For some time now the skeptical cardiologist has been obsessed with discovering the best tool to measure body fat.
It’s clear that the fat that gathers around our heart and within our abdomen, so-called visceral fat, has dire consequences for the cardiovascular system.
The standard way of measuring obesity, however, the body mass index doesn’t really tell us with high accuracy what is going on with visceral fat.
You can calculate your BMI using this online calculator. When I plug my numbers in I get a BMI of 22.3 which puts me in the “normal” range according to this chart from the NHLBI.
The BMI, however, is a very crude tool. A high BMI could be the result of a large amount of muscle mass, generally felt to be a good thing.
Conversely, it’s possible to have a normal BMI with a very high visceral fat percentage and low muscle mass. Such patients, the so-called “skinny fat” have the same risk as those with obesity as determined by BMI.
Due to perceived limitations of BMI as a predictor of body fat (and therefore true obesity), other methods of estimating body fat and/or visceral fat have been developed.
Waist Circumference and Waist Stature Ratio
Waist circumference (WC) is a simple, inexpensive and reliable test. Some studies have suggested WC correlates with visceral fat better than BMI. Despite recommendations that WC be made a routine measurement along with height and weight, very few doctors (including the skeptical cardiologist) have embraced routine WC measurement.
I measured my WC multiple times and it was always about 33 inches which puts me solidly under the 40-inch cut point for men. One study suggests the WC to stature ratio (WSR) is superior to WC and that we should aim for a ratio <0.5.
My ratio was slightly under 0.5.
It’s not clear to me that WC or WSR adds enough to BMI to justify performing it on my patients. A 2009 comparison of BMI, WC, and WSR to the gold-standard of dual x-ray absorptiometry (DEXA-scan) found that
BMI, WC, and WSR perform similarly as indicators of body fatness and are more closely related to each other than with percentage body fat
Using a special caliper it is possible to measure the thickness of the skin at various body locations. These measurements when normalized for age and gender give a fair estimate of body fat.
I purchased one of these devices a few years ago and made measurements on myself and many of my friends. When I added up my skinfold thickness from the anterior and posterior upper arm, the waist, and the shoulder blade regions I obtained a thickness of 29 mm. Using the chart that is shipped with the caliper, my fat % was calculated at 17.9%.
Many bathroom scales these days claim to measure fat mass, muscle mass at the same time they are weighing you. Such scales are using bioimpedance to infer body composition.
I have been using a QardioBase for my daily weights which gives me a readout that typically looks like this:
When I pulled up the chart below I realized that 24% body fat for men >60 years of age was at the upper range for healthy, bordering on “overfat.”
If I was a woman, on the other hand, I would be at the bottom end of the healthy range, bordering on “underfat.”
How Fat Am I?
After utilizing the commonly available modalities for assessing body fat, visceral fat, and obesity do we truly know how fat the skeptical cardiologist is?
BMI puts him solidly in the normal range.
Waist circumference puts him solidly in the normal range.
Waist to status ratio puts him close to obese.
Skinfold calipers give him normal body fat for age of 17.9%.
A bioimpedance scale gives him 24% body fat, bordering on “overfat.”
After undergoing a test last week I believe I can answer the burning question with confidence. More importantly, I believe I now have a convenient, inexpensive, and highly accurate tool that will provide precise estimates of my patient’s visceral body fat.
Empowered with such knowledge, hopefully, we can more successfully identify and treat cardiometabolic disease.
N.B. That is not my abdomen in the featured image.
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.
Increasingly, the skeptical cardiologist has been recommending to patients that they take BP meds at bedtime as evidence has mounted that this does a better job of normalizing asleep blood pressure and minimizing daytime side effects.
Now a study published in European Heart Journal in October has demonstrated that routine ingestion of BP meds at bedtime as opposed to waking results in improved 24 hour BP control with enhanced decrease in asleep BP and increased sleep-time relative BP decline (known as BP dipping.)
More importantly, bedtime BP med ingestion in this randomized trial of over 19 thousand hypertensive Spaniards resulted in highly significant reductions in cardiovascular events including death, heart attack, heart failure and stroke over a 6 year median follow-up
The so-called Hygia Chronotherapy Trial was extremely well done and the results are powerful and should modify clinical practice immediately.
This figure demonstrates the dramatic and highly significant 45% reduction in all types of cardiovascular events measured. Note that stroke rate was halved!
Here are the Kaplan-Meier curves showing early and progressive separation of the treatment curves.
There was no difference side effects or compliance between the two groups.
