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 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
If by now you are still taking fish oil supplements despite my last post on the topic I present three more reasons to stop wasting your money and destroying the ocean’s ecosystem.
The first nail: No Reason To Take Fish Oil Pills
A Cochrane review showing shows there is little or no effect of omega 3 supplements on our risk of experiencing heart disease, stroke or death.
This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia.
Second Nail. Peruvian Anchoveta: Put Them On A Pizza Not in A Pill
Paul Greenberg’s recently published book, The Omega Principle, emphasizes the damage the fish oil supplement business is doing to the ocean environment,
GREENBERG: So omega-3 supplements come from this critical layer of the ocean biosphere that are small – what are called pelagic fish. They’re the silvery, little fish like anchovies and herring and other fish called menhaden that most people haven’t heard of, but it’s actually the most caught fish in the lower 48 of the United States. These fish are really essential for ecosystem dynamics in the ocean.
So the way that oceans work is that all the energies coming from the sun – it goes – all that energy is processed by plankton, by phytoplankton. And it’s really these fish that are – these little fish that are used for omega-3 supplements that transfer the energy from plankton to larger fish. So in other words, you know, you have the solar energy going into the plankton. The little fish then eat the plankton. And then they are in turn eaten by larger fish. So if you harvest this middle layer – if you overharvest this middle layer of anchovies, of herring, of menhaden – if you take them out of the picture, there’s no way for the energy to be transferred from phytoplankton up to larger predators. So I guess that’s my main concern here.
So in particular, where are the omega-3 supplements coming from? Most of the omega-3 supplement oil is coming from a fish called a Peruvian anchoveta. And it is the most caught fish in the world. In some years, Peruvian anchoveta harvests have equaled as much as 10 million metric tons. Just to give you some perspective, that’s like one-eighth of all the fish caught in the world. And the crazy thing about it is that those fish are completely, totally edible. I’ve eaten them. They’re delicious. You can have them on a pizza. You could do anything with them. But 99 percent of those Peruvian anchoveta are ground up into animal feed, boiled down into oil and turned into supplements. So to me, to my mind, that is not necessarily the wisest use to be made of this really, really important source both for the ecology of the ocean but also for humans
Nail Three. Save the Krill!
The supplement industry is incredibly creative in their marketing. As the uselessness of fish oil supplementation has become clear, supplement manufacturers have begun touting krill oil as superior to fish oil.
Claims like the following are all over the internet:
Krill have an edge over your ordinary fish – when you take a krill oil supplement, you also get astaxanthin along with your DHA and EPA. It’s an antioxidant. In terms of antioxidant power of potency, it’s been found to be 500x to 6,000x stronger than regular vitamins like vitamin E and vitamin C.
This is just hogwash. There is no good clinical evidence to support any health claim for krill oil in general or astaxanthin in particular. Please read my post on the failure of anti-oxidant supplements and vitamins and recognize that claims of antioxidant power do not indicate any health benefit.
A technical paper from Greenpeace review the importance of krill to to the marine ecosystem in the Antarctic and this paper, entitled “License to Krill” details the problem.
Do you want to be responsible for starving penguins, whales and seals??!
the bottom line on fish oil supplements is that the most recent scientific evidence does not support any role for them in preventing heart attack, stroke, or death. There are potential down sides to taking them, including contaminants and the impact on the marine ecosystem. I don’t take them and I advise my patients to avoid them (unless they have triglyceride levels over 500.)
I mentioned at that time that Honey-Nut Cheerios was the #1 selling ready-to-eat breakfast cereal and Cheerios #4. This update indicates little has changed in the rankings or consumption of breakfast cereal since then despite a more widespread recognition that added sugar is the major toxin in our diet and that these food items are basically a vehicle for sugar.
Apparently, Americans believe honey is not sugar. But Honey Nut Cheerios contain 9 times as much sugar as cheerios. Here are the top ingredients:
General Mills tries to emphasize the healthiness of Honey Nut Cheerios, focusing on their close relationship with bees and the natural goodness of honey in its advertising along with other factors that we now know are not important (low fat, 12 vitamins and minerals, source of iron).
Little has changed with respect to the science supporting fiber consumption to reduce cardiovascular disease since 2014. It is still weak and based on observational studies and surrogate biomarkers.
