York Times article on this issue, entitled “Trump’s Physical Revealed Serious Heart Concerns, Outside Experts Say” however, presents a dramatically worrisome and misleading narrative.
It quotes several cardiologists who were very concerned about Trump’s high LDL level, weight and diet.
It’s interesting that some of the experts quoted in the NY Times piece feel that Trump’s Crestor dose should be increased in light of the recent NY Times piece questioning whether the elderly should take statins at all.
If we have serious concerns about Trump’s heart then we should have the same concerns about every 71 year old white man because he is totally average with regard to cardiac risk. In addition he is on a statin and on aspirin, the appropriate drugs to reduce risk.
In contrast to the average 71 year old male he has had a battery of cardiac tests which show exactly where he stands cardiac wise.
Most of these cardiac tests we would not recommend to an asymptomatic individual of any age. Jackson revealed that Trump had an EKG and an echocardiogram.
His ECG, or commonly EKG, was normal sinus rhythm with a rate of 71, had a normal axis, and no other significant findings.
He had a transthoracic echocardiogram done, which demonstrated normal left ventricular systolic function, an ejected fraction of 60 to 65 percent, normal left ventricular chamber size and wall thickness, no wall motion abnormalities, his right ventricle was normal, his atria were grossly normal, and all valves were normal.
So our President has a normal heart for a 71 year old white male. This automatically puts him at moderate risk for heart attack and stroke over the next 10 years but he is being closely monitored and appropriately treated and should do well.
N.B. I see that Trump’s LDL was reported previously as 93. The current LDL of 143 suggests to me that he has not been taking his Crestor.
N.B. Below is an excerpt from my prior post which explains coronary calcium
Regular readers of the skeptical cardiologist should be familiar with the coronary calcium scan or score (CAC) by now. I’ve written about it a lot (here, here, and here) and use it frequently in my patients, advocating its use to help better assess certain patient’s risk of sudden death and heart attacks.
The CAC scan utilizes computed tomography (CT) X-rays, without the need for intravenous contrast, to generate a three-dimensional picture of the heart. Because calcium is very apparent on CT scans, and because we can visualize the arteries on the surface of the heart that supply blood to the heart (the coronary arteries), the CAC scan can detect and quantify calcium in the coronary arteries with great accuracy and reproducibility.
Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium. Thus, the more calcium, the more plaque and the greater the risk of heart attack and death from heart attack.
The NY Times published an article earlier this month with the provocative title “You’re Over 75, and You’re Healthy. Why Are You Taking a Statin?”
It’s actually a balanced presentation of this difficult question (although it includes the seemingly obligatory anecdote of a patient getting severe muscle aches and weakness on Lipitor) and I agree with the concept that patients should demand a good thoughtful explanation from their PCP if they are on a statin. Shared physician and patient decision-making should occur irrespective of age when a statin is prescribed.
Unfortunately, the NY Times piece was triggered by and contains references to a weak observational study that was recently published in the Journal of the American Geriatric Society..
A much better article on this same topic was published earlier in January in what is arguably the most respected cardiology journal in the world (Journal of the American College of Cardiology).
It contains what I think is a very reasonable discussion of the problem: the elderly at are a substantially higher risk of adverse “statin-associated symptoms” but also at much higher risk of stroke, heart attack and cardiovascular-related death than the young.
Key Points To Consider For Use of Statins In Elderly
Some key points from that article to ponder for those over 75 years
Major European and North Americans national guidelines differ markedly in this area as this graphic illustrates
“At one end of the spectrum, the 2016 ESC/EAS guidelines miss great opportunities for safe, cheap, and evidence-based prevention in elderly individuals 66 to 75 years of age. At the other end of the spectrum, the 2014 NICE guideline provides near-universal treatment recommendations well into the very elderly >75 years of age where RCT evidence is sparse and more uncertain.”
2. Data on from 2 large primary prevention trial (JUPITER and HOPE-3) show that rosuvastatin (Ridker, et al)
reduced the risk of a composite endpoint (nonfatal MI, nonfatal stroke, or cardiovascular death) substantially by 49% (RR: 0.51; 95% CI: 0.38 to 0.69), and the risk was reduced by 26% (RR: 0.74; 95% CI: 0.61 to 0.91) in those ≥70 years of age. The efficacy was similar in individuals ≥70 and <65 years of age, indicating little heterogeneity in treatment effect by age. Today, nearly all apparently healthy elderly individuals have RCT evidence supporting statin efficacy.