The remarkable aspect of this intervention is that it costs nothing, introduces no new medications and has no increased side effects.
This study is practice-changing for me. We will be advising all hypertensive patients to take their once daily BP meds at bedtime.
h/t Reader Lee Sacry for bringing this study to my attention
The skeptical cardiologist this morning was greeted by headlines announcing that an international panel of 14 unbiased researchers had concluded that it was OK for humans to continue eating red meat and processed meat at current levels.
The startling news was a reversal of what the Dietary Guidelines for Americans, the AHA and the American Cancer Society have been telling us for years and threw the nutritional world into a tizzy. The bottom line recommendation, written in language suggesting a lack of certainty in the evidence and lack of confidence in the advice reads as follows:
The panel suggests that adults continue current unprocessed red meat consumption (weak recommendation, low-certainty evidence). Similarly, the panel suggests adults continue current processed meat consumption (weak recommendation, low-certainty evidence).
Volluz does her typically excellent job of explaining the science in a balanced way and includes some of the prominent voices who are outraged by the publication.
As I’ve pointed out (here and here and here) the science behind most nutritional recommendations is weak and often public health authorities make sweeping dietary recommendations that aren’t justified.
We are making gradual progress in rolling back bans on some healthy food, like eggs but unjustified bans on other healthy foods like full-fat yogurt and coconut oil persist.
When it comes to red meat consumption the systematic analyses reveal mild associations with poor health outcomes but these associations don’t prove causality and could easily be due to confounding factors or poor input data.
Thus, if you want to cut back your red meat consumption on the chance that these associations are truly reflective of causation go ahead. Especially if you have ethical or environmental concerns about production of red meat.
Just keep in mind that the calories you cut from less meat consumption should be replaced by more healthy nutrient-dense foods like non-starchy vegetables, nuts, dairy fat, avocado and olive oil and not by low quality carbs and ultra-processed food or you may be doing more harm than good.
I am happy to report that I survived the incident and am not concerned at all that my longevity has been compromised.
My 2013 summary of eggs, dietary cholesterol and heart disease (see here) is still valid and I highly recommend patients and readers read that post plus my updates on eggs with newer data (see here and here) rather than information related to the new egg study.
Although CNN and other news outlets lead with an inflammatory headline suggesting that eating those 3 eggs increased my risk of heart disease the new egg study could not possibly prove causation because it was an observational study.
Nutritional epidemiology has come under considerable criticism in the last few years for churning out these weak observational studies .John Ionaddis has been particularly vocal about these limitations, writing:
A large majority of human nutrition research uses nonrandomized observational designs, but this has led to little reliable progress. This is mostly due to many epistemologic problems, the most important of which are as follows: difficulty detecting small (or even tiny) effect sizes reliably for nutritional risk factors and nutrition-related interventions; difficulty properly accounting for massive confounding among many nutrients, clinical outcomes, and other variables; difficulty measuring diet accurately; and suboptimal research reporting. Tiny effect sizes and massive confounding are largely unfixable problems that narrowly confine the scenarios in which nonrandomized observational research is useful
This egg study contains the usual flaws that render it inconclusive:
First, the study relies on data collected from a food frequency questionnaire. Have you ever sat down and tried to recall exactly what you ate in the previous week? How accurate do you think your estimate of specific food items would be?
Ed Archer has written about the inaccuracy of the food frequency questionairres extensively. Here’s a sample from one of his devastating critiques;
In lieu of measuring actual dietary intake, epidemiologists collected millions of unverified verbal and textual reports of memories of perceptions of dietary intake. Given that actual dietary intake and reported memories of perceptions of intake are not in the same ontological category, epidemiologists committed the logical fallacy of “Misplaced Concreteness.” This error was exacerbated when the anecdotal (self-reported) data were impermissibly transformed (i.e., pseudo-quantified) into proxy-estimates of nutrient and caloric consumption via the assignment of “reference” values from databases of questionable validity and comprehensiveness. These errors were further compounded when statistical analyses of diet-disease relations were performed using the pseudo-quantified anecdotal data. These fatal measurement, analytic, and inferential flaws were obscured when epidemiologists failed to cite decades of research demonstrating that the proxy-estimates they created were often physiologically implausible (i.e., meaningless) and had no verifiable quantitative relation to the actual nutrient or caloric consumption of participants.
In addition to unreliable initial data the subjects were followed up to 30 years without any update on their food consumption. Has your food consumption remained constant over the last 30 years? Mine hasn’t. I went from avoiding eggs to eating them ad lib and without concern for my cardiovascular health about 5 years ago after looking at the science related to dietary cholesterol.
