For diagnosing high Lp(a) they chose a universal cut point of >100 nmol/L (approximately >50 mg/dl) which is at the 80th percentile in white Americans. This cut-off is not written in stone and may vary depending on risk, ethnicity, and comorbidities. Some labs report out Lp(a) in mg/dl, others in nmol/L. Pay attention to the units.
An individual’s Lp(a) level is 80-90% genetically determined in an autosomal codominant inheritance pattern with full expression by 1-2 years of age and adult-like levels achieved by approximately 5 years of age. Outside of acute inflammatory states, the Lp(a) level remains stable through an individual’s lifetime regardless of lifestyle.
High-quality evidence supports a link between Lp(a) levels and a variety of cardiovascular-related outcomes. See Table 1. The risk of heart attack and aortic stenosis is increased 3 to 4 fold.
4. The following populations should be considered for testing.
5. Neither diet nor lifestyle influences Lp(a) levels.
6. PCSK9 inhibitor drugs and niacin lower Lp(a) levels and but there are no data showing this changes clinical outcomes.
7. Similar to my approach, “the authors recommend initiating a moderate- to high-intensity statin therapy in adults aged 40-75 years with a 10-year ASCVD risk of 7.5% to ≤20% with a Lp(a) ≥100 nmol/L. High-risk patients with LDL-C ≥70 mg/dL (non-HDL-C ≥100 mg/dL) and a Lp(a) ≥100 nmol/L on maximally tolerated statin should be considered for more intensive therapies (ezetimibe and PCSK9 inhibitors) to lower LDL-C.”
8. Currently, novel therapies are being studied that selectively target Lp(a). A phase 2 trial of AKCEA apo(a)-LRx, an apo(a) antisense oligonucleotide, reduced Lp(a) up to 80%. A phase 3 study is being planned. Additionally, an oxPL antibody that binds and inactivates the pro-osteogenic activity of Lp(a) has promising in vitro data. These therapies, while promising, require additional research prior to becoming mainstream therapies.
The cost of the blood test for Lp(a) should be minimal. Medicare reimburses $14 for it. You can order it from Boston Heart Diagnostics for $11. Unfortunately, there is no telling what your local hospital lab will charge.
Since Lp(a) is inherited, patients with high levels should consider having first-degree relatives tested for Lp(a) to identify those who are going to be at high risk. This provides an early warning of who in the family is most at risk for cardiovascular complications early in life. Such patients should be considered for early screening for subclinical atherosclerosis. In addition, they should be additionally motivated to do everything possible to reduce their elevated risk by lifestyle changes.
N.B. In 2018 the Centers for Disease Control and Prevention (CDC) approved two ICD-10 codes for the diagnosis of elevated Lipoprotein(a), or Lp(a). The ICD-10 diagnosis codes help to identify asymptomatic patients with elevated Lipoprotein(a) (E78.41) and a family history of elevated Lipoprotein(a) (Z83.430)
N.B.2. Don’t confuse Lp(a) with Apolipoprotein A1 which is the major protein component of HDL particles in plasma. Also, please note that WordPress converted my little a into a capital A in the title and I have no idea how to prevent that conversion.
For far too long, many patients have undergone a cardiac test that carries grave risks with the misunderstanding that they are getting the definitive assessment of their coronary arteries.
Chances are if you have visited an emergency room in the USA with chest pain and you weren’t clearly having an acute heart attack, you ended up getting one of two tests: a stress test or an invasive coronary angiogram (ICA).
What Is A Cardiac Catheterization?
For decades the ICA (commonly termed “cardiac catheterization or cath”) was considered the “gold standard” for the assessment of the arteries to the heart (the coronary arteries.) This invasive test involves inserting a tube (catheter) into either an artery in the wrist or groin, threading the catheter up the artery to the aorta and injecting contrast dye directly into the coronary arteries.
The x-ray movie images (angiogram) obtained then show the dye within the lumen of the arteries. If the column of dye is impinged upon an obstruction is diagnosed. However, early plaque in the arteries doesn’t necessarily stick into the lumen and typically resides in the wall, hidden from these “lumenograms.”
Below are the freeze-frame images of the left coronary artery invasive angiogram from a man we shall call Jerry who underwent catheterization in his 40s for atypical chest pain. He was told he had normal arteries, that they were “clean”.
Given the news that his arteries had no plaque build-up, he felt no need to modify his lifestyle or take cholesterol medications in order to avoid the fate of early death from myocardial infarction that his father had suffered at age 50.
Limitations Of The Cardiac Cath In Identifying Atherosclerotic Plaque
When I first saw him a year after the cardiac cath I told him that although his previous cardiologist had told him all was fine with his coronary arteries he could, in fact, have significant diffuse subclinical atherosclerosis and still be at high risk for a heart attack.
This came as quite a shock to Jerry as he, like most laypeople, view the cardiac cath as the “gold standard” for assessment of the coronary arteries. For most patients, a normal cath has been viewed as a warranty against heart attack
Although ICA has been the gold standard for the diagnosis of coronary artery disease, lumenography only shows the internal arterial lumen and does not see the vessel wall with its developing atherosclerotic plaque. Previous studies analyzing serial angiograms from patients presenting with acute coronary syndrome (ACS) have suggested that in nearly two-thirds of the culprit lesions, the coronary angiogram obtained a few months before the acute event demonstrated a non-significant stenosis.
