Tag Archives: cholesterol

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.

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

 

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

Sheepshead Fish: Vulnerable and Gender Fluid Yet Mighty Tasty

The skeptical cardiologist and his Eternal Fiancee’ have escaped dreary and oceanopenic St. Louis and are spending a week in allegedly sunny and definitely beachy San Diego.

Upon arrival we took in a Farmer’s Market in Little Italy and stumbled into Ironside Fish and Oyster.screen-shot-2017-01-22-at-9-07-04-am
Always in search of heart-healthy, unique and local fish dishes, I spotted on the menu a luncheon special of sheepshead fish.

Kelly Fukushima is the local fisherman who caught my fish
Kelly Fukushima is the local fisherman who caught my fish.

California sheepshead (Semicossyphus pulcher), the existence of which I was previously unaware, turned out to be a fascinating and most delicious fish.

casheepshead

Before I could order it, I had to verify that I wasn’t contributing to the extinction of a species.  The IUCN Red List of Threatened species lists the CS as “vulnerable” because:

“The natural history of this species, including its limited geographic range along inshore habitat, the likely increasing interest in the fishery and the currently unsustainable fishing levels (according to the models of Alonzo et al. 2004), together with the difficulties in enforcing existing regulations strongly suggest that this species will continue to decline if stronger protective action is not put into place. “

After learning the CS was vulnerable, I had to make a critical decision: should I eat it before it disappeared, robbing me of a chance to ever taste it, or should I order something that wasn’t vulnerable, thus contributing to the preservation of the continuing biodiversity of the planet. I elected to taste it.

Gender Fluid Fish

Further research revealed that the CS transitions from a reproductively functional female at birth, to a functional male during the course of a lifespan in response to social factors (?reverse Bruce Jenner).

According to evolution.berkeley.edu this is termed sequential hermaphroditism:

In some sequentially hermaphroditic fish species, animals develop first as male and then switch to female (a condition called protandry), and in others, the individuals develop first as female and then switch to male (protogyny).

Clownfish (as in Finding Nemo) do the opposite of the sheepshead and are protandrous:

This species lives within sea anemones in groups of two large fish and many small fish. The two large fish are the only sexually mature fish and are a male and female breeding pair. All of the smaller fish are male. If the large breeding female is removed, her male mate changes sex to female and the next largest fish in the group rapidly increases in size and takes over the role as the sexually mature male.

While waiting for the vulnerable and sequentially hermaphroditic sheepshead to arrive, I sampled an equally

img_8160stupendous and heart-healthy side of cannelloni bean cassoulet. Chock full of Mediterranean diet essentials including kale, beans and mustard seeds, it worked really well as an appetizer.

 

Do not make the mistake of looking at this youtube video while waiting for your sheepshead entree’ as I did. The disturbing human-like teeth will not be part of your meal.

Finally, the 4 ounces of CS arrived, perfectly prepared a la plancha,

img_8162with an accompanying lemon butter sauce that was divine. Although butter is not officially a big part of the Mediterranean diet, frequent readers of the skepcard know that dairy fat does not make you fat or promote heart disease, and is fine (in moderation of course) as part of a heart-healthy diet.

Speaking of lingering bad dietary advice, if you investigate the nutritional content of sheepshead at a site like SELF Nutrition, the screen-shot-2017-01-22-at-10-18-54-amold canard that we should be limiting our dietary cholesterol raises its ugly head. Because sheepshead contain significant amounts of cholesterol (presumably from carnivorously munching on shellfish with its scary human-like choppers), the misguided nutritionists at SELF Nutrition and other would-be nutritionistas pronounce it as not optimally healthy.

Semiccossyphusilly Yours

-ACP

PS. If you’d really like to get your nerd on about sequential hermaphroditism check out this graphic showing the independent evolution of this feature across different phylogenetic lineages!

hermaphroditismtree

 

 

 

 

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.

 

 

 

Why Is The American College of Cardiology Distorting The 2015 Dietary Guidelines for Americans?