Between the lines below is my original post with current annotations in red.
The skeptical cardiologist usually eschews the breakfast offerings in the Doctor’s lounge. I’m not really interested in consuming donuts, muffins, or bagels with their high carbohydrate load. As I’ve ranted out about previously, the only yogurt available is Yoplait low fat , highly sugared-up yogurt which is arguably worse than starting the day with a candy bar.
A selection of breakfast cereals is available including Cheerios, Raisin Bran, and Frosted Flakes. Occasionally, when I have neglected to bring in my own full-faty yogurt, granola and/or fruit I will open up one of the Cheerios containers and consume a bowl mixed with 2% milk (full-fat, organic milk which I passionately advocate here and here is not available) (2018 update, I have said “cheerio” to all breakfast cereals and no longer eat Cheerios in the doctor’s lounge).
Pondering the Cheerios packaging and the cute little O’s made me wonder whether this highly processed and packaged food with a seemingly endless shelf life was truly a healthy choice.
The “Ready-To-Eat” And Allegedly Heart-Healthy Cereal
Cheerios and Honey-nut cheerios were the #4 and #1 breakfast cereals in the US in 2013, generating almost a billion dollars in sales. Both of these General Mills blockbusters undoubtedly have reached their popularity by heavily promoting the concept that they are heart healthy.
The Cheerios label is all about the heart. The little O’s sit in a heart-shaped bowl. A prominent red heart with a check inside it attests to the AHA having certified Cheerios as part of its checkmark.heart.org program. Additional text states “low in Saturated fat and cholesterol” and “diets low in saturated fat and cholesterol may reduce the risk of heart disease.”
Is The Fiber In Cheerios “Heart-Healthy” ?
Beta-glucan is a soluble fiber primarily located in the endosperm cell wall of oats. Early studies showed that oats and beta-glucan soluble fiber could reduce total and LDL (bad cholesterol) levels. The mechanism isn’t really known. (see the end of post for possible mechanisms). The Quaker oats web site oversimplifies the mechanism thusly :
“In your digestive tract, it acts as a sponge, soaking up cholesterol and carrying it out of the body”
This narrative fits with the oversimplified and now discredited descriptions of atherosclerosis which attribute it directly to consumption of cholesterol and fatty acids. See here if you’d like to appreciate how complex the process truly is.
The FDA Sanctions Oats As Heart Healthy
In 1997, the FDA reviewed 33 studies (21 showing benefit and 12 not) and decided to allow a health claim for foods that contain oats and soluble fiber. A minimum dose of 3 grams/day of oat beta-glucan was suggested for a beneficial reduction in blood cholesterol and (presumably, although never documented) a subsequent decline in coronary heart disease.
In 1998 Johnson, et al, published the results of a study funded by a grant from General Mills that showed that inclusion of whole grain oat ready to eat cereal providing 3 grams of beta-glucan as part of a low fat diet reduced LDL cholesterol by 4% after 6 weeks. HDL was unchanged. Patients in this study consumed 45 grams (1.5 oz) of cheerios at breakfast and then again in the evening. There was a total of 3 grams of soluble fibre in this amount of Cheerios. A control group consumed corn flakes in a similar fashion without change in LDL.
General Mills took this weak data and ran with it and began posting on Cheerios the following statements
“Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is … clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol.”
Although the FDA had approved verbiage indicating oats may reduce heart disease “when eaten as part of a diet low in saturated fat and cholesterol” the agency objected to General Mills claiming that Cheerios lowers cholesterol “when eaten as part of a diet low in saturated fat and cholesterol”.
The FDA issued a warning letter to General Mills in 2009 in which the agency alleged “serious violations” of the FDC Act in the label and labeling of Cheerios cereal.
Based on claims made on your product’s label, we have determined that your Cheerios® Toasted Whole Grain Oat Cereal is promoted for conditions that cause it to be a drug because the product is intended for use in the prevention, mitigation, and treatment of disease.
Lowering Cholesterol Is Not The Same As Preventing Heart Disease
The FDA was telling General Mills that it was OK to say that Cheerios may reduce heart disease but not that it can reduce cholesterol because that made it a drug. It makes no sense.
The only thing that had been demonstrated for oat soluble fiber and Cheerios in particular was a reduction in cholesterol. There has never been a study with oats showing a reduction in heart disease..
