Category Archives: Atherosclerosclerotic Cardiovascular Disease

Which Kind of Baby Aspirin Should I Take To Prevent Heart Attack? Chewable Versus Enteric Coated Versus Regular

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 US Preventive Services Task Force, on the other hand, recognizes certain individuals without heart disease who benefit from LDASA:

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?

Chewable Aspirin

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.

The most recent study showing this was published in 2017.

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.

Salicylically Yours,

-ACP

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.

Donald Trump Has Moderate Coronary Plaque: This Is Normal For His Age And We Already Knew It

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) .

Yesterday it was revealed by the White House doctor , Ronny Jackson, that Trump’s repeat score  was 133.

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.

Nonalarmingly Yours,

-ACP

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.

coronary calcium
Image from a patient with a large amount of calcium in the widowmaker or LAD coronary artery (LAD CA).

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.

Should You Take A Statin If You Are Over 75?: The Value of DeRisking in The Elderly

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

  1. 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.

Deriskingly Yours,

-ACP

Do You Need To Fast Before Your Cholesterol Test?

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.

A recent JACC article makes powerful arguments for using non fasting lipid profiles.

Rather than go through it in detail I’m going to post the “central illustration” which summarizes the authors points in graphic form.

The nonfasting profile is “evidence-driven” and also is time-efficient, patient, laboratory and physician-friendly.

So to my patients I say “you don’t need to fast before seeing me or prior to any blood work I order on you.”

To other patients whose physicians are still requiring fasting before a lipid profile I recommend challenging your doctor’s rationale.

If that doesn’t work, print out a copy of the above infographic and politely ask them to read the associated paper.

Hungrily  Yours,

-ACP

 

Top Skeptical Cardiology Stories of 2017

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”

Thus read the Vox headline for the ORBITA study which was published in November.

Indeed this was an earth-shattering study for interventional cardiologists, many of whom agreed with the NY Times headline “Unbelievable: Heart Stents Fail To Ease Chest Pain.”

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.

I’ve written previously (calcium supplements: would you rather a hip fracture or a heart attack) on the increased risk of heart attack with calcium supplementation.

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!

The skeptical cardiologist and his Eternal Fiancee marveling at the total eclipse of the sun (very accurately predicted by science) in St. Genevieve, Missouri

-ACP

 

Why Doesn’t The USA Have Graphic Warning Labels On Cigarette Packs Like The Netherlands?

While strolling the delightful (and typically debris-free) streets of Haarlem in The Netherlands the skeptical cardiologist espied an unusual cigarette pack on the ground.

In comparison to the typical American cigarette pack I noted a very prominent and disgusting picture of a leg which had been ravaged by peripheral artery disease.

The large print translates “smoking clogs your arteries.”

This is one of many potential warnings on Dutch cigarette packs. My favorite is

Roken kan leiden tot een langzame, pijnlijke dood

(Smoking can lead to a slow, painful death)

Perhaps, if such warning had been on American cigarette packs in the 1990s my mother would have been able to walk without severe pain in her legs (claudication) from the severe blockages caused by her decades of cigarette smoking.

When cigarette smoking patients tell me that “you have to die from something” I tell them that although they are greatly increasing their chance of dying from lung and cardiac disease, the smoking may not kill them but  leave them miserable and unable to walk or breath.

Experts on tobacco control note that these large, graphic and direct warnings are much more effective than the first small boxed warnings:

After the implementation of the first warning labels in 1966, the FTC’s 1981 report concluded that the original warning labels were not novel, overexposed and too abstract to remember and be personally relevant.46 Warning labels, like advertisements, wear out over time.47 Written warning labels wear out faster than graphic ones.48,49 In response, Congress passed a law mandating four rotating warnings. Studies on them began appearing in the late 1980s, demonstrating that several years after the implementation, those written labels on cigarette packs were also not noticed and not remembered by smokers and adolescents.5053 Since then, the diffusion and evolution of tobacco warning labels have been propelled by observational and experimental studies showing the effectiveness of large graphic warning labels in informing consumers about the health harms of smoking and reducing their smoking behavior.45,54