The 2015-2020 Dietary Guidelines for Americans (DGA) have finally been released and I’m sure that most of you could care less what they say. You may think that they can’t be trusted because you believe the original science-based recommendations have been altered by political, food and agribusiness forces.  Perhaps you don’t trust science to guide us in food choices. Perhaps, like the skeptical cardiologist, you realize that the DGA has created, in the past, more problems than they have corrected.

This time, the skeptical cardiologist believes they have made a few strides forward, but suffer from an ongoing need to continue to vilify all saturated fats.

As such, the DGA no longer lists a recommended limit on daily cholesterol consumption (step forward) but persists in a recommendation to switch from full fat to non fat or low fat dairy products, which is totally unsubstantiated by science, (see my multiple posts on this topic here).

By now you should have gotten the message that a healthy diet consists of lots of fruits, vegetables, nuts, legumes, fish, olive oil and whole grains. The DGA emphasizes this.

There is general consensus that processed foods and added sugar should be limited.

Most of the controversy is about what to limit and how much to limit foods that are considered unhealthy.

Red meat and processed meat remain in the crosshairs of the DGA (although not stated explicitly), but eggs and cholesterol have gotten a pass, something which represents a significant change for the DGA and which I have strongly advocated (here and here).

But hold on, my professional organization, the American College of Cardiology says otherwise.

Misleading Information From the American College of Cardiology

The American College of Cardiology sent me an email and posted on their website the following horribly misleading title:

“2015 Dietary Guidelines Recommend Limited Cholesterol Intake”

The first paragraph of the ACC post reads as follows:

“Physiological and structural functions of the body do not require additional intake of dietary cholesterol according to the 2015 Dietary Guidelines released on Jan. 7 by the U.S. Departments of Health and Human Services (HHS) and of Agriculture (USDA). As such, people should practice healthy eating patterns consuming as little dietary cholesterol as possible. – ”

While technically these statements can be found in the document (by digging way down) the executive summary (infographic below) says nothing about limiting cholesterol.

healthy eating pattern includes

The “Key Recommendations” list eggs as included under a “healthy eating pattern” along with other protein foods.

 

Screen Shot 2016-01-09 at 1.31.18 PM

In addition, there is no mention of cholesterol under what a healthy pattern limits.

 

 

In the same section on cholesterol that the ACC inexplicably has chosen to emphasize, is this sentence:

“More research is needed regarding the dose-response relationship between dietary cholesterol and blood cholesterol levels. Adequate evidence is not available for a quantitative limit for dietary cholesterol specific to the Dietary Guidelines.”

So the DGA recommends no specific limit on dietary cholesterol.

This is consistent with what the DG advisory committee recommended when they wrote “dietary cholesterol is no longer a nutrient of concern.”

The DGA goes on to state:

“A few foods, notably egg yolks and some shellfish, are higher in dietary cholesterol but not saturated fats. Eggs and shellfish can be consumed along with a variety of other choices within and across the subgroup recommendations of the protein foods group.”

The Vegan Agenda

I have a theory on why the ACC went so wildly astray in reporting this information: they are led by a vegan.

The current president of the ACC, Kim Williams, is an evangelical vegan, unrepentant, as this NY times article points out. Apparently, he tries to convert all his patients to the “plant-based diet.”

He is quoted extensively in the ACC blurb on the DGA and is clearly attempting to put a bizarre vegan spin on the new guidelines, ignoring the evidence and the progressive shift from the 2010 guidelines.

Can any information from the ACC be trusted if such basic and important science reporting was so heavily distorted by its President?

No wonder Americans tune out dietary advice: it can so easily be manipulated by those with an agenda.

-May the forks and knives be with you

-ACP

 

 

 

 

Saturated Fat: Traditionalists versus Progressives

Why is death from coronary heart disease declining in the US at the same time that obesity and diabetes rates are climbing?

Two editorials recently published in The Lancet show the widely varying opinions on the optimal diet for controlling obesity , diabetes and coronary heart disease that experts on nutrition, diabetes and heart disease hold.

fats
Typical innocent and usual suspects rounded up in the war on fat: Cheese-data show it lower heart disease risk Full fat yogurt (Trader’s Point Creamery)-data show it is associated with lower heart disease risk Butter-Delicious. Used in moderation not a culprit.

