Tag Archives: heart attack

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

 

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/)

 

What Pain Medications Are Safe For My Heart?

The skeptical cardiologist is frequently asked by patients if it is OK to take certain pain medications.

Yesterday, I got a variation on this  when a patient called and indicated that he had been prescribed meloxicam and tramadol by his orthopedic surgeon for arthritic leg joint pain. The orthopedic surgeon said to check with me to see if it was OK to take either of these medications. (Patients, if you want to skip to my answer skip down to the last two sections of the post and avoid the background information.)

What Is The Risk Of Pain Medications?

Cardiologists have been concerned about the increased risk of heart attack and heart failure with non steroidal anti-inflammatory drugs (NSAIDs) since Vioxx was withdrawn from the market in 2004.

NSAIDS have long been known to increase risk of gastrointestinal (GI) bleeding  by up to 4-5 fold, Scientists developed Vioxx, a COX-2 inhibitor, hoping to reduce that risk but Vioxx  turned out to  increase the risk of heart attack.

Since this revelation it has become clear that NSAIDS in general increase the risk of heart problems as well as GI problems

This includes the two over the counter (OTC) NSAIDS:

-ibuprofen (in the US marked most commonly as Motrin or Advil, internationally known as Nurofen). For extensive list of brand names see here.

-naproxen (most commonly sold as Aleve. Per wikipedia “marketed under various brand names, including: Aleve, Accord, Anaprox, Antalgin, Apranax, Feminax Ultra, Flanax, Inza, Maxidol, Midol Extended Relief, Nalgesin, Naposin, Naprelan, Naprogesic, Naprosyn, Narocin, Pronaxen, Proxen, Soproxen, Synflex, MotriMax, and Xenobid. It is also available bundled with esomeprazole magnesium in delayed release tablets under the brand name Vimovo.)

In 2015  the FDA mandated  warning labels on all prescription NSAIDs including

1) a “black box” warning highlighting the potential for increased risk for cardiovascular  (CV) events and serious life-threatening gastrointestinal  bleeding, ulceration, and perforation;

(2) statements indicating patients with, or at risk for, CV disease and the elderly may be at greater risk, and that these reactions may increase with duration of use;

(3) a contraindication for use after coronary artery bypass graft surgery on the basis of reports with valdecoxib/parecoxib;

(4) language that the lowest dose should be used for the shortest duration possible

5) wording in the warning section that there is no evidence that the concomitant use of aspirin with NSAIDs mitigates the CV risk, but that it does increase the GI risk

Since then, hardly a day goes by without me having a discussion with a patient about what drugs they can safely take for their arthritis.

A reasonable approach to using NSAIDS, balancing GI and CV risks, that I have used in the past comes from a 2014 review
This table and many authorities recommend naproxen as the NSAID of choice for patients with high CV risk.

Indeed prior to the publication of the PRECISION study in 2016 I believed that naproxen was the safest NSAID for my cardiac patients. I told them it was OK to use from a CV standpoint but to use the least amount possible for the shortest time in order to minimize side effects.

The PRECISION study compared a COX-2 NSAID (celecoxicib or Celebrex) to ibuprofen and naproxen in patients who required NSAIDS for relief of their joint pain.

The findings:

cardiovascular death (including hemorrhagic death), nonfatal MI, or nonfatal stroke, occurred in 2.3% of celecoxib-treated patients, 2.5% of the naproxen-treated patients, and 2.7% of the ibuprofen group.

There was no placebo in this trial so we can only look at relative CV risk  of the three NSAIDS and it did not significantly differ.

GI bleeding was less with celecoxib than the other two NSAIDS.

Although this study has flaws it throws into question the greater CV safety of naproxen and suggests that all NSAIDS raise CV risk.

My Current Patient Advice on Cardiac Safety of Pain Meds

Here is an infographic I came across from the Arthritis Foundation (complete PDF….here)

It’s a reasonable approach for these OTC drugs and I will start handing this out to my patients.

We should consider that all NSAIDS have the potential for increasing the risk of heart attack and heart failure, raising blood pressure, worsening renal function and causing GI bleeding.

Therefore, if at all possible avoid NSAIDS.

Acetaminophen (Tylenol) is totally safe from a heart standpoint and overall if you don’t have liver disease it is your safest drug for arthritis. However, it provides no anti-inflammatory effects and often is inadequate at pain relief.

Treating The Whole Patient

Meloxicam is an NSAID so my patient should , if at all possible, avoid it.