It’s Hard To Get Around Confounding Variables
Observational studies like this one try to take into account as many factors as they can which might influence outcomes. Invariably, however, there are factors which are unaccounted for, indeed unknowable, which could be influencing the results.
Individuals who were avidly trying to follow a healthy lifestyle in 1985 likely had drummed into their heads the message when these questionnaires were filled out that they needed to limit egg consumption. These individuals were also likely following other healthy habits, including exercising more, smoking less, and eating more fruits and vegetables and less junk food.
Observational studies cannot account for all these confounding variables.
At science-media centre.org they do a fantastic job of having independent experts in the field present their evaluation of scientific studies which have been popularized in the media. For the JAMA egg study their analyses can be found here.
Prof Kevin McConway, Emeritus Professor of Applied Statistics, The Open University emphasized the problem with residual confounding :
That’s because, for instance, there will be many other differences between people that eat many eggs and people that eat few other than their egg consumption. These other differences might be what’s causing higher death rates in people who eat a lot of eggs, rather than anything to do with the eggs themselves. The researchers point out that this has been a particular problem in some previous studies, and that this may have been a reason for inconsistency in the results of those studies. They have made considerable efforts to allow statistically for other differences in the new study. But they, correctly, point out that their own study is still not immune from this problem (known as residual confounding), and that therefore it’s impossible to conclude from this new study that eating eggs, or consuming more cholesterol in the diet, is the cause of the differences in cardiovascular disease rates and overall death rates that they observed.
For observational epidemiological studies like this egg study which show increased risks that are only “modest” it is highly likely that the next such study will find something different.
Eggs Are Not Eaten In Isolation
Finally, It’s important to remember that eggs, like most foods, are rarely consumed without accompanying food. This accompaniment is often bacon in the US. Eggs are often cooked in oil or butter and unless you cook them yourself you are unlikely to know the nature of the oil.
Eggs are frequently components of recipes.
We have no idea how these factors play into the results of the egg study.
So, rather than drastically cutting egg consumption I propose that there be a drastic cut in the production of weak observational nutrition studies and a moratorium on inflammatory media coverage of meaningless nutritional studies.
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 2010 President Obama signed into law the “Healthy, Hunger-free kids act (HHKA) of 2010” which funded child nutrition programs and free school lunch programs in schools. New nutrition standards for schools were a point initiative of then First Lady Michelle Obama as part of her fight against childhood obesity and her “Let’s Move” initiative.
That means 99,000 schools, feeding 30 million kids, can offer 1 percent chocolate and strawberry milk again, more refined white flour products, and, most importantly, freeze sodium levels in school lunches instead of reducing them further.
Criticism of the loosening implies that the original school lunch standards were appropriate and based on state of the art nutritional science, but were they?
The HHKA relied on guidance from the Institute of Medicine which established a committee to put together its report which was published in 2009 and was heavily based on the scientific guidance provided in the 2005 Dietary Guidelines for Americans and the IOM’s Dietary Reference Intake books”
Unfortunately, the 2005 Dietary Guidelines for Americans were not privy to dramatic changes in our understanding of nutritional science which have occurred in the 13 years since they were written.
The IOM report copied the 2005 DGA in recommending the consumption of low fat or non fat dairy and defined low fat as 1%.
To achieve its aim of reducing saturated fat intake to <10% the IOM chose to force schools to only utilize low fat or skim milk.
The IOM and school lunch program recommended eliminating whole milk entirely and only allowing
-fat-free (plain or flavored) or
-plain low-fat (meaning 1%) milk
In 2018 it is very clear to anyone who examines the relevant data (see here, here and here) that dairy fat, despite being predominantly saturated fat is not associated with higher rates of cardiovascular disease, obesity, diabetes or total mortality.
Remarkably few randomized clinical trials have examined the effects of reduced-fat milk (0% to 2% fat content) compared with whole milk on weight gain or other health outcomes. Lacking high-quality interventional data, beverage guidelines presume that the lower calo rie content of reduced-fat milk will decrease total calorie intake and excessive weight gain.. However, a primary focus on reducing fat intake does not facilitate weight loss compared with other dietary strategies, as shown in observational studies and clinical trials, perhaps because reduced-fat foods tend to have lower satiety value.
Therefore, one of the key components of the HHK is misguided and not science-based. It has in effect committed all of our children to a vast experiment with unknown health consequences.
How Do New USDA Guidelines Effect Dairy?