The first paper contains what I would  consider the saturated fat “traditionalist” viewpoint. This is a modification of the misguided concept that was foisted on the American public in the 1980s and resulted in the widespread consumption of industrially produced trans-fats and high sugar junk food that was considered heart healthy.

The traditionalists have shifted from condemning all fats to vilifying only saturated and trans fats. They would like to explain at least part of the reduction in coronary heart mortality as due to lower saturated fat consumption and the accompanying lowering of LDL (“bad”) cholesterol.

The SFA traditionalists fortunately are in decline and more and more in the last five years, prominent thinkers, researchers and scientists working on the connection between diet and the heart believe saturated fats are neutral but sugar and refined carbohydrates are harmful in the diet.

Darius Mozzafarian, a highly respected cardiologist and epidemiologist, who is dean of the School of Nutrition Science and Policy at Tufts, wrote the second editorial and is what I would term a saturated fatty acid (SFA) progressive.

He makes the following points which are extremely important to understand and which I have covered in previous posts. I’ve included his supporting references which can be accessed here.

Fat Doesn’t Make You Fat, Refined Starches And Sugar Do

"Foods rich in refined starches and sugars—not fats—seem to be the primary culprits for weight gain and, in turn, risk of type 2 diabetes. To blame dietary fats, or even all   calories, is incorrect
Although any calorie is energetically equivalent for short-term weight loss, a food's long-term obesogenicity is modified by its complex effects on satiety, glucose–insulin responses, hepatic fat synthesis, adipocyte function, brain craving, the microbiome, and even metabolic expenditure Thus, foods rich in rapidly digestible, low-fibre carbohydrates promote long-term weight gain, whereas fruits, non-starchy vegetables, nuts, yoghurt, fish, and whole grains reduce       long-term weight gain.123
Overall, increases in refined starches, sugars, and other ultraprocessed foods; advances in food industry marketing; decreasing physical activity and increasing urbanisation in developing nations; and possibly maternal–fetal influences and reduced sleep may be the main drivers of obesity and diabetes worldwide".

There Are Many Different Kinds of Saturated Fats With Markedly Different Health Effects: It Makes No Sense to Lump Them All Together 

"SFAs are heterogeneous, ranging from six to 24 carbon atoms and having dissimilar biology. For example, palmitic acid (16:0) exhibits in vitro adverse metabolic effects, whereas medium-chain (6:0–12:0), odd-chain (15:0, 17:0), and very-long-chain (20:0–24:0) SFAs might have metabolic benefits.4 This biological and metabolic diversity belies the wisdom of grouping of SFAs based on a single common chemical characteristic—the absence of double bonds. Even for any single SFA, physiological effects are complex: eg, compared with carbohydrate, 16:0 raises blood LDL cholesterol, while simultaneously raising HDL cholesterol, reducing triglyceride-rich lipoproteins and remnants, and having no appreciable effect on apolipoprotein B,  5 the most salient LDL-related characteristic. Based on triglyceride-lowering effects, 16:0 could also reduce apolipoprotein CIII, an important modifier of cardiovascular effects of LDL and HDL cholesterol. SFAs also reduce concentrations of lipoprotein(a) ,6 an independent risk factor for coronary heart disease."

The Effects of Dietary Saturated Fats Depend on Complex Interactions With The Other Ingredients in Food

"Dietary SFAs are also obtained from diverse foods, including cheese, grain-based desserts, dairy desserts, chicken, processed meats, unprocessed red meat, milk, yoghurt, butter, vegetable oils, and nuts. Each food has, in addition to SFAs, many other ingredients and characteristics that modify the health effects of that food and perhaps even its fats. Judging the long-term health effects of foods or diets based on macronutrient composition is unsound, often creating paradoxical food choices and product formulations. Endogenous metabolism of SFAs provide further caution against oversimplified inference: for example, 14:0 and 16:0 in blood and tissues, where they are most relevant, are often synthesised endogenously from dietary carbohydrate and correlate more with intake of dietary starches and sugars than with intake of meats and dairy.4"