Identifying Early Plaque Using Coronary Calcium Scans
I recommended the patient get a coronary artery calcium (CAC) scan to look for early coronary plaque and this demonstrated two small calcific plaques in the proximal portion of his LAD coronary artery. His calcium score was 9 which is higher than 82% of 45-year-old white males.
Now that we had visual proof of the plaque in his arteries he was motivated to change his lifestyle to reduce the risk of suffering his dad’s fate. In addition, he was now willing to take medications to further reduce risk.
A year later he was admitted to our hospital with palpitations and chest tightness. This time as I was his cardiologist we performed a noninvasive test-a coronary CT angiogram (CCTA). This demonstrated the two small areas of calcification in the LAD we had noted on the calcium scan but in addition, we were able to see surrounding those foci of calcification substantial premature build-up of soft plaque.
Following the CCTA and a more definitive assessment of his coronary artery status we were able to tell him there was no significant blockage of the coronaries and therefore no need for any stenting or bypass procedure.
Just as important, however, was the knowledge that he had a substantial plaque in the LAD which puts him at risk for heart attack.
With this knowledge, we were able to convince him to undergo substantial lifestyle changes to reduce his long term risk of heart attack and stroke. In addition, he was started on statin therapy to further reduce those risks.
The CCTA is performed using a special X-ray scanner and the risks are a small amount of radiation plus the risks of administration of intravenous radioiodine contrast. The injected dye material can cause allergic reactions in those predisposed and worsen kidney function in patients with underlying kidney disease.
Cardiac cath is usually very safe. A small number of people have minor problems. Some develop bruises where the catheter had been inserted (puncture site). The contrast dye that makes the arteries show up on X-rays causes some people to feel sick to their stomachs, get itchy or develop hives.
Even the NIH website downplays the risks, terming it a “relatively safe procedure” with rare complications.
However, the procedure is associated with substantial morbidity ranging from internal bleeding requiring surgery to disabling stroke. Although the risk of dying from the procedure has declined over the last 30 years it is still around .05%.
I have included a recent detailed summary of potential complications at the end of this post.
There are definite indications for getting a cardiac catheterization and I refer patients for this procedure on a daily basis. The clearest benefit is in patients presenting with clear evidence for myocardial damage (elevated troponin levels) from a myocardial infarction. In such patients the known benefits of opening tightly blocked coronary arteries outweigh the risks of the procedure.
However, patients should think twice and have an extensive discussion with the cardiologist recommending the test when there has been no evidence for myocardial damage.
Most importantly, patients should know that a declaration of “clean arteries” or “the arteries of a twenty-year-old” from the results of a cardiac cath do not guarantee freedom from cardiac events down the line. To detect early and premature atherosclerotic plaque build-up which corresponds to a very high lifetime risk of heart attack and stroke other techniques that look at the arterial wall and not the lumen are needed.
For the youngish, vascular ultrasound imaging for measurement of carotid IMT and soft plaque detection is useful, whereas CAC or CCTA is more useful in subjects over age 40 years of age.
N.B. As promised a long laundry list of complications for your edification.
The risk of major complications during diagnostic cardiac catheterization procedure is usually less than 1%, and the risk and the risk of mortality of 0.05% for diagnostic procedure. For any patient, the complication rate is dependent on multiple factors and is dependent on the demographics of the patient, vascular anatomy, co-morbid conditions, clinical presentation, the procedure being performed, and the experience of the operator. The complications can be minor as discomfort at the site of catheterization to major ones like death.
But there are very serious complications of the procedure that can result in death or serious disability.
These are among the most common complications seen after cardiac catheterization procedures. Hematomas are usually formed following poorly controlled hemostasis post sheath removal. Most hematomas are self-limiting and benign, but large rapidly expanding hematomas can cause hemodynamic instability requiring resuscitation with fluids and blood. The incidence of this complication is significantly reduced in transradial access. In patients with transfemoral access, retroperitoneal bleeding should be suspected if there is a sudden change in the hemodynamic stability of the patient with or without back pain as there may not be any visible swelling in the groin for some of these patients. The incidence of this complication is less than 0.2%. Strong clinical suspicion along with immediate imaging, usually with CT scan, helps make a diagnosis of this problem. Identification of the bleeding source is essential for patients with continued hemodynamic deterioration. These life-threatening bleeds are more frequent when the artery is punctured above the inguinal ligament. Most patients are managed with a reversal of anticoagulation, application of manual compression and volume resuscitation and observation. Patients with continued deterioration with need coiling of the bleeding source vessel, or balloon angioplasty or covered stents for bleeding from larger vessels.
When the hematoma maintains continuity with the lumen of the artery, it results in the formation of a pulsatile mass locally, defined as a pseudoaneurysm. This will be associated with bruit on examination. They happen following low access in the superficial femoral artery as opposed to the common femoral artery. These are usually diagnosed by ultrasound Doppler imaging or CT angiography. Small pseudoaneurysms of the less than 2 to 3 cm in size may heal of spontaneously and can be followed by serial Doppler examinations. Large symptomatic pseudoaneurysms can be treated by either ultrasound-guided compression of the neck of pseudoaneurysm or percutaneous injection of the thrombin using ultrasound guidance or may need surgical intervention.
Direct communication between the arterial and venous puncture sites with ongoing bleeding from the arterial access site leads to the fistula formation and are associated with a thrill or continuous bruit on examination. These usually will require surgical exploration as they are unlikely to heal spontaneously and may expand with time.