The change the USDA recently announced is to allow flavoring in 1% milk. Perdue is quoted as saying:
Because milk is a critical component of school meals, and providing schools with the discretion to serve flavored, 1 percent fat milk provides more options for students selecting milk as part of their lunch or breakfast, I am directing USDA to begin the regulatory process to provide that discretion to schools.
Prior to the mandated changes, the IOM report noted that dairy intake in children was predominantly from milk with >1% dairy fat.
17 percent of the total milk intake was from unflavored 2 percent milk, 16 percent from unflavored whole milk, and 9 percent from flavored milk
The dairy industry basically demanded the right to flavor 1% milk because the mandate to force all school children to drink low fat or skim milk has resulted in less children drinking milk.
And the government’s solution to making unpalatable skim milk tastier to children is to add sugar, something we have learned in the last decade we should not be doing to our food.
As Ludwig and Willet noted:
Consumption of sugar-sweetened, flavored (eg, chocolate) milk warrants special attention. While limit ing whole milk, some healthy beverage guidelines con done, and many schools provide, sugar-sweetened milk, with the aim of achieving recommended levels of total milk consumption in children. Not surprisingly, children prefer sweetened to unsweetened milk when given the choice, leading to a marked increase in the proportion of sweetened milk consumption in recent years. This trend may reflect, to some degree, compensation for the lower palatability and satiety value of fat-reduced milk. However, the substitution of sweetened reduced-fat milk for unsweetened whole milk—which lowers saturated fat by 3 g but increases sugar by 13 g per cup—clearly undermines diet quality, especially in a population with excessive sugar consumption.
The bulk of the dairy industry actually prefers you and your children drink skim milk (see here) and they are happy to adulterate the tasteless, nutritionless beverage with anything that makes it more palatable.
This is great news, not only for dairy farmers and processors, but also for schoolkids across the U.S.,” says John Rettler, president of FarmFirst Dairy Cooperative. “This is a step in the right direction in ensuring that school cafeterias are able to provide valuable nutrition in options that appeal to growing children’s taste buds. Their good habits now have the potential to make them lifelong milk-drinkers.”
Adding sugar to mandated unpalatable low fat milk might increase consumption of the beverage but it is definitely not a step forward for our kid’s health.
This unethical, unscientific experiment might be contributing already to higher rates of childhood obesity and diabetes.
Making Skepticism Great Again,
N.B. To help understand how skim milk despite having less calories than whole milk could actually worsen obesity Ludwig and Willet provide the following instructive paragraph:
Suppose a child, who habitually consumes a cup of whole milk and two 60-kcal cookies for a snack, instead had nonfat milk. Energy intake with that snack would not decrease if that child felt less satiated and consequently ate just extra cookie. Rather than weight loss, this substitution of refined starch and sugar (ie, high glycemic index carbohydrate) for fat might actually cause weight gain. Consumption of a low-fat, high glycemic index diet may not only increase hunger, but also adversely affect energy expenditure compared with diets with a higher proportion of fat. In an analysis of 3 major cohorts, high glycemic index carbohydrates, such as refined grains, sugary beverages, and sweet desserts, were positively associated with weight gain, whereas whole milk was not. Of particular relevance, prospective studies in young children, adolescents, and adults observed the same or greater rates of weight gain with consumption of reduced-fat compared with whole milk, suggesting that people compensate or overcompensate for the lower calorie content of reduced-fat milk by eating more of other foods.
The skeptical cardiologist had been avoiding reader pleas to comment on a paper recently published in the Lancet from the PURE study which showed that full fat dairy consumption is associated with a lower risk of mortality and cardiovascular disease. It felt like beating a dead horse since I’ve been writing for the last 5 years that the observational evidence nearly unanimously shows that full fat dairy is associated with less abdominal fat, lower risk of diabetes and lower risk of developing vascular complications such as stroke and heart attack. However, since bad nutritional advice in this area stubbornly persists and the PURE study is so powerful and universally applicable, I felt compelled to post my observations.
What Did the PURE Study Show?
The PURE (Prospective Urban Rural Epidemiology) study enrolled 136, 00 individuals aged 35–70 years from 21 countries in five continents. Dietary intakes of dairy products ( milk, yoghurt, and cheese) were recorded.. Food intake was stratified into whole-fat and low-fat dairy. The primary outcome was the composite of mortality or major cardiovascular events.
Consumption of 2 servings of dairy per day versus none was associated with a 16% lower risk of the primary outcome. The high dairy consumers had an overall 17% lower risk of dying. They had a 34% lower risk of stroke.