Here’s how Australia’s warnings have evolved

autralia-cigarette.jpg

 

 

 

 

 

 

 

In 2011 the US Congress passed legislation moving America towards such effective graphic warnings:

However, the law was challenged by Big Tobacco and has never been enacted. From the FDA site:

The Family Smoking Prevention and Tobacco Control Act requires the FDA to include new warning labels on cigarette packages and in cigarette advertisements. On June 22, 2011, the FDA published a final rule requiring color graphics depicting the negative health consequences of smoking to accompany the nine new textual warning statements. However, the final rule was challenged in court by several tobacco companies, and on Aug. 24, 2012, the United States Court of Appeals for the District of Columbia Circuit vacated the rule on First Amendment grounds and remanded the matter to the agency.[1] On Dec. 5, 2012, the Court denied the government’s petition for panel rehearing and rehearing en banc. In 2013, the government decided not to seek further review of the court’s ruling.

The FDA has been undertaking research related to graphic health warnings since that time.

[1] R.J. Reynolds Tobacco Co., et al., v. Food & Drug Administration, et al., 696 F.3d 1205 (D.C. Cir. 2012)

What Other Countries Are Doing

According to a Canadian Cancer Society report from late 2016,

More than 100 countries/jurisdictions worldwide have now required pictorial warnings, with fully 105 countries/jurisdictions having done so. This represents a landmark global public health achievement.

Increasingly, the United States stands alone, because of a constitutional doctrine privileging commercial speech above public health.

Here are the countries requiring pictorial warnings courtesy of that Canadian Cancer Society report.

And some of their warning pictures:

And this a picture that FDA would have required:

 

Skeptically Yours,

-AcP

Does Eating Saturated Fat Lower Your Risk of Stroke and Dying?: Humility and Conscience in Nutritional Guidelines

A study presented at the European Society of Cardiology  meetings in Barcelona and simultaneously published in The Lancet earlier this month caught the attention of many of my readers. Media headlines trumpeted  “Huge New Study Casts Doubt On Conventional Wisdom About Fat And Carbs” and “Pure Shakes Up Nutritional Field: Finds High Fat Intake Beneficial.”

Since I’ve been casting as much doubt as possible on the  conventional nutritional wisdom  to cut saturated fat, they reasoned, I should be overjoyed to see such results.

What Did the PURE Study Find?

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.)

Higher fat intake was associated with lower risk of total mortality.

Each type of fat (saturated, unsaturated, mono unsaturated ) was associated with about the same lower risk of total mortality. 

 

These findings are consistent with my observations that it is becoming increasingly clear that cutting back on  fat and saturated fat as the AHA and the Dietary Guidelines for Americans have been telling you to do for 30 years is not universally helpful (see here and  here ).

When you process the fat out of dairy and eliminate meat from your diet although your LDL (“bad”) cholesterol drops a little your overall cholesterol (atherogenic lipid) profile doesn’t improve (see here).

Another paper from the PURE study shows this nicely and concluded:

Our data are at odds with current recommendations to reduce total fat and saturated fats. Reducing saturated fatty acid intake and replacing it with carbohydrate has an adverse effect on blood lipids. Substituting saturated fatty acids with unsaturated fats might improve some risk markers, but might worsen others. Simulations suggest that ApoB-to-ApoA1 ratio probably provides the best overall indication of the effect of saturated fatty acids on cardiovascular disease risk among the markers tested. Focusing on a single lipid marker such as LDL cholesterol alone does not capture the net clinical effects of nutrients on cardiovascular risk.

Further findings from PURE:

-Higher saturated fat intake was associated with a lower risk of stroke

-There was no association between total fat or saturated fat or unsaturated fat with risk of heart attack or dying from heart disease.