This is an infrequent complication and occurs in patients with an increased atherosclerotic burden, tortuous arteries, or traumatic sheath placement. Non-flow limiting dissections usually heal spontaneously following sheath removal. A flow limiting large dissections could lead to acute limb ischemia and should be treated immediately with angioplasty and stenting. Vascular surgery is usually reserved for patients with failed percutaneous techniques.
Thrombosis and Embolism
This complication is extremely rare with the use of the low profile catheters and predisposing factors include small vessel lumen, and associated peripheral arterial disease, diabetes mellitus, female sex, large diameter sheath, and prolonged catheter dwell time. Treatment involves removal of the occlusive sheath, percutaneous thrombectomy in conjunction with vascular surgery consultation.
Vascular Complications after Transradial Access
The most frequent complication after transradial access is about a 5% risk of radial artery occlusion. This is a clinically insignificant complication if the Allen test is normal. Patients with incomplete palmar arch and abnormal Allen test may have symptoms of hand ischemia after radial artery occlusion.
Radial artery spasm is another frequent complication, and this can be avoided by the use of local vasodilatory medications and systemic anxiolytics. Perforation of the radial artery is an extremely rare complication and is usually managed with prolonged external compression and rarely requires vascular surgery intervention.
Other Major Complications
The incidence of death with cardiac catheterization has decreased progressively and is less than 0.05% for diagnostic procedures. Patients with depressed left ventricular systolic function and those presenting with shock in the setting of acute myocardial infarction are at increased risk. In some subsets of patients, the risk of mortality can be more than 1%. Other factors that would increase the risk include old age, the presence of multivessel disease, left main coronary artery disease, or valvular heart disease like severe aortic stenosis.
The reported incidence of periprocedural myocardial infarction for a diagnostic angiography is less than 0.1%. This is mostly influenced by patient-related factors like the extent and severity of underlying coronary artery disease, recent acute coronary syndrome, diabetes requiring insulin, and technique-related factors.
The overall risk of stroke in recently reported series is low at 0.05% to 0.1% in diagnostic procedures and can increase to 0.18% to 0.4% in patients undergoing intervention. This can be a very debilitating complication associated with a high rate of morbidity and mortality. The risk is higher in patients with extensive atherosclerotic plaque in the aorta and aortic arch, complex anatomy, procedures requiring multiple catheter exchanges or excessive catheter manipulation, or the need for large-bore catheters and stiff wires.
Dissection and Perforation of the Great Vessels
Dissection of the aorta, perforation of the cardiac chambers, perforation of the coronary arteries is an extremely rare complication. The risk is higher in procedures with intervention as opposed to diagnostic procedures only. Patients with type A aortic dissection involving the ascending aorta will require surgical correction. Patients with a cardiac chamber or coronary perforation resulting in the accumulation of the blood in the pericardial space will need urgent pericardiocentesis to restore hemodynamic stability and immediate surgical consultation.
Cholesterol emboli from friable vascular plaques can give rise to distal embolization in multiple vascular beds. These are usually recognized by digital discoloration (blue toes), livedo reticularis. This can also manifest as a neurological squeal or renal impairment. The risk of this complication is minimized by exchanging catheters over a long wire and minimizing the catheter exchanges. Retinal artery occlusion causes Hollenhorst plaque.
Allergic reactions can be related to the use of local anesthetic, contrast agents, heparin or other medications used during the procedure. Reactions to the contrast agents can occur in up to 1% of the patients, and people with prior reactions are pretreated with corticosteroids and antihistamines. Use of iso-osmolar agents decreases the risk compared to high osmolar agents. When severe reactions do occur, they are treated similarly to anaphylaxis with intravenous (IV) epinephrine (initial dose 1 ml of 1:10000 epinephrine).
Acute Renal Failure
The incidence of the reported contrast nephropathy is quite variable (range 3.3% to 16.5%) in the patients undergoing cardiac catheterization resulting in a transient increase in the serum creatinine levels after exposure to contrast material. In the National Cardiovascular Data Registry, the incidence of contrast-induced acute kidney injury was 7.1%, among the patients undergoing elective and urgent coronary intervention. The risk is higher in patients with underlying moderate to severe renal disease, people with diabetes, elderly, females, patients on diuretics, ACEI, and metformin. Adequate pre-hydration, use of iso-osmolar agents, and techniques to minimize the amount of dye used will help prevent this complication. Renal atheroemboli can also cause renal failure and are associated with other signs of embolization.
Cardiac catheterization is performed using sterile technique, and local or systemic infection is extremely rare. Routine prophylaxis for endocarditis is not recommended during cardiac catheterization procedures.
Radiation skin injury can occur if a patient is exposed to excessive doses of radiation to one particular area of the body and manifestation could range from mild erythema to deep ulceration. Skin biopsies should be avoided for these lesions as they would make the underlying condition worse. This complication should be managed by a combined team of cardiologists, dermatologists, and plastic surgeons.
The occurrence of the ventricular fibrillation or ventricular tachycardia during the procedure could be related to irritation or ischemia of the myocardium by the catheter, contrast material or occlusive balloons. These arrhythmias occur more frequently in people presenting with acute ST-elevation myocardial infarction and treatment includes cardioversion along with anti arrhythmic drugs and restoration of the flow to the occluded artery. Atrial tachyarrhythmias can occur following the irritation of the right atrium during right heart catheterization and is usually self-limiting.