It’s the heart disease, the atherosclerosis clogging our arteries and causing heart attacks and strokes that we want to prevent. We could care less about lowering cholesterol if it doesn’t prevent atherosclerosis.
A recent review of studies since the FDA ruling shows that 70% of studies show some reduction in LDL with beta-glucan. Interstingly, the studies which added beta-glucan to liquids were generally positive whereas addition to solids such as muffins usually did not show benefit.
I’m going to accept as evidence-based the claim that whole oats can lower your LDL about 7% if you consume a very large amount of them on a daily basis.
However, the critical question for any drug or dietary intervention is does it prevent atherosclerosis, the root cause of heart attacks and strokes. There has been in the past an assumption that lowering cholesterol by any means would result in lowering of atherosclerosis.
This theory has been disproven by recent studies showing that ezetimibe and niacin which significantly lower LDL do not reduce surrogate markers of atherosclerosis or cardiovascular events any more than placebo when added on to statin drugs. (There is now weak evidence that ezetimibe does lower cardiovascular events ). The recently revised cholesterol guidelines endorse the concept of treating risk of atherosclerosis rather than cholesterol levels.
I do like the food writer Michael Pollan’s simple rules to “Eat Food. Mostly Plants. Not Too Much.” and this NY Times piece summarizes much of what is in his short, funny and helpful Food Rules book:
you’re much better off eating whole fresh foods than processed food products. That’s what I mean by the recommendation to eat “food.” Once, food was all you could eat, but today there are lots of other edible foodlike substances in the supermarket. These novel products of food science often come in packages festooned with health claims, which brings me to a related rule of thumb: if you’re concerned about your health, you should probably avoid food products that make health claims. Why? Because a health claim on a food product is a good indication that it’s not really food, and food is what you want to eat.
If you follow Pollan’s dictum you will get plenty of fiber, soluble or otherwise and you will avoid the necessity to obsess over the macronutrients in your diet, fiber or otherwise. Throw in some Cheerios and oatmeal every once in a while if you like them; in their unadulterated state they are a heart-healthy food choice.
The skeptical cardiologist has a confession to make: he’s been adding ground flaxseed to his typical late morning full fat yoghurt plus berries and almonds.
Adding flaxseed seems dangerously close to dietary behaviour I have been advising against: supplementing instead of eating real food.
Also, I am philosophically opposed to going out of my way to eat any edible that is consistently promoted as a “super food” or a “functional food.” To me, these are meaningless terms and marketing blather
When I began writing this post in 2017 I was getting my flaxseed from Stober Farms (Est. 1901) who had been producing “for over 100 years the finest flax in the world.” Stober Farms provided me with “organic Golden Flax Seed which has been Cold-Milled Processed.”
Stober Farms (who have since mysteriously gone into bankruptcy) also informed me:
Flax is digested most effectively when ground. Some grinding methods generate heat when milled, spurring early omega-3 oxidation. Stober Farms uses a unique cold-milled process, which gently grinds the seed without significantly raising the temperature. This proprietary method preserves the nutrients, flavor and extends the shelf life to 22 months.
Honestly, I don’t recall exactly why I began “flaxing” but I suspect I felt it was a good way to boost the fat content in my full fat yoghurt (yes, I am now spelling yoghurt with an h) and berries and perhaps sufficiently satiate me that it would be the only food I would need to consume until dinner or late afternoon.
Two tablespoon (14 grams) is what I typically imprecisely add. These tablespoons provide 75 kcal of energy which comes from 3 grams of protein, 6 grams of fat, and 4 grams of carbs. Three of the four carb grams are soluble fibre.
About half of the fat in flaxseed is in the form of alpha-linolenic acid (ALA)(18:3) an omega-3 polyunsaturated (PUFA) fat. Flaxseed oil contains five times more ALA than walnut oil or canola oil, which are the next highest sources of ALA.
Is Flaxseed A Super Functional Food?
Many seemingly authoritative sites on the internet proclaim that flaxseed is incredibly healthy. For example, Healthline.com’s “Authority Nutrition” (they must be authoritative as authority is in their name) presents their 10 health benefits of eating flaxseed “backed by science” and concludes:
They can be used to improve digestive health, lower blood pressure and bad cholesterol, reduce the risk of cancer and may benefit people with diabetes.