People whose only dairy consumption consisted of whole-fat products had a significantly lower risk of the composite primary endpoint (29%).
Here’s how one of the authors of the PURE study summarized his findings (quoted in a good summary at TCTMD)
“We are suggesting that dairy consumption should not be discouraged,” lead investigator Mahshid Dehghan, PhD (McMaster University, Hamilton, Canada), told TCTMD. “In fact, it should be encouraged in low-to-middle income countries, as well as in high-income countries among individuals who do not consume dairy. We have people in North America and Europe who are scared of dairy and we would tell them that three servings per day is OK. You can eat it, and there are beneficial effects. Moderation is the message of our study.”
Despite these recent findings and the total lack of any previous data that indicates substituting low or no fat dairy for full fat dairy is beneficial, the American Heart Association (AHA)and major nutritional organizations continue to recommend skim or low fat cheese, yogurt and milk over full fat , non-processed dairy products.
The AHA Continues Its Misguided Vilification Of All Saturated Fat
“Currently with the evidence that we have reviewed, we still believe that you should try to limit your saturated fat including fat that this is coming from dairy products,” commented Jo Ann Carson, PhD, of UT Southwestern Medical Center in Dallas and a spokesperson for the American Heart Association.
“It is probably wise and beneficial to be sure you’re including dairy in that overall heart-healthy dietary pattern, but we would continue to recommend that you make lower fat selections in the dairy products,” Carson told MedPage Today regarding the study, with which she was not involved.
What is their rationale? A misguided focus on macronutrients. For decades these people have been preaching that saturated fat is bad and unsaturated fat is good. All saturated fat is bad. All unsaturated fat is good.
To deem even one product which contains a significant amount of saturated fat as acceptable would undermine the public’s confidence in the saturated fat dogma.
Bad Nutritional Advice From The AHA Is Not New
Of course, the AHA has been notoriously off base on its nutritional advice for decades. selling its “heart-check” seal of approval to sugar-laden cereals such as Trix, Cocoa Puffs, and Lucky Charms and promoting trans-fat laden margarine. These products could qualify as heart-healthy because they were low in cholesterol and saturated fat.
To this day, the AHA’s heart-check program continues to promote highly processed junk food as heart-healthy while raking in millions of dollars from food manufacturers.
The AHA’s heart-check program is still using low cholesterol as a criteria for heart-healthy food whereas the 2015 Dietary Guidelines concluded that dietary cholesterol intake was no longer of concern.
Why would anyone believe the AHA’s current nutritional advice is credible given the historical inaccuracy of the program?
I’ve noticed that the dairy industry has done nothing to counter the idea that Americans should be consuming skim or low fat dairy product and discussed this with a dairy farmer who only sells full fat products a few years ago.
Dr. Peter(Fritz) Kunz, a plastic surgeon, and his wife Jane, began selling milk from their farm after researching methods for rotational grazing , a process which allows the cows to be self-sustaining: the cows feed themselves by eating the grass and in turn help fertilize the fields, . After a few years of making sure they had the right grasses and cows, the Kunz’s opened Traders Point Creamery in 2003.
Two more studies (summarized nicely on ConscienHealth, an obesity and health blog) came out recently solidifying the extensive data supporting the health of dairy fat and challenging the nutritional dogma that all Americans should be consuming low-fat as opposed to full fat dairy.
The Dairy Industry’s Dirty Little Secret
Dr. Kunz opened my eyes to the dirty little secret of the dairy industry when i first talked to him: dairy farmers double their income by allowing milk to be split into its fat and non-fat portions therefore the industry has no motivation to promote full fat dairy over nonfat dairy.
Recently, I presented him with a few follow-up questions to help me understand why we can’t reverse the bad nutritional advice to consume low-fat dairy.
Skeptical Cardiologist: “When we first spoke and I was beginning my investigation into dairy fat and cardiovascular disease you told me that most dairy producers are fine with the promotion of non fat or low fat dairy products because if consumers are choosing low fat or skim dairy this allows the dairy producer to profit from the skim milk production as well as the dairy fat that is separated and sold for butter, cheese or cream products.”
I don’t have a clear idea of what the economics of this are. Do you think this, for example, doubles the profitability of a dairy?
Dr. Kunz: “Yes, clearly. Butter, sour cream, and ice cream are highly profitable products… All these processes leave a lot of skim milk to deal with, and the best opportunity to sell skim milk is to diet-conscious and heart-conscious people who believe fat is bad.”