It is available online and through an app for Apple and Android (search in the app store on “MESA Risk Score” for the (free) download.)
The MESA tool allows you to easily calculate how the CACS effects you or your patient’s 10 year risk of ASCVD.
The Multi-Ethnic Study of Atherosclerosis (MESA) is a study of the characteristics of subclinical cardiovascular disease (disease detected non-invasively before it has produced clinical signs and symptoms) and the risk factors that predict progression to clinically overt cardiovascular disease or progression of the subclinical disease. MESA researchers study a diverse, population-based sample of 6,814 asymptomatic men and women aged 45-84. Approximately 38 percent of the recruited participants are white, 28 percent African-American, 22 percent Hispanic, and 12 percent Asian, predominantly of Chinese descent.
To use the score you will need information on the following risk factors:
age, gender, race/ethnicity, diabetes (yes/no), current smoker (yes/no), total and HDL cholesterol, use of lipid lowering medication (yes/no), systolic blood pressure (mmHg), use of anti-hypertensive medication (yes/no), any family history of heart attack in first degree relative (parent/sibling/child) (yes/no), and a coronary artery calcium score (Agatston units).
In many cases the CACS dramatically lowers or increases the risk estimate.
In this example a 64 year old man with no discernible risk factors has a CACS of 175 The 10 year risk of a CHD event almost doubles from 4.7% to 7.6% when the CACS is added to the standard risk factors and moves into a range where we need much more aggressive risk factor modification.
On the other hand if we enter in zero for this same patient the risk drops to a very low 1.9%.
It’s also instructive to adjust different variables. For example, if we change the family history of heart attack (parents, siblings, or children) from no to yes, this same patient’s risk jumps to 7.2% (2.6% with zero calcium score and to 10.4% with CACS 175.)
It can also be used to help modify risk-enhancing behaviors. For example if you click smoker instead of non-smoker the risk goes from 4.7% to 7.5%. Thus, you can tell your smoking patient that his risk is halved if he stops.
Discussions on the value of tighter BP control can also be informed by the calculator. For example, if our 64 year old’s systolic blood pressure was 160 his risk has increased to 6.8%.
How Does Your CACS Compare To Your Peers?
A separate calculator let’s you see exactly where your score stands in comparison individuals with your same age, gender, and ethnicity
The Coronary Artery Calcium (CAC) Score Reference Values web tool will provide the estimated probability of non-zero calcium, and the 25th, 50th, 75th, and 90th percentiles of the calcium score distribution for a particular age, gender and race. Additionally, if an observed calcium score is entered the program will provide the estimated percentile for this particular score. These reference values are based on participants in the MESA study who were free of clinical cardiovascular disease and treated diabetes at baseline. These participants were between 45-84 years of age, and identified themselves as White, African-American, Hispanic, or Chinese. The current tool is thus applicable only for these four race/ethnicity categories and within this age range.
The calculator tells us that 75% of 64 year old white males have a non-zero CACS and that the average CACS is 61.
Unlike SAT scores or Echo Board scores you don’t want your CACS percentile status to be high. Scores >75th percentile typically move you to a higher risk category, whereas scores <25th percentile move you to a lower risk category, often with significant therapeutic implications.
Scores between the 25th and 75th percentile typically don’t significantly change the risk calculation.
Exploring Gender Differences In CACS
If we change the gender from male to female on our 64 year old the risk drops considerably from 4.7% down to 3.3%. This graph demonstrates that over 20% of women between the ages of 75 and 84 years will have zero calcium scores.
The graph for men in that same range shows that only around 10% will have a zero CACS.
I’ve been asked what the upper limit is for CACS but I don’t think there is one. I’ve seen numerous patients with scores in the high two thousands and these graphs show individuals in the lowest age decile having scores over 2981.
If you want to be proactive about the cardiovascular health of yourself or a loved one, download the MESA app and evaluate your risk. Ask your doctor if a CACS will help refine that risk further.
In October, 2016 the skeptical cardiologist predicted that Donald Trump’s coronary calcium score, if remeasured, would be >100 . At that time I pointed out that this score is consistent with moderate coronary plaque build up and implies a moderate risk of heart attack and stroke.
Trumps’ score gave him a seven-fold increase risk of a cardiovascular event in comparison to Hilary Clinton (who had a zero coronary calcium score) .
I was able to predict this score because we knew that Trump’s coronary calcium was 98 in 2013 and that on average calcium scores increase by about 10% per year.
I pointed out that his previous score was average for white men his age and his repeat score is also similar to the average white male of 71 years.
Entering Trump’s numbers into the MESA coronary calculator shows us he is at the 46th percentile, meaning that 46% of white men his age have less calcium.We can also calculate Trump’s 10 year risk of heart attack and stroke using the app from the ACC (the ASCVD calculator) and entering in the following information obtained from the White House press briefing:
Total Cholesterol 223
LDL Cholesterol 143
HDL Cholesterol 67
Systolic Blood Pressure 122
Never Smoked Cigarettes
Taking aspirin 81 mg and rosuvastatin (Crestor) 10 mg.
His 10 year risk of heart attack or stroke is 16.7%.
Given that his calcium score is average it doesn’t change his predicted risk and the conclusion is that his risk is identical to the average 71 year old white man-moderate.
We also know that Trump had an exercise stress echocardiogram which was totally normal and therefore can be reasonably certain that the moderate plaque build up in his arteries is not restricting the blood flow to his heart.