Given that most people still believe that saturated fat causes heart disease and are instructed by most national dietary guidelines to cut out animal and dairy fat this does indeed suggest that

Global dietary guidelines should be reconsidered …”

Amen!

Because the focus of dietary guidelines on reducing total and saturated fatty acid intake “is largely based on selective emphasis on some observation and clinical data despite the existence of several randomizesed trials and observational studies that do not support these conclusions.”

Pesky Confounding Factors

We cannot infer causality from PURE because like all obervational studies, the investigators do not have control over all the factors influencing outcomes. These confounding factors are legion in a study that is casting such a broad net across different countries with markedly different lifestyles and socioeconomic status.

The investigators did the best job they could taking into account household wealth and income, education, urban versus rural location and the effects of study centre on the outcomes.

In an accompanying editorial, Christopher E Ramsden and Anthony F Domenichiello, prominent NIH researchers,  ask:

“Is PURE less confounded by conscientiousness than observational studies done in Europe and North American countries?

 

“Conscientiousness is among the best predictors of longevity. For example, in a Japanese population, highly and moderately conscientious individuals had 54% and 50% lower mortality, respectively, compared with the least conscientious tertile.”

“Conscientious individuals exhibit numerous health-related behaviours ranging from adherence to physicians’ recommendations and medication regimens, to better sleep habits, to less alcohol and substance misuse. Importantly, conscientious individuals tend to eat more recommended foods and fewer restricted foods.Since individuals in European and North American populations have, for many decades, received in influential diet recommendations, protective associations attributed to nutrients in studies of these populations are likely confounded by numerous other healthy behaviours. Because many of the populations included in PURE are less exposed to in influential diet recommendations, the present findings are perhaps less likely to be confounded by conscientiousness.”

It is this pesky conscientiousness factor (and other unmeasured confounding variables) which limit the confidence in any conclusions we can make from observational studies.

I agree wholeheartedly with the editorial’s conclusions:

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.

 

Ah, if only the field of nutrition had been injected with a healthy dose of humility and a nagging conscience thirty years ago when its experts declared confidently that high dietary fat and cholesterol consumption was the cause of heart disease.!

Current nutritional experts and the guidelines they write will  benefit from a keen awareness of the unintended consequences of recommendations which they make based on weak and insufficient evidence  because such recommendations influence the food choices  (and thereby the quality of life and the mechanisms of death) of hundreds of millions of people.

PUREly Yours,

ACP

Do Statins Cause Memory Loss? The Science, The Media, The Statin-Denialist Cult, and The Nocebo Effect

The Skeptical Cardiologist was recently contacted by a television reporter  working on a segment about statins. and looking for a cardiologist to interview who “is concerned about the cognitive side effects of these drugs.”

Since I regularly prescribe statin drugs to my patients to reduce their risk of heart attack and stroke,  I am very concerned about any possible side effects from them, cognitive or otherwise. However, in treating hundreds of patients with statins, I have not observed a consistent significant effect on brain function.

When the U.S. Food and Drug Administration (FDA) issued a statement in 2012 regarding rare postmarketing reports of ill-defined cognitive impairment associated with statin use it came as quite a surprise to most cardiologists.

The FDA made a change in the patient information on all statin drugs which stated:

Memory loss and confusion have been reported with statin use. These reported events were generally not serious and went away once the drug was no longer being taken

This FDA statement was surprising because prior observational and randomized controlled trials had suggested that patients who took statins were less likely to have cognitive dysfunction than those who didn’t.

Early studies implied that statins might actually protect against Alzheimer’s disease.

In fact these signals triggered two studies testing if statins could slow cognitive decline in patients with established Alzheimer’s disease  One study used 80 mg atorvastatin versus placebo and a second 40 mg simvastatin versus placebo and both showed no effect on the decline of cognitive function over 18 months.

More recently, multiple reviews and meta-analyses have examined the data and concluded that there is no significant effect of statins on cognitive function. Importantly, these have been written by reputable physician-scientists with no financial ties to the pharmaceutical industry.