3. The elderly compared to the younger are much more likely to have a nonfatal event which does not reduce their longevity but impacts their quality of life.
Thus, patient preferences are critical important for well-informed shared decision-making. If a patient only values longevity, there are little data to support primary prevention with statins in people >65 years of age. On the other hand, if preventing nonfatal and potentially disabling MI or stroke is of value to the patient, it might be reasonable to initiate statin therapy. From this perspective, it is noteworthy that the relative importance that people assign to avoiding death compared with avoiding nonfatal events appears to be highly age dependent. Although younger individuals <65 years of age weigh avoiding death highest, elderly individuals ≥65 years put a much higher weight on avoiding MI or stroke than death, These differences are compatible with elderly individuals having a greater focus on quality of life and avoiding disability than on extending life.
The Value of Derisking and Deprescribing
In my practice, I do a fair amount of deprescribing statins in the elderly. I have a very low threshold for initiating a trial of temporary statin cessation if there is any question that a patient’s symptoms could be statin-related (see here.)
The older the patient, the higher the bar for initiating statins and I think in all patients a search for subclinical atherosclerosis (coronary calcium scan or vascular ultrasound) helps inform the decision.
Previously, I had no term for this higher bar but I like the term the JACC paper introduces, derisking:
A promising approach to personalize treatment in elderly people is “derisking” by use of negative risk markers (i.e., absence of coronary artery calcification) to identify those at so low risk that statin therapy may safely be withheld . In the BioImage study of elderly individuals, for example, absence of coronary artery calcification was prevalent (≈1 of 3) and associated with exceptionally low ASCVD event rates
If you are >75 ponder all these factors and have an intense discussion with your doctor about taking a statin.
If you are still on the fence after this discussion consider a compromise approach that I have outlined here.
When the skeptical cardiologist trained in medicine and cardiology in the 1980s the standard protocol for obtaining a lipid profile (LDL and HDL cholesterol plus triglycerides) involved having the patient fast for >8 hours before the blood was drawn.
Beginning in 2009, however, various national organizations began recommending the use of nonfasting lipid profiles. In 2011 the American Heart Association endorsed the fasting lipid profile and shortly thereafter I began telling my patients they did not need to fast for these tests.
Old habits and ideas are hard to kill and to this day most of my patients think that fasting is a requirement. Lab personnel seem to be stuck in the past as well and I typically instruct my patients to lie if they are asked if they have eaten.
Science continued to progress in the field of cardiology in 2017. Some cardiology interventions were proven to be more beneficial (TAVR) and some less (coronary stents). A class of cholesterol lowering drugs had a big winner and a big loser. A supplement that many thought, based on observational studies, was crucial to prevent heart disease, turned out to be unhelpful. More evidence emerged that saturated fat is not a dietary villain.
From the skeptical cardiologist’s viewpoint, the following were the major scientific studies relevant to cardiology:
1. “Thousands of heart patients get stents that may do more harm than good”
Cardiologists have known for a decade (since the landmark COURAGE study) that outside the setting of an acute heart attack (acute coronary syndrome or ACS), stents don’t save lives and that they don’t prevent heart attacks.
Current guidelines reflect this knowledge, and indicate that stents in stable patients with coronary artery disease should be placed only after a failure of “guideline-directed medical therapy.” Despite these recommendations, published in 2012, half of the thousands of stents implanted annually in the US continued to be employed in patients with either no symptoms or an inadequate trial of medical therapy.
Yes, lots of stents are placed in asymptomatic patients. And lots of patients who have stents placed outside the setting of ACS are convinced that their stents saved their lives, prevented future heart attacks and “fixed” their coronary artery disease. It is very easy to make the case to the uneducated patient that a dramatic intervention to “cure” a blocked artery is going to be more beneficial than merely giving medications that dilate the artery or slow the heart’s pumping to reduce myocardial oxygen demands.
Stent procedures are costly in the US (average charge around $30,000, range $11,000 to $40,000) and there are significant risks including death, stroke and heart attack. After placement, patients must take powerful antiplatelet drugs which increase their risk of bleeding. There should be compelling reasons to place stents if we are not saving lives.