The other drug he was prescribed, tramadol, is an opiod. Opiods have their own set of problems including, most importantly,  addiction and abuse.

A recent review concluded

 reliable conclusions about the effectiveness of long-term opioid therapy for chronic pain are not possible due to the paucity of research to date. Accumulating evidence supports the increased risk for serious harms associated with long-term opioid therapy, including overdose, opioid abuse, fractures, myocardial infarction, and markers of sexual dysfunction; for some harms, the risk seems to be dose-dependent.

As his cardiologist I am concerned about his heart, of course, but a good cardiologist doesn’t just focus on one organ, he looks at what his recommendations are doing to the whole person.

I certainly don’t want to have him become addicted to narcotics in order to avoid a slightly increased risk of a heart attack. On the other hand, the risks of the NSAIDS involve multiple organs, most of which don’t fall in the domain of the cardiologist.

My patient’s risk of taking either the meloxicam or the tramadol is best assessed by his primary care physician, who has the best understanding of his overall medical condition and the overall risk of dangerous side effects from these drugs.

Ultimately, I think the decision of which pain pill to take for chronic arthritis has to be made by an informed patient in discussion with his  informed (and informative) primary care physician. Only the patient can decide how much pain he is having and how much risk he/she wants to assume in relieving that pain.

Analgesically Yours,

-ACP

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

 

 

 

More Incredibly Bad Science From Dr. Esselstyn’s Plant-Based (Vegan) Diet Study

A while back the skeptical cardiologist exposed “The incredibly bad science behind Dr. Esselstyn’s plant-based diet.

The diet has the catchy slogan “eat nothing with a face or a mother” and Esselstyn was featured in the vegan propaganda film “Forks Over Knives.”

After detailing the lack of science I concluded:

Any patients who were not intensely motivated to radically change their diet would have avoided this crazy "study" like the plague.

This "study" is merely a collection of 18 anecdotes, none of which would be worthy of publication in any current legitimate medical journal.

Three of the 18 patients have died, one from pulmonary fibrosis, one presumably from a GI bleed, and one from depression. Could these deaths be related to the diet in some way? We can't know because there is no comparison group.

The post garned little attention initially but in the last few months several hundred visitors per day apparently read it and Essesltyn followers have started leaving me testimonials to the diet along with nasty comments.

Here’s are some typical ones (with my comments in red)

“If your (sic) not backed by some meat industry or cardiac bypass group I would be much surprised.”

I am completely free of bias. Nobody is paying me anything to do the research and writing I do. My only purpose is to find the truth about diet in order to educate my patients properly. I have  saved many more patients from bypass surgery than I have referred for the procedure.

“it is so arrogant to think the only science could come from clinical studies which may be funded by an interested party.”

Doctors like randomized (and preferably blinded) clinical studies because they minimize the bias introduced by interested parties like patients and zealous investigators (like Dr. E)  motivated to see positive outcomes. Small, non-randomized studies can only generate ideas and hypotheses which larger, randomized studies can prove with a greater degree of certainty.

“the entire nentire western medical system is skewed due to the big pharma influence…unfortunately western medicine believes the only science is the pen and the scalpel..whereas …history is the best teacher of all…”

By pen I assume you mean medications. If we examine history as  you suggest we see that life expectancy was 50 years in 1945  but today in developed countries it is around 80 years. This advance corresponds to (among other things) advances in vaccines, antibiotics, anti-cancer drugs, cardiac and blood pressure medications and surgery: the pen and the scalpel. It does not correspond to following a vegan diet.

“Your foolishness is the embarrassment.”

Thank you for this insightful comment! I’m considering it as my epitaph.

One man felt that changing to the Esselstyn diet dramatically improved his cardiac situation and commented:

“Nothing like bashing something that works just because you want to eat meat. .”

I do enjoy meat in moderation but I also really enjoy vegetables, nuts, fish, legumes, olive oil and avocados. I looked into Esselstyn’s diet in detail because it stands out as particularly misguided in banning nuts, avocados, fish and olive oil to heart patients.

..”.So sicking (sic) to see people talk trash about something that works so well… It saved my life…”

I’m happy you are doing well with your cardiac condition but it is impossible to know what would have happened to you on a more reasonable diet such as the Mediterranean diet (which actually has legitimate scientific studies supporting it). And again criticizing Esselstyn’s ideas and “study” can hardly be considered trash talk.