Dietary Saturated Fat Should Not Be a Target for Health Promotion

"These complexities clarify why total dietary SFA intake has little health effect or relevance as a target. Judging a food or an individual's diet as harmful because it contains more SFAs, or beneficial because it contains less, is intrinsically flawed. A wealth of high-quality cohort data show largely neutral cardiovascular and metabolic effects of overall SFA intake.7 Among meats, those highest in processing and sodium, rather than SFAs, are most strongly linked to coronary heart disease.7Conversely, higher intake of all red meats, irrespective of SFA content, increases risk of weight gain and type 2 diabetes; the risk of the latter may be linked to the iron content of meats.28 Cheese, a leading source of SFAs, is actually linked to no difference in or reduced risk of coronary heart disease and type 2 diabetes.910 Notably, based on correlations of SFA-rich food with other unhealthy lifestyle factors, residual confounding in these cohorts would lead to upward bias, causing overestimation of harms, not neutral effects or benefits. To summarise, these lines of evidence—no influence on apolipoprotein B, reductions in triglyceride-rich lipoproteins and lipoprotein(a), no relation of overall intake with coronary heart disease, and no observed cardiovascular harm for most major food sources—provide powerful and consistent evidence for absence of appreciable harms of SFAs."

Dietary Saturated Fats May Raise LDL cholesterol But This Is Not Important: Overall Effects On Obesity and Atherosclerosis Are What Matters

"a common mistake made by SFA traditionalists is to consider only slices of data—for example, effects of SFAs on LDL cholesterol but not their other complex effects on lipids and lipoproteins; selected ecological trends; and expedient nutrient contrasts. Reductions in blood cholesterol concentrations in Western countries are invoked, yet without systematic quantification of whether such declines are explained by changes in dietary SFAs. For example, whereas blood total cholesterol fell similarly in the USA and France between 1980 and 2000, changes in dietary fats explain only about 20% of the decline in the US and virtually none of that which occurred in France.11Changes in dietary fats11 simply cannot explain most of the reductions in blood cholesterol in Western countries—even less so in view of the increasing prevalence of obesity. Medication use also can explain only a small part of the observed global trends in blood cholesterol and blood pressure. Whether decreases in these parameters are caused by changes in fetal nutrition, the microbiome, or other unknown pathways remains unclear, thus highlighting a crucial and greatly underappreciated area for further investigation."

Dietary Saturated Fats Are Neutral For Coronary heart Disease Risk

Finally, SFA traditionalists often compare the effects of SFAs only with those of vegetable polyunsaturated fats, one of the healthiest macronutrients. Total SFAs, carbohydrate, protein, and monounsaturated fat each seem to be relatively neutral for coronary heart disease risk, likely due to the biological heterogeneity of nutrients and foods within these macronutrient categories.7Comparisons of any of these broad macronutrient categories with healthy vegetable fats would show harm,12 so why isolate SFAs? Indeed, compared with refined carbohydrates, SFAs seem to be beneficial.7

The overall evidence suggests that total SFAs are mostly neutral for health—neither a major nutrient of concern, nor a health-promoting priority for increased intake. 

Focusing On Reducing Saturated Fats Leads To Unhealthy Dietary Choices

I’ve written about this a lot. The most baffling aspect of this is the promotion of low or non-fat dairy.

There is no evidence that low fat dairy products are  healthier than full fat dairy products.

Non-fat yogurt filled with sugar should be considered a dessert, not a healthy food.

"Continued focus on modifying intake of SFAs as a single group is misleading—for instance, US schools ban whole milk but allow sugar-sweetened skim milk; industry promotes low-fat foods filled with refined grains and sugars; and policy makers censure healthy nut-rich snacks because of SFA content.13 "

It is extremely hard to change most people’s opinions on dietary fat.

My patients have been hearing the SFA traditionalist dogma for decades and thus it has become entrenched in their minds.