Here is what Dr. Jackson said about the stress echo:
He had an exercise stress echocardiogram done, which demonstrated above-average exercise capacity based on age and sex, and a normal heart rate, blood pressure, and cardiac output response to exercise. He had no evidence of ischemia, and his wall motion was normal in all images. the stress echo:
The New York Times article on this issue, entitled “Trump’s Physical Revealed Serious Heart Concerns, Outside Experts Say” however, presents a dramatically worrisome and misleading narrative.
It quotes several cardiologists who were very concerned about Trump’s high LDL level, weight and diet.
It’s interesting that some of the experts quoted in the NY Times piece feel that Trump’s Crestor dose should be increased in light of the recent NY Times piece questioning whether the elderly should take statins at all.
If we have serious concerns about Trump’s heart then we should have the same concerns about every 71 year old white man because he is totally average with regard to cardiac risk. In addition he is on a statin and on aspirin, the appropriate drugs to reduce risk.
In contrast to the average 71 year old male he has had a battery of cardiac tests which show exactly where he stands cardiac wise.
Most of these cardiac tests we would not recommend to an asymptomatic individual of any age. Jackson revealed that Trump had an EKG and an echocardiogram.
His ECG, or commonly EKG, was normal sinus rhythm with a rate of 71, had a normal axis, and no other significant findings.
He had a transthoracic echocardiogram done, which demonstrated normal left ventricular systolic function, an ejected fraction of 60 to 65 percent, normal left ventricular chamber size and wall thickness, no wall motion abnormalities, his right ventricle was normal, his atria were grossly normal, and all valves were normal.
So our President has a normal heart for a 71 year old white male. This automatically puts him at moderate risk for heart attack and stroke over the next 10 years but he is being closely monitored and appropriately treated and should do well.
N.B. I see that Trump’s LDL was reported previously as 93. The current LDL of 143 suggests to me that he has not been taking his Crestor.
N.B. Below is an excerpt from my prior post which explains coronary calcium
Regular readers of the skeptical cardiologist should be familiar with the coronary calcium scan or score (CAC) by now. I’ve written about it a lot (here, here, and here) and use it frequently in my patients, advocating its use to help better assess certain patient’s risk of sudden death and heart attacks.
The CAC scan utilizes computed tomography (CT) X-rays, without the need for intravenous contrast, to generate a three-dimensional picture of the heart. Because calcium is very apparent on CT scans, and because we can visualize the arteries on the surface of the heart that supply blood to the heart (the coronary arteries), the CAC scan can detect and quantify calcium in the coronary arteries with great accuracy and reproducibility.
Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium. Thus, the more calcium, the more plaque and the greater the risk of heart attack and death from heart attack.
Although most nutritional authorities are now admitting that reducing saturated fat consumption by substituting carbohydrates was really bad advice, they, for the most part, are still sticking to the overall concept of limiting all saturated fats to <10% of daily calories and substituting “healthy” polyunsaturated fats for “unhealthy” saturated fats whenever possible.
The recommendation to limit intake of calories from saturated fats to less than 10 percent per day is a target based on evidence that replacing saturated fats with unsaturated fats is associated with reduced risk of cardiovascular disease. The limit on calories from saturated fats is not a UL set by the IOM. For most calorie levels, there are not enough calories available after meeting food group needs to consume 10 percent of calories from added sugars and 10 percent of calories from saturated fats and still stay within calorie limits.
Recommendations to limit saturated fatty acids (SFAs) to <10% of calories persist, despite a spate of recent meta-analyses showing no relationship between saturated fat consumption and coronary heart disease (CHD, also known as ischemic heart disease (IHD)).
In addition, it should be abundantly clear by now that not all SFAs behave the same with respect to our lipids or our IHD risk.
Wide Variety Of Saturated Fats
Most SFAs come from animal origins, including meat and dairy products. The types of SFAs differ markedly between meat and dairy products; the associated nutrients and their interaction with SFAs also differs widely and all of this is likely to affect the risk of IHD.
For example, in the MESA (Multi-Ethnic Study of Atherosclerosis) study, each 5-g/d intake of dairy SFAs was associated with a 16% lower risk of IHD, whereas each 5-g/d intake of meat SFAs was related to a 29% higher risk of IHD.
Despite this, current guidelines continue to repeat the unsubstantiated recommendation to consume low fat dairy over full fat dairy.
Lower Risk Of Heart Disease With Dairy Saturated Fats
This study found that higher intakes of SFA in 35,597 Dutch men and women were associated with lower risks of ischemic heart disease (IHD).
In other words, the more SFA the Dutch eat, the less their chance of having a heart attack.
And, the association “did not depend on the substituting macronutrient.” Those who ate less saturated fats and more “healthy” polyunsaturated fats did no better than those who substituted carbohydrates.
The association was dependent “on the chain length and food source of SFAs.”
The authors noted that the lower risk of IHD was driven by consumption of:
short-to-medium chain SFAs (myristic acid, the sum of pentadeclyic and margaric acids, and SFAs from dairy sources including butter, cheese, and milk and milk products.
Skeptics amongst my readers might think that this study was funded by the dairy industry, but as Marion Nestle pointed out on her Food Politics blog, support came from Unilever, who would have a vested interest in promoting their low saturated fat/high polyunsaturated fat margarines as substitutes for butter fat. This is only one of 11 industry-funded studies with findings different from what the sponsors would have liked, versus 105 studies with findings supporting products of the sponsors (since Marion has been tracking such studies).