I, along with the vast majority of cardiologists, still recommended stents for those patients with tightly blocked coronary arteries and stable symptoms, which were not sufficiently helped by medications. ORBITA calls into question even this indication for stenting.
The ORBITA study investigators recruited 230 patients to whom most American cardiologists would have recommended stenting. These patients appeared to have a single tightly blocked coronary artery and had chest pain (angina) that limited their physical activity.
They treated the patients for 6 weeks with aspirin/statins/ and medications that reduce anginal symptoms such as beta-blockers, calcium-channel blockers or long-acting nitrates. At this point patients were randomized to receive either a stent or to undergo a catheteriation procedure which did not result in a stent, a so-called sham procedure.
The performance of a sham procedure was a courageous move that made the study truly double-blinded; neither the patients nor the investigators knew which patients had actually received a stent. Thus, the powerful placebo effects of having a procedure were neutralized.
Surprisingly, the study found that those patients receiving stents had no more improvement in their treadmill exercise time, angina severity or frequency or in their peak oxygen uptake on exercise.
ORBITA hopefully will cause more cardiologists to avoid the “oculo-stenotic” reflex wherein coronary artery blockages are stented without either sufficient evidence that the blockage is causing symptoms or that a medical trial has failed.
Although this was a small study with a very narrowly defined subset of patients, it raises substantial questions about the efficacy of coronary stenting. If ORBITA causes more patients and doctors to question the need for catheterization or stenting, this will be a very good thing.
2. Vitamin D Supplementation Doesn’t Reduce Cardiovascular Disease (or fractures, or help anything really).
One of my recurring themes in this blog is the gullibility of Americans who keep buying and using useless vitamins, supplements and nutraceuticals, thereby feeding a $20 billion industry that provides no benefits to consumers (see here and here).
Vitamin D is a prime player in the useless supplement market based on observational studies suggesting low levels were associated with increased mortality and cardiovascular disease
Despite well done studies showing a lack of benefit of Vitamin D supplementation, the proportion of people taking more than 1,000 IU daily of Vitamin D surged from just 0.3 percent in 1999-2000 to 18 percent in 2013-2014.
Most recently a nicely done study showed that Vitamin D supplementation doesn’t reduce the risk of heart disease.
In a randomized clinical trial that included 5108 participants from the community, the cumulative incidence of cardiovascular disease for a median follow-up period of 3.3 years was 11.8% among participants given 100 000 IU of vitamin D3 monthly, and 11.5% among those given placebo.
Aaron Carroll does a good job of summarizing the data showing Vitamin D is useless in multiple other areas in a JAMA forum piece:
Last October, JAMA Internal Medicine published a randomized, controlled trial of vitamin D examining its effects on musculoskeletal health. Postmenopausal women were given either the supplement or placebo for one year. Measurements included total fractional calcium absorption, bone mineral density, muscle mass, fitness tests, functional status, and physical activity. On almost no measures did vitamin D make a difference.
The accompanying editor’s note observed that the data provided no support for the use of any dose of vitamin D for bone or muscle health.
Last year, also in JAMA Internal Medicine, a randomized controlled trial examined whether exercise and vitamin D supplementation might reduce falls and falls resulting in injury among elderly women. Its robust factorial design allowed for the examination of the independent and joined effectiveness of these 2 interventions. Exercise reduced the rate of injuries, but vitamin D did nothing to reduce either falls or injuries from falls.
In the same issue, a systematic review and meta-analysis looked at whether evidence supports the contention that vitamin D can improve hypertension. A total of 46 randomized, placebo controlled trials were included in the analysis. At the trial level, at the individual patient level, and even in subgroup analyses, vitamin D was ineffective in lowering blood pressure.
Finally, if the Vitamin D coffin needs any more nails, let us add the findings of this recent meta-analysis:
calcium, calcium plus vitamin D, and vitamin D supplementation alone were not significantly associated with a lower incidence of hip, nonvertebral, vertebral, or total fractures in community-dwelling older adults.
3. PCSK9 Inhibitors: Really low cholesterol levels are safe and reduce cardiac events
I reported the very positive results for evolocumab and disappointing results for bosocizumab on the physician social media site SERMO in March but never put this in my blog.