“I personally have followed dr. esselstyn’s program for what will be 5 years in 11/17 and have made tremendous gains in my cardio pulmonary function….my cardiologist looks at me in wonder…why are you here? and often says , if everyone did what you have…Id be out of business…so…isnt that telling and sad?”

I’m glad you’re doing well with the program, most patients can’t follow this kind of diet for more than a few months.  But perhaps we shouldn’t judge its effectiveness until  we make sure you don’t suffer a heart attack next week. Your cardiologist is wrong: see what I wrote about “dealing with the cardiovascular cards you’ve been dealt.” Some individuals inherit genes that guarantee progressive and accelerated atherosclerosis that will kill them at an early age despite the best lifestyle.

“…the phrase “follow the money” comes to mind…and since theres no big money to be made….science will attempt to dispell the results and thousands of years of history that proves this dietary system works…”

Using a scientific approach to analyze Esselstyn’s diet (which tries to claim a scientific basis) seemed appropriate to me but I wasn’t motivated by money. I’m looking for what is best for my patients, pure and simple.

The Plural of Anecdote Is Not Data

One man wrote:

“But since this is only anecdotal evidence – it must be junk science…”

Esseslstyn devotees like to post what their personal experience is with the diet but as skeptical medicine has pointed out “the plural of anecdote is not data.” 

One woman described in detail a good response her husband had after starting the diet following a heart attack:

I’m concerned about the skeptical cardiologist going after the person of dr. Esselstyn versus the science, such as quoting how you States dr. Esselstyn came up with the diet. So there may be a personal bias there. I’m sure there are more people out there on the esselstyn diet that are not noted in the study years ago. I hope there is another book coming out

I’ve reviewed in detail my comments about how Esselstyn came up with the diet but I am at a loss to find any ad hominem attack.

This woman went on to say

We will keep you posted, as my husband is willing to get another cardiac Cath and 12 months to visually see the difference after the diet.

I have to point out that if his cardiologist performs a cardiac cath (which carries risks of stroke, heart attack and death) for the sole purpose of checking the effect of the diet he is engaging in unethical medical behavior and likely insurance fraud. By the way, I hope that your husband is on a statin like most of Dr. Esselstyn’s are!:)

and a man wrote

Calling Essylstein ilk shows a little too much biased hatred on your part

Please note the definition of ilk “a type of people or things similar to those already referred to.” No pejorative there. And no ad hominem attack.  I wrote:

 It is possible that the type of vegan/ultra-low fat diets espoused by Esselstyn and his ilk have some beneficial effects on preventing CAD, but there is nothing in the scientific literature which proves it.

I should be able to criticize the methods and ideas of Dr. E without it being considered an attack on his person

Completely wrong. Esselstyn has saved my life. His book explains it all, how the endothelium cells get ruined, inflammation … heart attack proof (his words). One does not continue as head of the Cleveland Wellness Center if one is a quack.

Words are easy to come by on the interweb but Dr. E’s are not supported by science and as for the “Cleveland Wellness Center” it is probably not wise to get me started. Dr. E ‘s program is listed as being part of the Cleveland Clinic Wellness Center which is an attempt to capitalize on the market for pseudoscientific enterprises. He is not the director. The director recently came under intense criticism for promoting anti vaccine quackery. (See here).

The Wellness Center promotes so-called functional, integrative, complementary and alternative approaches. (Functional medicine is fake medicine!) These are approaches that have not been proven to work and could arguably be called quackery. (Let me be clear, however, I am not calling Dr. Esselstyn a quack but the fact that he is part of the Wellness Center does not add any scientific validity to his work.)

“I’m sure there are more people out there on the esselstyn diet that are not noted in the study years ago. I hope there is another book coming out”

Fake News, Fake Science

As a matter of fact, Dr. E has been hard at work over the last 30 years and has added a grand total of 176 patients who are considered “adherent” to the diet: about 6 per year. The “original research” was published in The Journal of Family Practice in 2014. Unfortunately the bad science present in the original publication has only been amplified.

In addition to any randomization or suitable control group for comparison, the data collection techniques are unacceptable:

“In 2011 and 2012 we contacted all participants by telephone to gather data. If a participant had died, we obtained follow-up medical and dietary information from the spouse, sibling, off-spring or responsible representative.”

In other words, there was no actual systematic review of medical records, autopsies or death certificates, just word of mouth from whomever answered the phone.

“Patients who avoided all meat, fish, dairy, and knowingly, any added oils throughout the program were considered adherent.”