When I present to them the new progressive and science-based approach to fat and saturated fat some find it so mind boggling that they become skeptical of the skeptical cardiologist!

Hopefully, in the next few years, the progressive SFA recommendations will become the norm and maybe , some day in the not too distant future, the inexplicable recommendations for low-fat or non fat dairy will disappear.

As more data accumulates we may become SFA enthusiasts!

Saturatingly Yours,

-ACP

For another viewpoint (?from an SFA enthusiast) and  a detailed description of both editorials see Axel Sigurdsson’s excellent post here.

PCSK9: The canine that escalates Your LDL

Yes. PCSK9 is a factor in escalating LDL cholesterol levels. The point was brought home as I rode the escalator up from the first to the top pcsk9floor of the San Diego Convention Center at this year’s American College of Cardiology meetings. I suspsect if I had taken an elevator I would have seen a sign proclaming that PCSK9 is a factor in elevating cholesterol levels.
And PCSK9 signage is everywhere in this meeting.

 

 

Proprotein convertase subtilisin/kexin type 9, also known as PCSK9, is an enzyme that appears to degrade LDL receptors.

If you are born with a mutation that produces less active PCSK9 you have more LDL receptors and consequently more LDL is taken out of circulation leading to lower LDL levels.

Mutations leading to gain of PCSK9 function result in lower LDL receptors, higher LDL levels and substantial clinical evidence for premature atherosclerosis.

Amgen has produced all the PCSK9 signs that abound at the ACC meetings because they have produced a fully humanized monoclonal antibody (utilizing Chinese hamster ovaries) that inhibits PCSK9 and does a great job of lowering LDL without significant adverse effects.

At a late-breaking clinical trial session, results of longer term follow up of the company’s Osler randomized trials were presented and simultaneously published here.

The results were remarkably good. Not only did evolocumab drop LDL by 61% (from 120 down to 48) it showed significant improvement in cardiovascular outcomes.

“The rate of cardiovascular events at 1 year was reduced from 2.18% in the standard-therapy group to 0.95% in the evolocumab group (hazard ratio in the evolocumab group, 0.47; 95% confidence interval, 0.28 to 0.78; P=0.003).”

According to the biotech website fiercebiotech:

“The antibody is expected to win FDA approval by Aug. 27, trailing Sanofi ($SNY) and Regeneron’s ($REGN) alirocumab, which, thanks to some regulatory opportunism, is likely to hit the market a month or so before. Pfizer ($PFE) is in third place, working through Phase III with its bococizumab. Analysts say each treatment could bring in more than $3 billion a year at its peak…”

More study is needed of these drugs before approval in my opinion for a number of reasons. There is evidence of a small, but significant increase in neurocognitive side effects for one.

Although with evolocumab these were not related to the level of LDL achieved, there are concerns that extremely low LDL levels may interfere with neural development and such effects may not manifest for years.

The study authors did a good job of pointing out other limitations including small number of events, open-label design and patients selected who were free of adverse events. Hopefully, the FOURIER study will resolve these issues.

This post was also posted at SERMO, the physician social network. I would encourage physicians to join in the robust discussions on medicine and other topics at this site.

Skeptically Yours,

ACP

Since Dietary Cholesterol Isn’t Important Can I Stop Taking My Cholesterol Drug

A year ago one of my patients began experiencing  chest pain when he walked up hills. Subsequent evaluation revealed that atherosclerotic plaque (95% narrowing of a major coronary artery ) was severely reducing the blood flow to his heart muscle and was the cause of his chest pain. When this blockage was opened up with a stent he no longer had the pain.

Along with other medications (aspirin and plavix to keep his stent open) I had him start atorvastatin, the generic version of Lipitor, a powerful statin drug that has been shown to prevent progression of atherosclerotic plaque and thereby reduce subsequent heart attacks, strokes and death in patients like him

I saw him in the office the other day in follow up and he was feeling great . He asked me “Doc I read  your post yesterday.s Since you say that cholesterol in the diet doesn’t matter anymore, does that mean I don’t have to take my cholesterol drug anymore.?”