It’s likely that some saturated fats, especially when eaten immoderately, without an otherwise balanced and diverse diet, can increase your risk of heart disease.
However, the saturated fats that come from dairy products are clearly not contributing to heart disease risk or obesity and our nutritional guidelines should recommend full fat dairy, not low fat or non fat products that require addition of added sugar to maintain palatability.
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.
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.1, 2, 3
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.2, 8 Cheese, a leading source of SFAs, is actually linked to no difference in or reduced risk of coronary heart disease and type 2 diabetes.9, 10 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
"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!
For another viewpoint (?from an SFA enthusiast) and a detailed description of both editorials see Axel Sigurdsson’s excellent post here.
The skeptical cardiologist recently spent a week in the Basque region of Spain intensively researching dietary and lifestyle choices of this unique area.
Spain borders the Mediterranean and is often included in those countries that are considered to be the source of the Mediterranean diet (MD) which I recommend to my patients.
For a good summary of the Mediterranean “diet pyramid” check out this 1995 article.
The definition of the MD varies, often based on what bias the definer has for particular foods or macronutrients, but initially was considered to be the food patterns typical of Crete, much of the rest of Greece and southern Italy in the early 1960s. The reason for choosing this time era and geography was based on:
very high adult life expectancy with very low rates of coronary heart disease, certain cancers and diet-related chronic disease
Data suggested common characteristics of food availability and dietary intake
Epidemiological studies throughout the world on populations with similar dietary patterns suggested a benefit
The diet is closely tied to traditional areas of olive cultivation in the Mediterranean region.
The MD of the early 1960s had the following characteristics:
an abundance of plant foods (fruit, vegetables, breads, other forms of cereals, potatoes, beans, nuts and seeds)
minimally processed, seasonally fresh and locally grown foods
fresh fruit as the typical daily dessert
sweets containing concentrated sugar or honey consumed a few time per week
olive oil as the principal source of fat
dairy products (principally cheese and yogurt and full fat) consumed in low to moderate amounts
fish and poultry consumed in low to moderate amounts
zero to four eggs consumed weekly
red meat consumed in low amounts
wine consumed in low to moderate amounts, normally with meals
I stayed in a small beach town, Deba, in Spain which is half way between Bilbao (famous for its Guggenheim museum) and San Sebastian. There were very few non-Spanish tourists in Deba so presumably the dietary and lifestyle choices I observed are representative of current Basque choices although likely different from the early 1960s.
I found the Basque people in Deba to be welcoming and joyful and European statistics show the Basque to be among the most satisfied with their overall life and job conditions.
Interestingly, the life expectancy of the Basque population in 2000 in years was 75.8 for men and 83.8 for women, and by 2011 it had increased to 79.3 and 86.1, respectively. The Basque women live longer than women in any other country in Europe.
Walking around the squares of Deba I observed two activities which I would ordinarily have presumed would result in a low life expectancy: lots of cigarette smoking and lots of Jamón consumption.
Ham was everywhere in Deba, from the supermarkets to the cafes. A typical appetizer choice was a plate full of Jamón Ibérico. Most of the pintxos (Basque-style tapas) we saw consisted of Jamon on bread.
From jamon.com (dedicated to the fine art of ham):
“Picture paper-thin strips of dark red ham like petals ringing a hand painted plate. Imagine big honest hams curing in the mountain air. Picture individual hams resting on stands in family kitchens throughout Spain with a long slim knife at hand for any and all to slice a treat.
In Spain, Jamón is hospitality. Jamón is Spain. Of all the European hams, jamón from Spain is the Gold Standard.”
Jamón, dry-cured ham, has been eaten in Spain and other Mediterranean countries since ancient times. There are basically two kinds: hams from rustic and free range pigs (Iberia, Corsican or Cinta Senese) and hams from intensively-reared white pigs (Serrano, Parma, Bayonne).
Both hams involve a moderate salting and a ripening period of 7-14 months for white pigs and over 20 months for Iberian hams.
When they are finished curing, they have an incredibly complex taste, distinct marbling, a deep red color and an intense ham flavor.
The most sought after ham is Jamón Ibérico de Bellota: a sub category of Jamón Ibérico” where the pigs are free to roam the meadows of the ‘dehesa’. During the autumn prior to their sacrifice, they are encouraged to gorge on acorns (bellotas) from the holm oak and cork trees, sometimes gaining as much as a kilo of weight a day.”
Health Consequences of Eating Jamón Ibérico.
A 100 g serving of Jamon Iberico contains 375 calories, 200 of them from fat. Of the total 22 grams of fat, 6.5 grams is saturated, 2 grams polyunsaturated, and 13 grams monounsaturated . There are 43 grams of protein and a lot of sodium ( 1.1 grams).
If we follow most current nutritional guidelines we would be advised to avoid Jamon because it is a considered a processed meat and it contains lots of salt and saturated fat.
Despite eating lots of Jamon, however, the Spanish and Basque do very well in terms of longevity and rates of heart disease.
The Basque good health could be related to any number of factors. They consume lots of fresh fish caught in nearby ports and prepared with lots of garlic and olive oil. (I had the best monkfish of my life in a cider house in the hills near Deba). Fish and olive oil are clearly beneficial dietary components.
They also drink alcohol in varied forms, including locally sourced apple cider, beer and fine local wines from Rioja.