Imagine, if you will, that your husband died 10 years ago and you received a call from Dr. E’s office or perhaps Dr. E himself and he asks you if your husband “avoided all meat, fish, dairy and added oils.”  For one thing, it would be very difficult for you to answer that question with any degree of accuracy: was your husband cheating on Dr. E’s diet when you weren’t looking, do you remember his entire diet from 10 years ago?

For another thing, you know that the caller has an agenda. If your husband died of a heart problem the caller is not going to be happy until he/she gets you to admit that your husband had some guacamole on Cinco de Mayo in 2002. If he’s alive and doing well, the caller is likely to be satisfied with a simple answer that , yes, he’s following the diet.

Yes, we have more data from Dr. E but it turns out to be even more incredibly bad than the first lot.

Let the anecdotes and ad hominem attacks begin!

-ACP

Are You On The Fence About Taking A Statin Drug?

The father of the eternal fiancee’ of the skeptical cardiologist (FOEFOSC, let’s call him “Geo”) is a typical 61 year old white male. A year ago his primary care physician informed him that he needed to start taking a statin drug because his cholesterol was high. The note accompanying this recommendation also stated “work harder on diet and exercise to get LDL<130.”  No particulars on how to change his current diet and exercise program were provided.

Neither of Geo’s parents and none of his siblings have had heart problems at an early age and Geo is very active without any symptoms. His diet is reasonably free of processed food and added sugar, he is not overweight and his blood pressures are fine. Due to concern about side effects he had read about on the internet and because he doesn’t like taking medications , Geo balked at taking the recommended statin,

Reluctance to start a new and likely life-long drug is understandable especially when combined with a constant stream of internet-based bashing of statins.

My advice was sought and I suggested a few things that would be helpful in making a more informed decision:

-Calculate Geo’s 10 year risk of heart attack and stroke using the ACC ASCVD Risk estimator app.

-Assess for early or advanced build-up of atherosclerotic or fatty plaque in the carotid arteries (vascular ultrasound) and coronary arteries (coronary calcium scan).

As I’ve pointed out before (here), the vast majority of men over the age of 60 move into a 10 year risk category >7.5%, no matter how great their lifestyle is, and Geo was no exception with a risk of 8.4%. His total cholesterol was 249, LDL (bad) 154, HDL (good) 72 and triglycerides 116.

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.

When Geo presented these findings to his PCP, he seemed unaware of the ASCVD risk estimator (recommended by AHA/ACC guidelines first published in 2013), which no longer suggests LDL levels as goals. His PCP also seemed miffed that he had gotten the coronary calcium scan. Geo felt like the PCP’s attitude was “shut up and do what I tell you.”

Geo’s PCP’s approach exemplifies a not-uncommon traditional doctor-patient relationship, but a better approach is shared decision-making (see here). Geo, like many patients, welcomes more information on the risks and benefits of any recommended treatment so that he can participate in deciding the best course of action.

I steer patients who want more complete information towards my  evidence-based blog posts on statins (see here for discussion on statin side effects and here for statin benefits beyond cholesterol lowering.)

By giving patients more information on the risks, side effects, and benefits of the statin drugs along with a better understanding of their overall risk of heart disease and stroke, we can hopefully move more patients “off the fence” and onto the most appropriate treatment.

Stay tuned to find out what The Skeptical Cardiologist Recommended for Geo.

Decisively Yours

-ACP

For more discussion on the value of coronary artery calcification (CAC) and the value of statin in lower risk patients see this recent paper entitled “Refining Statin Prescribing in Lower-Risk Individuals: Informing Risk/Benefit Decisions”(PDF refining-statin-prescribing-in-lower-risk-individuals-informing-riskbenefit-decisions)

If you’d like to read the recently published recommendations of the US Preventive Services Task Force on statins for primary prevention of cardiovascular disease see here. Importantly this panel of unbiased experts concluded that statin therapy significantly reduced overall mortality and cardiovascular mortality. In addition, the review found no increased risk of diabetes overall with statin therapy. The only trial that identified an increased risk was using high intensity statin therapy (Crestor (rosuvastatin) >20 mg).

And,  since the internet is jammed with people who believe statins robbed them of their brain power, I would advise noting that the writers concluded  “These findings are consistent with those from a recent systematic review of randomized trials and observational studies that found no adverse associations of statins with incidence of Alzheimer disease, dementia, or decreased scores on tests of cognitive performance.”

 

 

Do You Know What’s On Garry Shandling’s And Your Parent’s Death Certificate?