But typical of Authority Nutrition’s overblown claims these are not truly proven by science. The studies cited are weak; typically short-term tests of biomarkers or animal studies or human studies with very small numbers. Most importantly. these studies , which are often funded by flaxseed promoters are highly likely to be biased in favor of positive results.
Most websites tout the cardiovascular benefits of the omega-3 PUFA in flaxseed, the high percentage of soluble fibre and the benefits of a chemical which cannot be named (due to a name which is too difficult to pronounce), SDG.
Omega-3 PUFAs and fibre I’ve touched on previously (and positively) but what about the mysterious and unpronounceable SDF. Per a 2010 review article
Flaxseed is the richest source of the lignan secoisolariciresinol diglucoside (SDG). After ingestion, SDG is converted to secoisolariciresinol, which is further metabolised to the mammalian lignans enterodiol and enterolactone. A growing body of evidence suggests that SDG metabolites may provide health benefits due to their weak oestrogenic or anti-oestrogenic effects, antioxidant activity, ability to induce phase 2 proteins and/or inhibit the activity of certain enzymes, or by mechanisms yet unidentified.
Like so many putative wonder phytochemicals, SDG has a “growing body of evidence” for lots of things but actual proof that it does anything worthwhile in humans is lacking and awaits well done randomized clinical trials
Poorly researched articles on flaxseed are highly likely to tout its anti-inflammatory properties. These properties are seen in rats but unfortunately haven’t been proven in my favorite species, Homo Sapiens , Flaxseed doesn’t seem to decrease the inflammatory marker CRP in humans as reported in this systematic review and meta-analysis.
ALA and Cardiovascular Disease
As I’ve indicated in previous posts, evidence supports fatty fish consumption as beneficial in reducing cardiovascular disease presumably by increasing levels of marine omega-3 PUFAs in the body.
The value of fish oil supplementation, however, is not proven (see here).
How does ALA compare to the seafood omega 3s in preventing cardiovascular disease (CVD)?
Their introductory paragraph nicely lays out why ALA could be very important to public health:
A large body of evidence supports a potential protective effect of seafood omega-3 (n−3) fatty acids, particularly EPA (20:5n−3) and DHA (22:6n−3), on coronary heart disease (CHD. However, fewer studies have evaluated how the plant-derived omega-3 fatty acid α-linolenic acid (ALA; 18:3n−3) relates to risk of CHD and other cardiovascular disease (CVD) outcomes, and the results have been inconsistent As an essential fatty acid that cannot be synthesized by humans, ALA is mainly consumed from plant sources, including soybeans, walnuts, and canola oil. Compared with seafood omega-3 fatty acids, ALA from plant sources is more affordable and widely available globally. Thus, whether ALA can reduce the risk of CVD is of considerable public health importance.
If plant-derived ALA can provide our omage-3 PUFA needs then perhaps we can stop stripping the ocean of all the menhaden.
In the Harvard analysis when all 27 studies were combined the authors found a significant risk reduction of 14% in CVD events with flaxseed.
There were lots of issues with the data which I won’t bore you with leading the authors to conclude that “ALA consumption may be beneficial “. They emphasized the need for additional well-designed observational studies and randomized clinical trials in the area.
Since observational studies cannot prove causality, I await a good randomized clinical trial of ALA supplementation before I can recommend ALA supplementing to prevent heart disease.
After Performing This Review Is The Skeptical Cardiologist Still “Flaxing”?
I am. Because I’ve found that when I consume flaxseed I feel 20 years younger, full of vitality. and with a youthful golden sheen to my hair, nails and skin.
Actually, that last sentence is untrue.
I’m still adding ground flaxseed to my yoghurt but not with any expectation that it is reducing my risk of heart attack and definitely not because I perceive it as a super or functional food.
I like the taste, the convenience, and the extra (presumably healthy) calories it provides but I’m still an advocate of just eating real food rather than trying to identify specific nutrients, nutraceuticals or supplements and add them to your diet.
N.B. I did not touch on omega-6/omega-3 ratios in the diet. I’ve been examining that inflammatory (enjoy the pun) topic for years and once I come across a good study that adds to understanding in the area I will likely publish a post on it.