 

Data Show No Evidence of Causality Despite Case Reports

The FDA added the warning to statin patient information based on case reports  Occasional reports of patients developing memory loss on a statin do not prove that statins are a significant cause of cognitive dysfunction.

Case reports have to  be viewed in the context of all the other scientific studies indicating no consistent evidence of negative effects of the statins. Case reports are suspect for several reasons:

First, patients receiving statins are at increased risk for memory loss because of associated risk factors for atherosclerosis and advancing age. A certain percentage of such patients are going to notice memory loss independent of any medications.

Second. The nocebo effect: If a patient taking a statin is told that the drug will cause a particular side effect,that patient will be more likely to notice and report that particular side effect.

A recent study in The Lancet looked at reported side effects in patients taking atorvastatin versus placebo and found substantial evidence for the nocebo effect.

Analysis of the trial data revealed that when patients were unaware whether they were taking a statin or a placebo, the number of side effects reported was similar in those taking the statin and those taking placebo. However, if patients knew they were taking statins, reports of muscle-related side effects in particular increased dramatically, by up to 41 per cent.

Third, a review of the FDA post-marketing surveillance data showed the rate of memory loss with statins is not significantly higher than for other non-statin cardiovascular medications (1.9 per million prescriptions for statins , 1.6 per million prescriptions for losartan) and clopidogrel (1.9 per million prescriptions for clopidogrel.)

What Most Media Prefer: Controversy And Victims

I thought my experience and perspective on statins and cognitive function might be useful for a wider audience of patients to hear so I agreed to be interviewed. After I expressed interest the  reporter responded:

I would like to interview you and also a person who has experienced memory and/or thinking problems that they attribute to statin use.  
 I responded with “let me see what I can find,”  although I was concerned that  this reporter was searching for a cardiologist to support attention-grabbing claims of  severe side effects of statins rather than seeking a balanced, unbiased perspective from a knowledgeable and experienced cardiologist.
If I produced a “victim” of statin-related memory loss this would boost ratings.
I then began racking my brain to come up with a patient who had clearly had statin-related memory loss or thinking problems. I asked my wonderful MA Jenny (who remembers details about patients that I don’t) if she could recall any cases. Ultimately, we both came up without any patients for the interview. (Any patient of mine reading this with definite statin memory loss please let me know and I will amend my post. However, I won’t be posting anecdotes outside of my practice.)
I have had a few patients relate to me that they feel like their memory is not as good as it was and wonder if it could be from a medication they are on.  Invariably, the patient has been influenced by one of the  statin fear-mongering sites on the internet (or a friend/relative who has been influenced by such a site.)
I wrote about one such site in response to a patient question a while back:
The link appears to be a promotional piece for a book by Michael Cutler, MD. Cutler’s website appears to engage in fear-mongering with respect to statins for the purpose of selling his books and promoting his “integrative” practice. I would refer you to my post entitled “functional medicine is fake medicine”. Integrative medicine is another code word for pseudoscientific medicine and practitioners should be assiduously avoided.
The piece starts with describing the case of Duane Graveline, a vey troubled man who spent the latter part of his life attempting to scare patients from taking statins. Here is his NY Times obituary.
You can judge for yourself if you want to base decisions on his recommendations.
There is no scientific evidence to suggest statins cause dementia.
An Internet-Driven Cult With Deadly Consequences
Steve Nissen recently wrote an eloquent article which accuses statin deniers of  being  an “internet–driven cult with deadly consequences.”  Nissen has done extremely important research helping us better understand atherosclerosis  and is known for being a patient advocate: calling out drug companies when they are promoting unsafe drugs.
I have immense respect for his honesty, lack of bias, and his courage to be outspoken .  He writes:

“Statins have developed a bad reputation with the public, a phenomenon driven largely by proliferation on the Internet of bizarre and unscientific but seemingly persuasive criticism of these drugs. Typing the term statin benefits into a popular Internet search en- gine yields 655 000 results. A similar search using the term statin risks yields 3 530 000 results. One of the highest-ranking search results links to an article titled “The Grave Dangers of Statin Drugs—and the Surprising Benefits of Cholesterol”. We are losing the battle for the hearts and minds of our patients to Web sites de- veloped by people with little or no scientific expertise, who often pedal “natural” or “drug-free” remedies for elevated cholesterol levels. These sites rely heavily on 2 arguments: statin denial, the proposition that cholesterol is not related to heart disease, and statin fear, the notion that lowering serum cholesterol levels will cause serious adverse effects, such as muscle or hepatic toxicity— or even worse, dementia.”

He goes on to point out that this misinformation is contributing to a low rate of compliance with taking statins. Observational studies suggest that noncompliance with statins significantly raises the risk of death from heart attack.

The reasons for patient noncompliance, Nissen goes on to say, can be related to the promotion of totally unproven supplements and fad diets as somehow safer and more effective than statin therapy:

“The widespread advocacy of unproven alternative cholesterol-lowering therapies traces its origins to the passage of the Dietary Supplement Health and Education Act of 1994 (DSHEA). Incredibly, this law places the responsibility for ensuring the truthfulness of dietary supplement advertising with the Federal Trade Commission, not the U.S. Food and Drug Administra-tion. The bill’s principal sponsors were congressional representatives from states where many of the companies selling supplements are headquartered. Nearly 2 decades after the DSHEA was passed, the array of worthless or harmful dietary supplements on the market is staggering, amounting to more than $30 billion in yearly sales. Manufacturers of these products commonly imply benefits that have never been confirmed in formal clinical studies.”

Dealing With Statin Side Effects In My Practice

When a patient tells me they believe they are having a side effect from the statin they are taking (and this applies to any medication they believe is causing them side effects), I take their concerns very seriously. After 30 years of practice, I’ve concluded that in any individual patient, it is possible for any drug to cause  side effects.  And, chances are that if we don’t address the side effects the patient won’t take the medication.

If the side effect is significant I will generally tell the patient to stop the statin and report to me how they feel after two to four weeks.

If there is no improvement I have the patient resume the medication and we generally reach a consensus that the side effect was not due to the medication.

If there is a significant improvement, I accept the possibility that the side effect could be from the drug. This doesn’t prove it, because it is entirely possible that the side effect resolved for other reasons coincidentally with stopping the statin. Muscle and joint aches are extremely common and they often randomly come and go.

At this point, I will generally recommend a trial at low dose of another statin (typically rosuvastatin or livalo.)  If the patient was experiencing muscle aches and they return we are most likely dealing with a patient with statin related myalgias. However, most patients are able to tolerate low dose and less frequent administration of rosuvastatin or Livalo.

For all other symptoms, it is extremely unusual to see a return on rechallenge with statin and so we continue statin long term therapy.

Today a patient told me he thought the rosuvastatin we started 4 weeks ago was causing him to have more diarrhea. I informed him that there is no evidence that rosuvastatin causes diarrhea more often than a placebo and had no reason based on its chemistry to suspect it would. (Although I’m sure there is a forum somewhere on the internet where patients have reported this). Fortunately he accepted my expert opinion and will continue taking the drug.

If the symptoms persist and the patient continue to believe it is due to the statin, we will go through the process I described above. And, since every patient is unique, it is possible that my patient is having a unique or idiosyncratic reaction to the statin that only occurs in one out of a million patients and thus is impossible to determine causality.

Since statins are our most effective and best tolerated weapon in the war against our biggest killer, it behooves both patients and physicians to have a high threshold  for stopping them altogether. Having such a high threshold means filtering out the noise from attention-seeking media and the internet-driven denials cult thus minimizing the nocebo effect

Antinocebonically Yours

-ACP

N.B. It turns out the reporter had an open mind about the issue of statin-related memory loss. We had a good discussion  and at some point you may see the skeptical cardiologist on TV being interviewed on the topic.