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Better Call Saul’s Bob Odenkirk and Kathy Griffin “hanging” with an apparently healthy Larry Sanders on March 20. These two appeared on Shandling’s brilliant Larry Sanders TV show.

When someone who had appeared to be healthy dies suddenly, it is often assumed that he/she died of “a massive heart attack.” Certainly, this was the case in the recent unexpected sudden death of Garry Shandling, the actor and comedian.  Shandling, aged 66, died March 24 of this year.

ET online reported:

“His publicist Alan Nierob told the ET that Shandling had no history of heart problems, but that doctors believe he died as the result of a heart attack.”

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.

The LA Coroner’s office could not get Sanders’ physician to sign his death certificate and the cause of death has still apparently not been determined, pending toxicology testing which typically takes 6 weeks.

What’s On Your Parent’s Death Certificate

More important than what is on Garry Shandling’s death certificate is what is on your parent’s death certificate, and whether it is accurate. If one of your parents died prematurely and suddenly, it is  important to know with precision what caused it. If the cause was an heritable cardiovascular condition, hopefully, appropriate testing can determine if you have that condition, and steps can be taken to prevent your premature demise.

Examples of inherited cardiovascular conditions (in addition to heart attack (myocardial infarction) or pulmonary embolism) that can cause sudden and unexpected death include aortic aneurysm dissection, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasis, and long QT syndrome.

Unfortunately I find that, at least in my patients, uncertainty about the cause of death of one’s parents is the norm.

Many of my patients, for example, tell me one of their parents died of a “massive heart attack” and they assume that they are at increased risk of the same fate. When I press for details, typically no autopsy was performed.  Mom or dad may have been found dead at home, or they may have suddenly keeled over but not survived to make it to the hospital for a definitive diagnosis.

Without an autopsy in such circumstances, it is not possible to be sure of the cause of death.

Even if you have a cause of death listed on your parent’s death certificate, there is no guarantee that it is accurate.  The doctor that filled it out, without an autopsy in many circumstances, is just speculating on the cause based on what he/she knew about prior medical conditions and the circumstances surrounding the death.

I was recently asked to fill out the death certificate of an elderly patient of mine who had atrial fibrillation and congestive heart failure and was living in a nursing home.

One night she was noted by the staff to be very short of breath and was taken to a local  emergency room where she was pronounced dead.

Based on the information available to me, I had no idea what caused her death. Although she had quite signifiant cardiac problems, when I last saw her she was stable and I have numerous patients with the same conditions who live for decades.

I filled out the death certificate, listing all of her conditions, and entered in that the cause of death was unknown.

Although the CDC guide for physicians filling out death certificates clearly states that this is acceptable, I was subsequently informed that the funeral home did not accept unknown cause of death and that they had found another doctor to fill in a cause  of death.

I guarantee you, whatever he put on as the cause of death was total speculation.

Jerry Seinfeld was good friends with Garry Shandling and, oddly enough, not too long ago, featured him in an episode of his internet series “Comedians in Cars Getting Coffee” entitled “It’s Great That Garry Shandling Is Still Alive.

Screen Shot 2016-07-03 at 7.04.14 AM

Shandling mentions “I had hyperparathyroidism,” making a joke that “the symptoms are so much like being an older Jewish man, no one noticed!”

James Fallows, the excellent The Atlantic writer, highlights his own experience with hyperparathyroidism (a disease that leads to high calcium levels and is easily treated with surgery), in a recent Atlantic article. The subtitle of this article, “a rare and under-publicized condition that can sometimes be fatal,” suggests that hyperhyperparathyroidism might have led to Shandling’s death.

I don’t think this is likely because Shandling suggests that the disease is in the past tense (i.e. he has already had the surgery), and sudden death from hyperparathyroidism would be extremely unlikely.

Fortunately, Shandling is getting a full examination and autopsy to fully determine the cause of his death. If he has offspring, this will be extremely helpful to them in understanding what medical conditions they can expect later in life.

If he was not a celebrity, his death, like many of your parents’, most likely would have been ascribed to a “massive heart attack.”

 

 

Death Knell For Niacin For Lipids Sounded by FDA?

The skeptical cardiologist stopped writing new prescriptions for niacin extended release tablets in 2011. For any patient who was taking niacin, I recommended stopping it.

Because niacin had favorable effects on the cholesterol profile, physicians had been utilizing it for many years in high risk patients on statins who had low HDL  (good cholesterol) and/or high triglycerides.