Skeptical Cardiologist:” I’ve been baffled by public health recommendations to consume low fat dairy as the science would suggest the opposite. The only reason I can see that this persists is that the Dairy Industry Lobby , for the reason I pointed out above, actually has a vested interest from a profitability standpoint in lobbying for the low fat dairy consumption.. Do you agree that this is what is going on? ”
Dr. Kunz: “Yes, definitely. The obsession with low-fat as it relates to diet and cardiac health has been very cleverly marketed. Fat does NOT make you fat.
Skeptical Cardiologist: “Also, I have had trouble finding out the process of production of skim milk. I’ve come across sites claiming that the process involves injection of various chemical agents but I can’t seem to find a reliable reference source on this. Do you have any information/undestanding of this process and what the down sides might be? I would like to be able to portray skim milk as a “processed food” which, more and more, we seem to be recognizing as bad for us.”
Dr. Kunz: “The PMO pasteurized milk ordinance states that when you remove fat you have to replace the fat soluble vitamins A & D. Apparently the Vitamin A & D have to be stabilized with a chemical compound to keep them miscible in basically an aqueous solution. The compound apparently contains MSG!! We were shocked to find this out and it further confirmed that we did not want to do a reduced fat or skim milk product.”
Skeptical Cardiologist: ” Any thoughts on A2? Marion Nestle’, of Food Politics fame, was recently in Australia where there is a company promoting A2 milk as likely to cause GI upset. It has captured a significant share of the Aussie market.”
Dr. Kunz: “We have heard of this and have directed our farm to test and replace any A1 heterozygous or homozygous cows. We believe that very few of our herd would have A1 genetics because of the advantage of using heritage breeds like Brown Swiss and Jersey instead of Holstein. Because few people are actually tested for lactose intolerance and because of the marketing of A2, it’s imperative not to be left behind in this – whether or not it turns out to be a true and accurate cause of people’s GI upset.
Skeptical Cardiologist:” I like that your milk is nonhomogenized. Seems like the less “processing” the better for food. I haven’t found any compelling scientific reasons to recommend it to my patients, however. Do you have any?”
Dr. Kunz: The literature is fairly old on this subject, but xanthine oxidase apparently can become encapsulated in the fat globules and it can be absorbed into the vascular tree and cause vascular injury. I will look for the articles. Anyway, taking your milk and subjecting it to 3000-5000 psi (homogenization conditions) certainly causes damage to the delicate proteins and even the less delicate fat globules. Also remember that dietary cholesterol is not bad but oxidized cholesterol is very bad for you. That’s why overcooking egg yolks and high pressure spray drying to make powder products can be very dangerous – like whey protein powders that may contain some fats.
Skeptical Cardiologist: I spend a fair amount of time traveling in Europe and am always amazed that their milk is ultrapasteurized and sits unrefrigerated on the shelves. any thoughts on that process versus regular pasteurization and on pasteurization in general and its effects on nutritional value of dairy.
Dr. Kunz :“Absolutely crazy bad and nutritionally empty.. don’t know why anyone would buy it. The procedure is known as aseptic pasteurization and is how Nestle makes its wonderful Nesquik. If they made a full fat version of an aseptically pasteurized product it may have more oxidized cholesterol and be more harmful than no fat!!”
So there you have it, Straight from the doctor dairy farmer’s mouth:
Skimming the healthy dairy fat out of milk is a highly profitable process. Somehow, without a shred of scientific support, the dairy industry, in cahoots with misguided and close-minded nutritionists, has convinced the populace that this ultra-processed skim milk pumped full of factory-produced synthetic vitamins is healthier than the original product.
The two recent articles (mentioned in this post) supporting full fat dairy are:
which concluded ‘In two prospective cohorts, higher plasma dairy fatty acid concentrations were associated with lower incident diabetes. Results were similar for erythrocyte 17:0. Our findings highlight need to better understand potential health effects of dairy fat; and dietary and metabolic determinants of these fatty acids
Four years ago the skeptical cardiologist wrote the (in his extremely humble and biased opinion) the definitive post on aspirin and cardiovascular disease. Entitled “Should I take aspirin to prevent stroke or heart attack“, it pointed out that although Dr. Oz had recently told almost all middle-aged women to take a baby aspirin and fish oil, there was, in fact no evidence to support that practice.
The publication of the ASPREE (Aspirin in Reducing Events in the Elderly) trial results in the latest issue of the New England Journal of Medicinefurther strengthens the points I made in 2014.
Between 2010 and 2014 the ASPREE investigators enrolled over 19,000 community-dwelling persons in Australia and the United States who were 70 years of age or older (or ≥65 years of age among blacks and Hispanics in the United States) and did not have cardiovascular disease, dementia, or disability.