His question gets at the heart of the  “diet-heart hypothesis”. The concept that dietary modification, with reduction of cholesterol and fat consumption can reduce coronary heart disease.

The science supporting this hypothesis has never been strong but the concept was foisted on the American public and was widely believed. It was accepted I would  say because it has a beautiful simplicity which can be summarized as follows:

“If you eat cholesterol and fat it  will enter  your blood stream and raise cholesterol levels. This excess cholesterol will then  deposit in your arteries, creating fatty plaque , clogging them and leading to a heart attack.”

This concept was really easy to grasp and simplified the public health recommendations.

However, cholesterol blood levels are determined more by cholesterol synthesized in the liver and predicting  how dietary modifications will effect these levels is not easy.

Since the public has had the diet-heart hypothesis fed to them for decades and given its beautiful simplicity it is hard to reverse this dogma. My patient’s question reflects a natural concern that if science/doctors got this crucial question so wrong, is everything we know about cholesterol treatment and heart disease wrong?

In other words, are doctors promoting a great cholesterol hoax?

Evidence Strongly Supports Statins in Secondary Prevention 

For my patient the science supporting taking a  cholesterol-lowering statin drug is very solid. There are multiple excellent studies showing that in patients with established coronary artery disease taking a statin drug substantially reduces their risk of heart attack and dying.

These studies are the kind that provide the most robust proof: randomized, prospective and blinded.

level of evidenceWhen cardiologists rate the strength of evidence for a certain treatment (as done for lifestyle intervention here) we use  a system that categorizes the evidence as Level A, B, or C quality.

LeveleA quality (or strong) evidence consists of multiple,large, well-done, randomized trials such as exist for statins in patients with coronary heart disease.

Level B Evidence comes from a single randomized trial or nonrandomized studies.

Level C evidence is the weakest and comes from “consensus opinion of experts, case studies or standard of care.”

When treatment recommendations are based on Level C evidence they are often reversed as more solid data is obtained. Level A recommendations almost always hold up over time.

The level of evidence supporting restricting dietary cholesterol and fat to reduce heart attacks and strokes has always been at or below Level C and now it is clear that it is insufficient and should be taken out of guideline recommendations.

Evidence Strongly Supports Atherogenic Cholesterol is Related to Coronary Heart Disease

There are other lines of evidence that strongly support  the concept that  LDL cholesterol (bad cholesterol) or an atherogenic form of LDL cholesterol is strongly related to the development of atherosclerosis. If you are born with really high levels you are at very high risk for coronary heart disease, conversely if you are born with mutations that cause extremely low levels you are highly unlikely to get coronary heart disease.

Thus, the cholesterol hypothesis as it relates to heart disease is very much till intact although the diet-heart hypothesis is not.

Conflating the Diet-Heart Hypothesis and the Cholesterol Hypothesis

There is an abundance of misinformation on the internet that tries to conflate these two concepts. Sites with titles like “The Great Cholesterol Lie” , “The”  Cholesterol Hoax”, The Cholesterol Scam”  abound .

These sites proclaim that cholesterol is a vital component of cell membranes (it is) and that any attempt by diet or drugs to lower levels will result in severe side effects with no benefit

Doctors, according to these types of sites, in collusion with Big Pharma, have inflated the benefits of statin drugs and overlooked the side effects in the name of profit. Often, a “natural” alternative to statins is promoted.  In all cases a book is promoted.

The Great Cholesterol Truths

It’s unfortunate that nutritional guidelines have promoted restriction of cholesterol and fat for so long. These guidelines (like most of nutritional science)  were based on flawed observational studies. They should not have been made public policy without more consensus from the scientific community.  The good news is that ultimately the truth prevails when enough good scientific studies are done.

It is right to question the flimsy foundation of nutritional recommendations on diet and heart disease but the evidence for statin benefits in patients with established coronary heart disease is rock solid.

Hopefully, the less long-winded explanation I provided my patient in the office will persuade him to keep on taking his atorvastatin pills while simultaneously allowing him to eat eggs, shrimp and full fat dairy without guilt.