The rationale was that, since high HDL was associated with lower risk of heart attacks, raising the HDL would lower that risk. Similarly, lowering the triglycerides would improve cardiovascular risks.

While niacin certainly improved the cholesterol profile, there was no good evidence that starting it in a patient already on statin would improve cardiovascular outcomes. The cholesterol profile is a surrogate endpoint: the actual treatment goal is reducing cardiovascular disease.

In 2011, the AIM-HIGH study proved there was no benefit to adding niacin to good statin therapy despite increasing HDL from 35 to 42 mg/dl, lowering triglycerides and lowering LDL. This and other studies showing no benefit of niacin therapy (and worrisome adverse effects) should have resulted in the total cessation of niacin prescriptions, especially  in patients on statins.

Unfortunately, old habits die hard amongst physicians, and the allure of raising HDL and lowering triglycerides with niacin persisted despite a lack of evidence of any benefit in lowering cardiovacular risk.

Yesterday, the FDA announced it was removing from the market two  drugs made by Abbvie, Advicor and Simcor, which are combinations of extended release niacin plus lovastatin or simvastatin, and removed its approved indication for niacin ER plus statin for lowering CHD risk stating:

“Based on the collective evidence from several large cardiovascular outcome trials (Refs. 1-3), the Agency has concluded that the totality of the scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events. Consistent with this conclusion, FDA has determined that the benefits of niacin ER tablets and fenofibric acid DR capsules for coadministration with statins no longer outweigh the risks, and the approvals for this indication should be withdrawn.”

This is good news for patients whose physicians were keeping them on the unproven brand name combination drugs, Advicor and Simcor.

There are still legitimate uses of niacin to prevent vitamin deficiencies but If you are still taking some form of niacin ER for the purpose of preventing heart disease with or without a statin I recommend presenting your doctor with the link to the FDA pronouncement above and having a good discussion with him about the rationale for staying on it.

The other drug mentioned in the announcement, fenofibric acid,  is far less often prescribed and is not available as a combination. It is the most effective drug we have for extremely high triglyceride levels over 500 mg/dl which can cause pancreatitis. I have a few patients on the generic fenofibric acid strictly for the purpose of lowering their dangerously high triglycerides but not for the indication of lowering their cardiovascular risk.

Nonsurrogateingly Yours

-ACP

 

The Skim Milk Scam: Words of Wisdom From a Doctor Dairy Farmer

The skeptical cardiologist only consumes full fat dairy and recommends this to his patients.

Full fat dairy is associated with less abdominal fat, lower risk of diabetes and lower risk of developing vascular complications such as stroke and heart attack.
quart_whole_milk_yogurt-293x300I’ve been consuming  full fat yogurt and milk  from Trader’s Point Creamery in Zionsville, Indiana almost exclusively since visiting the farm and interviewing its owners a few years ago.

Dr. Peter(Fritz) Kunz, a plastic surgeon, and his wife Jane, began selling milk from their farm after researching methods for rotational grazing , a process which allows  the cows to be self-sustaining: the cows feed themselves by eating the grass and in turn help fertilize the fields,  . After a few years of making sure they had the right grasses and cows, the Kunz’s opened Traders Point Creamery in 2003.

Two more studies (summarized nicely on ConscienHealth, an obesity and health blog)  came out recently solidifying the extensive data supporting the health of dairy fat and challenging the nutritional dogma that all Americans should be consuming low-fat as opposed to full fat dairy.

The Dairy Industry’s Dirty Little Secret

Dr. Kunz opened my eyes to the dirty little secret of the dairy industry when i first talked to him: dairy farmers double their income by allowing milk to be split into its fat and non-fat portions therefore the industry has no motivation to promote full fat dairy over nonfat dairy.

Recently, I  presented him with a few follow-up questions to help me understand why we can’t reverse the bad nutritional advice to consume low-fat dairy.

Skeptical Cardiologist: “When we first spoke and I was beginning my investigation into dairy fat and cardiovascular disease you told me that most dairy producers are fine with the promotion of non fat or low fat dairy products because if consumers are choosing low fat or skim dairy this allows the dairy producer to profit from the skim milk production as well as the dairy fat that is separated and sold for butter, cheese or cream products.”
I  don’t have a clear idea of what the economics of this are. Do you think this, for example, doubles the profitability of a dairy?

Dr. Kunz:Yes, clearly. Butter, sour cream, and ice cream are highly profitable products… All these processes leave a lot of skim milk to deal with, and the best opportunity to sell skim milk is to diet-conscious and heart-conscious people who believe fat is bad.”