They are active and they have long stretches of beautiful coastline to hike (including this geopark), some of the best surfing beaches in the world, and hills for cycling.
Ultimately, a healthy lifestyle consists of enjoyable and sustainable exercise and an enjoyable, sustainable and palatable diet composed of a combination of foods (mostly plants) , interacting in myriad unmeasurable ways. Focusing on specific fat (other than industrially produced trans fats) or sodium content is not a particularly useful approach.
I think Jamon can be considered part of a healthy Mediterranean diet when consumed in moderation and when combined with an active physical lifestyle. It makes a wonderful addition to anyone’s diet.
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.
When 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.
The updated AHA/ACC Cardiovascular Prevention Guidelines (CPG) which include the excessively wordy “The Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults Risk” were published late last year and immediately were the center of controversy.
After working with them for 9 months and using the iPhone app to calculate my patients’ 10 year risk of atherosclerotic cardiovascular disease (ASCVD, primarily heart attacks and strokes) it has become clear to me that the new guidelines will recommend statin therapy to almost all males over the age of 60 and females over the age of 70.
As critics have pointed out, this immediately adds about 10 million individuals to the 40 million or so who are currently taking statins.
Should we be starting all elderly Americans on statin drugs?
My simple answer is no. It doesn’t make sense to do this, because clearly not all elderly individuals have atherosclerosis or will ever develop its consequences of heart attack and stroke. Many have inherited the genes that allowed their parents to live free of heart disease into their 90s and will not benefit at all from long term statin therapy; they may actually suffer the expense and side effects instead.
How can we better decide who among the elderly will benefit from statin therapy?
If you have read my previous posts on searching for subclinical atherosclerosis here and here you probably know the answer. Let’s look at a specific case and apply those principles.
Robert is 69 years old. I see him because, in 2010, the posterior leaflet of his mitral valve ruptured, resulting in the mitral valve becoming severely incompetent at its job of preventing back flow from the left ventricle into the left atrium. I sent him to a cardiac surgeon who repaired the ruptured leaflet. Although he has a form of “heart disease,” this is a form that has nothing to do with cholesterol, hypertension or diabetes and is not associated with ASCVD.
However, it is my job to assess in him, like all individuals, the risk of developing coronary heart disease or ASCVD.
He has no family history of ASCVD and he feels great since the surgery, exercising aerobically 4-5 times per week.
His BMI is 23.87 which is in the normal range. His BP runs 116/80.
His total cholesterol is 210 and LDL or bad cholesterol is 142. Good or HDL cholesterol is 56 and triglycerides 59. The total and LDL cholesterol levels are considered “high,” but they could be perfectly acceptable for this man.
When I ran his 10 year ASCVD risk (risk of developing a heart attack or stroke over the next 10 years), it came back as 14%. The new guidelines would suggest having a conversation with him about starting a statin if his risk is over 7.5%. His risk is double this and statins are definitely recommended in this intermediate risk range. Interestingly, I cannot enter a cholesterol level or blood pressure for a man of this age that yields a risk less than 7.5%.
When I had my discussion with him about his risk for ASCVD, I plugged his numbers into my iPhone and showed him the results and gave him the guideline recommendation.
Lifestyle Changes to Lower Cholesterol
The new Cardiovascular Prevention Guidelines have a section devoted to Lifestyle Management to Reduce Cardiovascular Risk. Unfortunately, none of the lifestyle changes they recommend have been shown to reduce ASCVD risk in an individual like Robert. He already exercises the recommended amount, is at his ideal body weight and eats a healthy diet. If we were to tighten up on his diet by, say reducing red meat, eggs and high fat dairy, all we would accomplish would be to lower his LDL and HDL cholesterol levels and make his life and meals less satisfying. The lower total cholesterol and LDL cholesterol would not lower his risk of ASCVD and the calculated 10 year ASCVD risk would still be in the range where statins are recommended.
Therefore, I am not going to tell Robert that he should reduce his saturated fat consumption (he already has incorporated that into his diet since he’s been bombarded with the low fat mantra for 30 years).
Searching for Subclinical Atherosclerosis
I’m going to tell Robert that we need to know if he has atherosclerosis, the disease that we are attempting to modify.
We started with an ultrasound to look at the lining of the large arteries in his neck that supply blood to the brain, the carotid arteries (a process I describe in more detail here). Although severe atherosclerotic blockages in these arteries put one at risk of a stroke, I was much more interested in the subtle changes in the arteries that precede symptoms and are an early harbinger of atherosclerosis.
Careful ultrasound recording and measurement of the main common carotid arteries from both the left and right side showed that the IMT or thickness was lower than average for his age, gender and ethnicity. His carotid IMT was at the average for a 60 year old, therefore, his so-called vascular age was 60 years, younger than his chronological age. If I plug that age into the ASCVD risk estimator, I get an 8.2% 10 year risk, just barely above the statin treatment cut-off.
Careful scrutiny with ultrasound of the entire visible carotid system in the neck on both sides did not reveal any early fatty plaques or calcium in the lining of the carotid arteries. He had no evidence for atherosclerosis, even very subtle early forms, in this large artery, a finding which is usually predictive of what is going on in the other large arteries in the body, including the coronary arteries, which supply blood to the heart.
At this point, I think, we could have stopped the search for subclinical atherosclerosis and agreed that no statin therapy was warranted. However, Robert wanted further reassurance that his coronary arteries were OK, therefore we set him up with a coronary calcium study (see my full description of this test here).