(It’s important to look closely at the precise inclusion and exclusion criteria in randomized studies to understand fully the implications of the results (for example, what qualified as cardiovascular disease) and I’ve listed them at the end of this post.)
Study participants were randomly assigned to receive 100 mg of enteric-coated aspirin or placebo. At the end of the study about 2/3 of participants in both groups were still taking their pills.
When I wrote about aspirin in 2014 I focused on cardiovascular disease. At that time, there was some reasonable evidence that aspirin might lower the risk of colorectal cancer. But when we look at outcomes the bottom line is how the drug influences the overall mix of diseases and deaths.
The ASPREE researchers chose disability-free survival, defined as survival free from dementia or persistent physical disability (inability to perform or severe difficulty in performing at least one of the six basic activities of daily living that had persisted for at least 6 month) as their primary end-point which makes a lot of sense-patients don’t want to just live longer, they want to live longer with a good quality of life. If aspirin, to take a totally hypothetical example) is stopping people from dying from heart attacks but making them demented it’s not benefiting them overall.
After 5 years there was no difference in the rate of death, dementia or permanent physical disability between the aspirin group (21.5 events per 1000 person-years) and placebo group (21.2 per 1000).
However those taking aspirin had a significantly higher rate of major bleeding (3.8%) than those taking placebo (2.8%).
The risk of death from any cause was 12.7 events per 1000 person-years in the aspirin group and 11.1 events per 1000 person-years in the placebo group.. Cancer was the major contributor to the higher mortality in the aspirin group, accounting for 1.6 excess deaths per 1000 person-years.
And, despite prior analyses suggesting aspirin reduces colorectal cancer the opposite was found in this study. Aspirin takers were 1.8 times more likely to die from colorectal cancer and 2.2 times more likely to die from breast cancer.
After a median of 4.7 years of follow-up, the rate of cardiovascular disease was 10.7 events per 1000 person-years in the aspirin group and 11.3 events per 1000 person-years in the placebo group (hazard ratio, 0.95; 95% confidence interval [CI], 0.83 to 1.08). The rate of major hemorrhage was 8.6 events per 1000 person-years and 6.2 events per 1000 person-years, respectively (hazard ratio, 1.38; 95% CI, 1.18 to 1.62; P<0.001).
The ASPREE study confirms what I advised in 2014 and hopefully will further reduce the inappropriate consumption of aspirin among low risk individuals.
I’ve taken more patients off aspirin since 2014 than I’ve started on and what I wrote then remains relevant and reflects my current practice. Especially in light of the increase cancer risk noted in ASPREE patients should only take aspirin for good reasons.
Aspirin is a unique drug, the prototypical two-edged sword of pharmaceuticals. It t has the capability of stopping platelets, the sticky elements in our blood, from forming clots that cause strokes and heart attacks when arterial plaques rupture, but it increases the risk of serious bleeding into the brain or from the GI tract. Despite these powerful properties, aspirin is available over the counter and is very cheap, thus anyone can take it in any dosage they want.
Who Should Take Aspirin?
For the last five years I’ve been advising my patients who have no evidence of atherosclerotic vascular disease against taking aspirin to prevent heart attack and stroke. Several comprehensive reviews of all the randomized trials of aspirin had concluded by 2011 that
The current totality of evidence provides only modest support for a benefit of aspirin in patients without clinical cardiovascular disease, which is offset by its risk. For every 1,000 subjects treated with aspirin over a 5-year period, aspirin would prevent 2.9 MCE and cause 2.8 major bleeds.
(MCE=major cardiovascular events, e.g. stroke, heart attack, death from cardiovascular disease)
Dr. Oz, on the other hand, came to St. Louis in 2011 to have lunch with five hundred women and advised them all to take a baby aspirin daily (and fish oil, which is not indicated for primary prevention as I have discussed here). When I saw these women subsequently in my office I had to spend a fair amount of our visit explaining why they didn’t need to take aspirin and fish oil.
After reviewing available data, the FDA this week issued a statementrecommending against aspirin use for the prevention of a first heart attack or stroke in patients with no history of cardiovascular disease (i.e. for primary prevention). The FDA pointed out that aspirin use is associated with “serious risks,” including increased risk of bleeding in the stomach and brain. As for secondary prevention for people with cardiovascular disease or those who have had a previous heart attack or stroke (secondary prevention), the available evidence continues to support aspirin use.