Skeptical Cardiologist:” I’ve been baffled by public health recommendations to consume low fat dairy as the science would suggest the opposite. The only reason I can see that this persists is that the Dairy Industry Lobby , for the reason I pointed out above, actually has a vested interest from a profitability standpoint in lobbying for the low fat dairy consumption.. Do you agree that this is what is going on? ”

 Dr. Kunz: “Yes, definitely. The obsession with low-fat as it relates to diet and cardiac health has been very cleverly marketed. Fat does NOT make you fat. 

Skeptical Cardiologist: “Also, I have had trouble finding out the process of production of skim milk. I’ve come across sites claiming that the process involves injection of various chemical agents but I can’t seem to find a reliable reference source on this. Do you have any information/undestanding of this process and what the down sides might be? I would like to be able to portray skim milk as a “processed food” which, more and more, we seem to be recognizing as bad for us.”

Dr. Kunz: “The PMO pasteurized milk ordinance states that when you remove fat you have to replace the fat soluble vitamins A & D. Apparently the Vitamin A & D have to be stabilized with a chemical compound to keep them miscible in basically an aqueous solution. The compound apparently contains MSG!! We were shocked to find this out and it further confirmed that we did not want to do a reduced fat or skim milk product.”

Skeptical Cardiologist: ” Any thoughts on A2? Marion Nestle’, of Food Politics fame, was recently in Australia where there is a company promoting A2 milk as likely to cause GI upset. It has captured a significant share of the Aussie market.”

Dr. Kunz: “We have heard of this and have directed our farm to test and replace any A1 heterozygous or homozygous cows.  We believe that very few of our herd would have A1 genetics because of the advantage of using heritage breeds like Brown Swiss and Jersey instead of Holstein.  Because few people are actually tested for lactose intolerance and because of the marketing of A2, it’s imperative not to be left behind in this – whether or not it turns out to be a true and accurate cause of people’s GI upset.

Skeptical Cardiologist:” I like that your milk is nonhomogenized. Seems like the less “processing” the better for food.  I haven’t found any compelling scientific reasons to recommend it to my patients, however. Do  you have any?”

Dr. Kunz: The literature is fairly old on this subject, but xanthine oxidase apparently can become encapsulated in the fat globules and it can be absorbed into the vascular tree and cause vascular injury.  I will look for the articles.  Anyway, taking your milk and subjecting it to 3000-5000 psi (homogenization conditions) certainly causes damage to the delicate proteins and even the less delicate fat globules.  Also remember that dietary cholesterol is not bad but oxidized cholesterol is very bad for you. That’s why overcooking egg yolks and high pressure spray drying to make powder products can be very dangerous – like whey protein powders that may contain some fats.

Skeptical Cardiologist: I spend a fair amount of time traveling in Europe and am always amazed that their milk is ultrapasteurized and sits unrefrigerated on the shelves. any thoughts on that process versus regular pasteurization and on pasteurization in general and its effects on nutritional value of dairy.

Dr. Kunz :“Absolutely crazy bad and nutritionally empty.. don’t know why anyone would buy it. The procedure is known as aseptic pasteurization and is how Nestle makes its wonderful Nesquik. If they made a full fat version of an aseptically pasteurized product it may have more oxidized cholesterol and be more harmful than no fat!!”
So there you have it, Straight from the  doctor dairy farmer’s mouth:
Skimming the healthy dairy fat out of  milk is a highly profitable process. Somehow, without a shred of scientific support,  the dairy industry, in cahoots with misguided and close-minded nutritionists, has convinced the populace that this ultra-processed skim milk pumped full of factory-produced synthetic vitamins is healthier than the original product.
Lactosingly Yours
-ACP
The two  recent articles supporting full fat dairy are:

Circulating Biomarkers of Dairy Fat and Risk of Incident Diabetes Mellitus Among US Men and Women in Two Large Prospective Cohorts

which concluded ‘In two prospective cohorts, higher plasma dairy fatty acid concentrations were associated with lower incident diabetes. Results were similar for erythrocyte 17:0. Our findings highlight need to better understand potential health effects of dairy fat; and dietary and metabolic determinants of these fatty acids

and from Brazilian researchers

Total and Full-Fat, but Not Low-Fat, Dairy Product Intakes are Inversely Associated with Metabolic Syndrome in Adults1

 

What Happens To Cholesterol Levels When You Switch To Low Or Non Fat Dairy

When individuals  discover that they have abnormal  cholesterol readings they are often told to initiate  lifestyle changes to try to correct them.