Searching for Subclinical Atherosclerosis: The Calcium Score
Robert’s coronary calcium score came back at 21 (all in the LAD coronary artery) , which put him at the 26th percentile compared to normal men of his age and gender. A score of 21 is average for a 59 year old man and 82% of men aged 69 have a score greater than zero. Robert had much less calcium in his coronaries than men his age, another factor putting him in a low risk category.
Given the low risk findings from both the vascular screening and the coronary calcium, I felt comfortable recommending no statin therapy and going against the guidelines.
Statins: Better Targets for The Two-edged Sword
This is not an unusual scenario; many of my older patients without heart attacks, strokes or diabetes fall into the risk category that would warrant statin therapy and if they have no clinical or subclinical evidence of atherosclerosis, I don’t advise statin therapy. My patients are free to follow the guidelines and take statin drugs after this advice, but most are very grateful that another pill (which they likely have heard bad things about on the internet or from friends with adverse experiences) can be avoided.
Statins are wonderful drugs when utilized in the right population, but they also carry a 9% increased risk of diabetes and about a 10% real world risk of developing muscle aches and weakness (myalgia).
I think it is essential to aim these two-edged swords at the right targets if we are to maximize the overall health benefits.
After a week of trying to track my salt consumption I have learned two things
1. Tracking salt consumption (unless you make all your meals at home from scratch or buy from fast food restaurants) is very tedious.
2. My salt consumption is low: less than the 1.5 grams per day recommended by the American Heart Association (AHA) every day (unless I attend a Cardinals game)
After reviewing the latest scientific publications on salt, however, I have to think that for most people, it is not worth the effort to track daily salt consumption.
Yes , this is nutritional heresy and goes against what my patients have been reading from authoritative nutritional sources for decades.
The AHA 1.5 gram/day limit for all Americans comes from a small, short term (4 weeks) study (Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med2001;344:3-10.)
The findings are not applicable to all Americans because more than 50% of participants in the DASH study had hypertension or prehypertension, more than 50% of participants were of African ancestry, potassium intake was markedly lower than in the general U.S. population, the trial involved only 412 persons, and a limited range of sodium intake was studied (1.5 to 3.3 g per day).
I asked most of my patients this week about their salt consumption. None of them could tell me what their average daily salt consumption was. However, almost to a man (or woman) they told me they had been consciously limiting their consumption of salt because they knew that this was healthy.
Thus, the 35 year old white woman with a blood pressure of 110/50 , palpitations and periodic dizzy spells is following the same recommendations to limit salt consumption as the 70 year old African-American with poorly controlled hypertension.
In the last few years this focus on lower salt consumption has been questioned after close analysis by the Institute of Medicine and the Cochrane Analysis.
Two articles in the prestigious New England journal of Medicine published a few weeks ago have convinced me that most individuals who are following a Mediterranean diet do not need to be concerned about their salt consumption.
Salt and Blood Pressure
In the first PURE study paper,(a prospective cohort study that included 101,945 people from five continents)
very few participants had an estimated sodium intake of less than 2.3 g per day, and almost none had an intake of less than 1.5 g per day. This suggests that, at present, human consumption of extremely low amounts of sodium for prolonged periods is rare.
The PURE Study looked at sodium excretion versus blood pressure and
found a steep slope for this association among study participants with sodium excretion of more than 5 g per day, a modest association among those with sodium excretion of 3 to 5 g per day, and no significant association among those with sodium excretion of less than 3 g per day.
This graph of data from the PURE study shows that lower levels of sodium excretion , below about 3 grams per day were associated with a higher risk of death.
Starting above about 5 grams per day the risk of death increased with increasing amounts of sodium excretion.
This is quite a shocker for those of us who have assumed for the last 20 years that the less salt we consumed the longer we would live.
Drawing less controversy were the findings from these two studies on potassium consumption. Higher levels of potassium consumption were associated with lower blood pressures and lower risk of death. The authors point out that high potassium intake may simply be a marker of healthy dietary patterns that are rich in potassium (e.g., high consumption of fruit and vegetables).
You can read more about these papers, including critical and positive comments at the heart.org here.
My Recommendations on Salt Consumption
Here is what I will be telling my patients about salt after a week of tracking my consumption and reading the relevant scientific literature.
Spend a day or two accurately tracking your consumption of salt to educate yourself. I found this app to be really helpful. I’ll expand on this in a future post.
Recognize that not everybody needs to follow a low salt diet. If your blood pressure is not elevated and you have no heart failure you don’t need to change your salt consumption.
If your blood pressure is on the low side and especially if you get periodic dizzy spells, often associated with standing quickly liberalize your salt intake, you will feel better.
If you have high blood pressure, you are the best judge of how salt effects your blood pressure. In the example I gave in a previous post, my patient realized that all the salt he was sprinkling on his tomatoes was the major factor causing his blood pressure to spike.
The kidneys do a great job of balancing sodium intake and sodium excretion if they are working normally. If you have kidney dysfunction you will be more sensitive to the effects of salt consumption on your blood pressure and fluid retention.
If you are following a Mediterranean diet with plenty of fresh fruits and vegetables you are going to be in the ideal range for both potassium and sodium consumption.
Public health experts are always seeking a “one size fits all” message to give the public. In the case of salt consumption, however, the message of less is better does not apply to all.