I could bring to the interview one of  my many patients who since starting to take statins have  not had a heart attack or stroke and who have taken statins for decades without side effects.

Now that would make for some compelling and exciting TV!

For a nice discussion of Nissen’s article see Larry Husten’s excellent piece at Cardiobrief.org here (/nissen-calls-statin-denialism-a-deadly-internet-driven-cult/)

 

Unsure About Taking A Statin For High Cholesterol? Consider A Compromise Approach

In an earlier post the skeptical cardiologist introduced Geo, a 61 year old male with no risk factors for heart attack or stroke other than a high cholesterol. His total cholesterol was 249, LDL (bad) 154, HDL (good) 72 and triglycerides 116.

His doctor had recommended that he take a statin drug but Geo balked at taking one due to concerns about side effects and requested my input. My first steps were to gather more information.

-I calculated his 10 year risk of stroke or heart attack at 8.4% (treatment with statin typically felt to benefit individuals with 10 year risk >7.5%) and as I have previously noted, this is not unusual for a man over age 60.

-I assessed him for any hidden  or subclinical atherosclerosis and found

The vascular ultrasound showed below normal carotid thickness and no plaque and his coronary calcium score was 18,  putting him at the 63rd  percentile. This is slightly higher than average white men his age.

So Geo definitely has atherosclerotic plaque in his coronary arteries. This puts him at risk for heart attack and stroke but not a lot higher risk than most men his age.

Strictly speaking, since he hasn’t already had a heart attack or stroke, treating him with a statin is a form of primary prevention. However, we know that atherosclerotic plaque has already developed in his arteries and at some point, perhaps years from now it will have consequences.

What is the best approach to reduce Geo’s risk?

It’s essential  to look closely at lifestyle changes in everyone to reduce cardiac risk.

The lifestyle components that influence risk are

  1. Cigarette Smoking (by far the strongest)
  2. Diet
  3. Exercise
  4. Obesity (Obviously related to #1 and #2)
  5. Stress
  6. Sleep

Patients who try to change to what they perceive as a heart healthy diet by switching to non-fat dairy and eliminating all red meat will not substantially lower risk (see here.) Even if you are possess the rock-hard discipline to stay on a radically low fat diet like the Esselstyn diet or the Pritikin diet there are no good data supporting their  efficacy in preventing cardiac disease.

Geo was not far from theMediterranean diet I recommend but would probably benefit from increased veggie and nut consumption. He was not overweight and he doesn’t smoke. I encouraged him to engage in 150 minutes of moderate exercise weekly.

Low Dose, Intermittent Rosuvastatin

I engaged in shared decision-making with Geo.  Informing him, as best I could, of the potential side effects and benefits of statin therapy.

After a long discussion we decided to try a compromise between no therapy and the guideline recommended moderate intensive dose statin therapy.

This approach utilizes a low dose of rosuvastatin taken intermittently with the goal of minimizing any statin side effect but obtaining some of the benefits of statin drugs on  cardiovascular risk reduction.

I have many patients who have been unable to tolerate other statin drugs in any dosage due to statin related muscle aches but who tolerate this particular  treatment and I  see substantial reductions in the LDL (bad) cholesterol with this approach.

Studies have shown that rosuvastatin 5–10 mg or atorvastatin 10–20 mg given every other day produce LDL-C reduction of 20–40 %

Studies have also shown that In patients with previous statin intolerance, rosuvastatin administered once or twice weekly (at a mean dose of 10 mg per week) achieved an LDL-C reduction of 23–29% and was well tolerated by 74–80 % of patients.

In a recent report from a specialized lipid clinic, 90 % of patients referred for intolerance to multiple statins were actually able to tolerate statin therapy, although the majority was at a reduced dose and less-than-daily dosing.

Results in Geo

After several months of taking 5 mg rosuvastatin twice weekly Geo felt fine with no discernible side effects. He obtained repeat cholesterol  levels:

His LDL had dropped 52% from 140 to 92.