Based on what physicians and patients have been taught  over the last twenty years, the likely dietary change recommended and the easy , first step is likely  to be to cut back on dairy fat.

IMG_6135
Yoplait Original-25% Less Sugar.(but still with 18 grams per 6 oz serving). A typical supermarket/doctor’s lounge yogurt with lots of ingredients added in (sugar, modified corn starch, Vitamin A Acetate, Vitamin D3)to replace the natural good taste and nutrients found in dairy fat.
IMG_6272 (1)
Traders Point Creamery plain yogurt. Ingredients= milk and cultures. Taste =fantastic. Grams of sugar=zero.

After all, it’s a pretty easy transition to start using skim milk and non fat yogurt because these line the supermarket shelves and have been filled with chocolate or added sugar to taste more palatable.

You might miss the great taste that butter adds to bread or cooking but for your health you would be willing to switch to non butter spreads and cut down on the cheese in your diet because  based on what you have heard from numerous media sources this is a giant step toward reducing your cholesterol numbers.

 

 

 

 


 

Unfortunately, it is a horribly misguided  step.

Although, the switch to low or non fat dairy lowers your cholesterol numbers, it is  not lower cholesterol numbers that you want: what you want is a lower risk of developing stroke or heart attack or the other complications of atherosclerosis.

Let me repeat: Don’t worry about your cholesterol numbers, worry about your overall risk of developing heart attack or stroke.

Due to 30 years of misinformation, the concept that lowering your cholesterol means lower risk of heart disease has become firmly entrenched in the public’s consciousness-but in the case of dietary intervention this has never been documented.

I take care of a 69 year old woman who has an abnormal heart rhythm and chest pain. As part of her evaluation for chest pain we performed a coronary CT angiogram (CCTA) which showed advanced but not obstructive atherosclerotic plaque in her right and left anterior descending coronary arteries.

This lady was not overweight, followed a healthy diet and exercised regularly. Her mother, a sedentary, heavy smoker, suffered a heart attack at age 54.

Her PCP had obtained lipid values on her 6 months before I saw her which were abnormal but the patient had been reluctant to start the recommended statin drug because of concerns about side effects.

After seeing her CCTA I advised that she begin atorvastastin 10 mg daily and aspirin to help reduce her long term risk of heart attack, stroke.

She decided without telling me not to take the statin, again due to side effect concerns, but started the aspirin, and began to pursue what she felt were healthy dietary changes.

When I saw her back in the office she told me  “I don’t eat butter or cheese anymore and I’ve switched to skim milk.” She had substituted olive oil for butter.

Here are her lipid values before and after her dietary changes (TC=total cholesterol, LDL= bad cholesterol, HDL=good cholesterol, trigs=triglycerides)

Date              TC             LDL       HDL   trigs            ASCVd 10 year risk

3/2015         275          173       72       149                         7.9%

10/2015      220           122       43      274                         8.3%

At first glance, and especially if we focus only on the total and bad cholesterol, this appears to be a successful response to dietary changes:  a 29% reduction in the bad cholesterol and a 25% drop in the total cholesterol.

However, although the LDL or bad cholesterol has dropped a lot, the HDL or good cholesterol has dropped by  more: 40%!

This is the typical change when patients cut out dairy fat-the overall ratio of bad  to good cholesterol actually rises.

In addition, the pattern she has now, with a low HDL and high triglycerides is typical of the metabolic syndrome which is recognized as likely to contribute to early  atherosclerosis: so-called “atherogenic dyslipidemia.”

When I plugged both sets of numbers into the ASCVD 10 year risk calculator app (see here) her estimated 10 year risk of heart attack and stroke had actually increased from 7.9% to 8.3%.

Hopefully, this anecdote will reinforce what population studies show:

  • There is NO evidence that dairy fat consumption increases risk of cardiovascular disease (see here)
  • Current recommendations to consume non or low fat dairy (often  accompanied by increase in added sugars) are not supported by scientific studies.

Finally, my patient is another example of an inherited tendency to development of premature atherosclerosis: her diet, exercise, body weight were all optimal and could not be tweaked to lower her risk.

Such patients must deal with the cardiovascular cards they have been dealt. If they have advanced atherosclerosis, as much as they may dislike taking medications, statins are by far the most effective means of reducing their long term risk of heart attack and stroke.