As a practicing cardiologist I’ve been struggling with how to utilize the two available PCSK9 inhibitors (Amgen’s Repatha (evolocumab) and Sanofi’s Praluent (alirocumab) in my clinical practice. I would love to use them for my high risk statin-intolerant patients but the high cost and limited insurance coverage has resulted in only a few of my patients utilizing it.
The lack of outcomes data has also restrained my and most insurance companies enthusiasm for using them.
The opening session at this year’s American College of Cardiology Scientific Sessions in DC I think has significantly changed the calculus in this area with two presentations: the first showing Amgen’s “fully humanized” evolocumab significantly lowers CV risk in high risk patients on optimal statin therapy and the second showing that Pfizer’s “mostly humanized” bococizumab loses efficacy over time and will likely never reach the market.
The FOURIER study of evolocumab randomized 27, 564 high risk but stable patients who had LDL>70 with prior MI, prior stroke or symptomatic PAD to receive evolocumab or placebo on top of optimized lipid therapy. 69% of patients were recieving high intensity statin therapy and the baseline LDL was 92. LDL was reduced by 59% to average level of 30 in the treated patients. The reduction in LDL was consistent through the duration of the study.
IN 1/4 of the patients LDL was <20! These are unprecedented low levels of LDL.
Active treatment significantly reduced the primary endpoint by 15% and reduced the secondary endpoinf of CV death, MI, stroke by 20%. absolute difference 2% by 3 years.
There was no difference in adverse effects between placebo and Evo.
The next presentation featured data using Pfizer’s candidate in the PCSK9 wars and the acronym SPIRE (Studies of PCSK9 Inhibition and the Reduction in vascular Events (SPIRE) Bococizumab Development Program).
Paul Ridker presented the outcomes data for bococizumab which was actually similar to evolocumab data but given the declining efficacy and development of antibodies to the Pfizer drug over time these were very disappointing for Pfizer and I would presume their drug will never reach the market.
How will these results impact clinical practice?
I am now more inclined to prescribe evolocumab to my very high risk patients who have not achieved LDL< 70. I’m willing to do what I can to jump through insurance company hoops and try to make these drugs affordable to my patients.
I am less worried about extremely low LDL levels and have more faith in the LDL hypothesis: the lower the LDL the lower the risk of CV disease.
Cost is still going to be an issue for most of my patients I fear and the need for shared decision-making becomes even more important.
4. “Pure Shakes Up Nutritional Field: Finds High Fat Intake Beneficial.”
As one headline put it.
I recorded my full observations on this observational international study here
Here is a brief excerpt:
The Prospective Urban Rural Epidemiology (PURE) study, involved more than 200 investigators who collected data on more than 135000 individuals from 18 countries across five continents for over 7 years.
There were three high-income (Canada, Sweden, and United Arab Emirates), 11 middle-income (Argentina, Brazil, Chile, China, Colombia, Iran, Malaysia, occupied Palestinian territory, Poland, South Africa, and Turkey) and four low-income countries (Bangladesh, India, Pakistan, and Zimbabwe)
This was the largest prospective observational study to assess the association of nutrients (estimated by food frequency questionnaires) with cardiovascular disease and mortality in low-income and middle-income populations,
The PURE team reported that:
-Higher carbohydrate intake was associated with an increased risk of total mortality but not with CV disease or CV disease mortality.
This finding meshes well with one of my oft-repeated themes here, that added sugar is the major toxin in our diet (see here and here.)
I particular liked what the editorial for this paper wrote:
Initial PURE findings challenge conventional diet–disease tenets that are largely based on observational associations in European and North American populations, adding to the uncertainty about what constitutes a healthy diet. This uncertainty is likely to prevail until well designed randomised controlled trials are done. Until then, the best medicine for the nutrition field is a healthy dose of humility
I wish for all those following science-based medicine a healthy dose of humility. As science marches on, it’s always possible that a procedure we’ve been using might turn out to be useless (or at least much less beneficial than we thought), and it is highly likely that weak associations turn out to be causally nonsignificant. Such is the scientific process. We must continually pay attention, learn and evolve in the medical field.
Happy New Year to Be from the Skeptical Cardiologist the EFOSC!