Hopefully, this LDL reduction plus the non-cholesterol lowering beneficial properties of statins (see here) will substantially lower Geo’s risk of heart attack and stroke.

We need randomized studies testing long-term outcomes using this approach to make it evidence-based. But in medicine we frequently don’t have studies that apply to  specific patient situations. In these cases shared decision-making in order to find solutions that fit the individual patient’s concerns and experience becomes paramount.

Faithfully Yours,

-ACP

 

 

 

What Can We Learn About Heart-Healthy Lifestyle From The Tsimane People of the Amazon Rainforest ?

The skeptical cardiologist has been in Washington, DC attending the Scientific Sessions of the American College of Cardiology for the last three days in an attempt to upgrade his cardiology knowledge and obtain CMEs for all the various areas he needs CME (echo/nuclear/CT/vascular).

I’ve written some posts for SERMO, a physician social media site,  on interesting presentations from the meeting.

Here’s my take on one paper (published simultaneously in The Lancet) that is of general interest:

I’m a big advocate of coronary artery calcium (CAC) scans for helping make decisions on individual patients with intemediate risk for CAD. Several speakers at this year’s American College of Cardiology Meetings presented convincing data supporting this approach, providing more information to get patients off the fence about taking statins.

However, CAC apparently would be a useless test in the Tsimane (pronounced chee-MAH-nay) people according to a study presented at  the ACC meeting and published simultaneously in The Lancet.

Researchers performed CT scans on 700 of  these “forager-horticulturalist”  people, indigenous to the Bolivian Amazon Rainforest and found very little calcium suggesting that they have an amazingly low rate of atherosclerosis compared to we who have to live in the industrialized world.

Obviously CT scanners are not portable so the Tsimane traveled by river and jeep from the Amazon rainforest to Trinidad, a city in Bolivia and the nearest city with a CT scanner. It took tribe members one to two days to reach the nearest market town by river, and then another six hours driving to reach Trinidad.

85% of the Tsimane people studied had CAC scores of 0. In those over age 75 years, 65% had CAC scores of 0, and just four individuals in their 80s had moderately elevated CAC (> 100). The incidence of CAC > 100 in the entire Tsimane population was 3%, which is about one tenth the prevalence in a matched industrialized population. In addition, incidences of obesity, hypertension, high glucose concentrations, and cigarette smoking were rare overall.

The Tsimane live a subsistence lifestyle that includes hunting, gathering, fishing, and farming. They don’t eat at McDonalds and the men spend almost 7 hours pers day on physical labor. Their diet consists mostly of unprocessed fiber-rich carbohydrates with rice, plantain, manioc, corn, wild nuts, and fruit composing their staples. Fat consumption is 9% of calories versus 23% in the U.S.

Supporters of plant-based diets, of course, seized on these data to support the unsubstantiated claim that meat and dairy consumption is the main cause of atherosclerosis in western civilization.

Hillard Kaplan, one of the authors and a Professor of anthropology at the University of New Mexico said:

 “Their lifestyle suggests that a diet low in saturated fats and high in non-processed fibre-rich carbohydrates, along with wild game and fish, not smoking and being active throughout the day could help prevent hardening in the arteries of the heart. The loss of subsistence diets and lifestyles could be classed as a new risk factor for vascular aging and we believe that components of this way of life could benefit contemporary sedentary populations.”

However, the real cause of the low levels of coronary artery calcification in the Tsimane remains a mystery because this kind of observational study cannot establish causality. Perhaps it is the 17,000 steps a day that they walk  engaging in foraging and horticulturalism. Could it be due to the absence of processed food and added sugar? The Tsimane have high levels of parasitic infections: perhaps that is protecting them.

Of two things I am certain:

-The Tsimane don’t need statins.

-I prefer my lifestyle to munching on manioc and foraging all day.

Semihorticulturally Yours,

-ACP