Subclinical Atherosclerosis and Aspirin usage
As I’ve discussed previously, however, many individuals who have not had a stroke or heart attack are walking around with a substantial burden of atherosclerosis in their arteries. Fatty plaques can become quite advanced in the arteries to the brain and heart before they obstruct blood flow and cause symptoms. In such individuals with subclinical atherosclerosis aspirin is going to be much more beneficial.
Guided Use of Aspirin
We have the tools available to look for atherosclerotic plaques before they rupture and cause heart attacks or stroke. Ultrasound screening of the carotid artery, as I discussed here, is one such tool: vascular screening is an accurate, harmless and painless way to assess for subclinical atherosclerosis.
Coronary calcium is another, which I’ve written extensively about.
In my practice, the answer to the question of who should or should not take aspirin is based on whether my patient has or does not have significant atherosclerosis. If they have had a clinical event due to atherosclerotic cardiovascular disease (stroke, heart attack, coronary stent, coronary bypass surgery, documented blocked arteries to the legs) I recommend they take one 81 milligram (baby) uncoated aspirin daily. If they have not had a clinical event but I have documented by either
Incidentally discovered significant plaque in the aorta or peripheral arteries (found by CT or ultrasound done for other reasons)
then I recommend a daily baby aspirin (assuming no high risk of bleeding).
There are no randomized trials testing this approach but in the next few years several large aspirin trials will be completed and hopefully we will get a better understanding of who benefits most from aspirin for primary prevention.
Until then remember that aspirin is a powerful drug with potential for good and bad effects on your body. Only take it if you and your health care provider have decided the benefits outweigh the risks after careful consideration of your particular situation
The inclusion criteria for ASPREE define significant cardiovascular disease as follows
a past history of cardiovascular or cerebrovascular event or established CVD, defined as myocardial infarction (MI), heart failure, angina pectoris, stroke, transient ischemic attack, >50% carotid stenosis or previous carotid endarterectomy or stenting, coronary artery angioplasty or stenting, coronary artery bypass grafting, abdominal aortic aneurysm
With the recent recall of valsartan due to carcinogenic Chinese contaminants the issue of where one’s generic medication is manufactured has become more important.
I take two generics: ramipril for my hypertension and rosuvastatin for my cholesterol/atherosclerosis and I had no idea where they came from when I discussed the rise of generics manufactured in China recently.
Where Is My Ramipril Made?
I called my St. Lukes pharmacist, Robert, and asked him if he could give me information on the origin of these pills.
Robert told me that my 10 mg ramipril capsule was distributed by a company called West-Ward located in New Jersey. West-Ward was an independent Columbus, Ohio company but was purchased in 2016 by a very large pharmaceutical company , Hikma, based in Aaman, Jordan. Now the Hikma web site indicates West-Ward is no more and is simply called Hikma in the US.
Hikma Pharmaceuticals Plc projects it will end 2017 with about $2 billion revenue, about $600 million of which is from generic drugs made by its U.S. subsidiary West-Ward. In the spring, the company had projected $800 million in generics sales.
Customer service at Hikma informs me that my ramipril was made in their Columbus, Ohio plant.
Where Is My Rosuvastatin Made?
My rosuvastatin (generic of Crestor) was made by Glenmark Pharmaceuticals which, per wikipedia
Glenmark received FDA approval to market their generic rosuvastatin in the US in July, 2016. and at that time had 115 products authorized for distribution in the US market and 61 drugs pending approval with the US FDA.
My rosuvastatin according to Robert was made in India although the Glenmark product catalog does not reveal this information.
Generic versus Brand Name
I’ve talked about Crestor/rosuvastatin a few times on this blog and the development of a generic version has been very helpful for many of my patients. Looking online today I see that generic rosuvastatin goes for about 10$ per month compared to 260$ for Crestor.
Is it worth paying an extra 250$ per month to get brand name Crestor if, let’s say it was manufactured in the US? For most people it isn’t. For one thing, there is no guarantee of where your brand name drug is manufactured.
Crestor used to be made in a factory in Bristol, UK but this was shut down in 2017 and now I can’t tell where Astra-Zeneca makes the stuff. Frankly, I’m surprised that they are selling any of the drug which used to account for 5 billion dollars of their annual sales.
So my cholesterol drug is made in India by an Indian company and my blood pressure drug is made in Columbus, Ohio by a Jordanian company.
I never realized how globalized the pharmaceutical industry has become. Hopefully, the FDA is doing a good job of monitoring the safety and quality of products we rely on for our wellbeing which are manufactured all over the globe.
Addendum: I have an updated post which includes more generic ARB recalls here