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If you have high blood pressure—or even high blood pressure that is being controlled with medication as Timothy wrote yesterday—there are certain anti-stress poses that you should not be doing. Although inverted poses can lower blood pressure due to the interaction between your baroreceptors and your nervous system (see Why You Should Love Your Baroreceptors), going upside down initially raises your blood pressure before feedback from the baroreceptors to the nervous system causes the Relaxation Response to kick in. This initial rise in blood pressure is why the poses are considered dangerous for those whose blood pressure is already high (and perhaps for those whose blood pressure is being controlled with medication as Timothy wrote in Keeping Yoga Safe for People with High Blood Pressure), because there is concern it could cause a stroke.
Timothy didn’t list exactly which inverted poses besides Headstand that people with high or even controlled high blood should be avoiding, so I decided to talk with Baxter about the topic in order to list them out for you. The good news is that Baxter considers three of the most effective stress-reducing inversions to be generally safe. I’ve divided the inverted poses into same three groups I used in my post All About Supported Inversions. So here goes: Full Inversions: Poses to Avoid
Handstand (Adho Mukha Vrksasana)
Forearm Balance (Pincha Mayurasana)
Scorpion (Vrschikasana)
Headstand (Sirsasana)
Shoulderstand (Sarvagasana), including the chair version
Plow (Halasana), including the chair/bench version
Because you are fully inverted in these poses, the blood quickly rushes toward your head, initially raising your blood pressure. In addition, most of these poses are stressful to perform, especially for beginners, and the stress itself can raise your blood pressure. Half Inversions: Poses to Evaluate
Downward-Facing Dog pose (Adho Mukha Svanasana)
Standing Forward Bend (Uttanasana), with or without support
Wide-Legged Standing Forward Bend (Prasarita Padottanasana)
Poses where your head and torso are inverted but your legs not, such as Standing Forward Bend, are probably safe. But Baxter recommends that you ask your teacher to look at you while you are doing the poses. The same questions about how you look in the pose that Timothy listed yesterday would be helpful for assessing the suitability of these poses for you or, if you’re a teacher, for your student.
“Does the student appear to have the strength and flexibility to do the pose safely? How is their breathing in the pose? Do they look uncomfortable? Are they able to maintain a healthy curve in the neck? Are their neck veins bulging? How do they say they feel in the pose? It is even possible, if you've got a blood pressure device, to measure the pressure to make sure it isn't spiking in the pose or poses you're concerned about.”
If the pose is difficult or stressful for you, you may want to exclude it from your practice. If you decide to exclude these poses, you can practice Half Downward-Facing Dog pose at the Wall instead. Gentle Inversions: Poses that are Generally Safe
Legs Up the Wall pose (Viparita Karani)
Easy Inverted pose (Viparita Karani with bent legs)
Supported Straight Leg Bridge pose (Setubanda Sarvangasana)
According to Baxter, gentle inversions where your heart is only slightly higher than your head and your body slopes gradually down, such as Legs Up the Wall pose, do not seem to cause an initial rise in blood pressure (he has done some informal testing). Therefore, he feels comfortable in saying they are generally safe. One caveat might be that if your blood pressure is wildly out of control, it might make sense for you to do a different type of practice for stress reduction (see below).
Safe Ways to Lower Blood Pressure
Remember, there is no need for you to do any inverted poses! If you are at all concerned about going upside down, you can choose from several other very effective and safe techniques for lowering your blood pressure. Any yoga or meditation technique that triggers the Relaxation Response (see The Relaxation Response and Yoga) will lower your blood pressure (this was proven in the 70s by Dr. Herbert Bensen and described in his book The Relaxation Response, which I highly recommend). Probably the easiest thing to do is just to sit quietly and observe your breath or recite a mantra. But you can practice any form of mediation, practice Yoga Nidra, any guided Savasana, or any form of Relaxation pose (Savasana) with a mental focus. You could also practice your favorite restorative poses (see Mini Restorative Practice, also with a mental focus. Just be sure to take a non-judgmental attitude toward your practice, give yourself at least 10 to 20 minutes of practice, as it takes a while for the Relaxation Response to kick in, and don’t fall asleep (sleeping is different than conscious relaxation).
All of these options are wonderful for anyone who experiences “situational” high blood pressure (when getting stressed out or angry causes... well, you know!) And practicing conscious relaxation on a regular basis will also enhance your health in the short term (bolstering your immune system) and the long term (helping to prevent heart disease, strokes, and other diseases of aging).
I recently taught a course on Yoga for High Blood Pressure on Yoga U Online. During the program I suggested that doing certain inverted poses such as Headstand (Sirsasana) may not be a good idea, even for some people whose blood pressure (BP) is “well controlled” by medications. But one listener had heard during her teacher training that inversions were okay in this situation. Her instructors had consulted a local cardiologist and shown the doctor the poses in question, and he had said he didn't have a problem with them in people whose BP was under control.
The concern is that when you go upside down, the pressure in the head increases, which could at least theoretically increase the risk of a stroke. I say theoretically, because actually no one really knows how large the risk is, though it's likely very, very small. As I've written elsewhere, more than likely yoga greatly decreases the overall risk of a stroke. But that doesn't mean it's a good idea to push your luck.
Interestingly, blood pressure is one area where yoga teachers are sometimes more conservative than doctors. Aadil Pahkivala, the teacher I worked with on the high blood pressure chapter of my book Yoga as Medicine, has found that some people with well-controlled BP nonetheless demonstrate jitteriness when they do some inversions and strong backbends. This nervous system agitation, which can be visible to the teacher and palpable to the student (at least the ones who have developed their internal awareness though their yoga practices), suggests a potential problem.
In medical school, we were taught to always weigh risks vs. benefits of any test, drug or medical procedure under consideration. In medicine, this comes under the category of “first do no harm.” In yoga, we've got the same idea with the notion of ahimsa, non-harming, which is considered the foundation of any yoga practice. Again, the risk of a stroke when inverting with “well-controlled” high blood pressure is likely very small, but even a tiny risk of something very bad should be factored in when deciding whether or not to do a particular yoga pose. In yoga, a crucial way to assess safety is to study your student—or yourself, if you're the student in question—as they do the practice in question.
So rather than simply saying, “The doctor says it's okay to do Headstand so let's do it,” a more prudent approach is to let that be the beginning of your evaluation. If you're a teacher, consider the following questions: Does the student appear to have the strength and flexibility to do the pose safely? How is their breathing in the pose? Do they look uncomfortable? Are they able to maintain a healthy curve in the neck? Are their neck veins bulging? How do they say they feel in the pose? It is even possible, if you've got a blood pressure device, to measure the pressure to make sure it isn't spiking in the pose or poses you're concerned about. And if you're a student concerned about high blood pressure, ask your teacher to help you do this evaluation.
Especially when the risks are uncertain, the more information you can get the better. And after you have all the information, it’s time to practice ahimsa.
In our new series on shaping up, Healthy Food Guide’s art director Tina Betts starts on her journey towards a proper exercise plan to supplement her day-to-day walking…
By Tina Betts
How did it happen? I’m 43, and things are starting to sag. I haven’t changed my eating and drinking habits, so age is starting to catch up with me. I inherited my ‘walk everywhere’ gene from my Dad. I don’t have a car, so think nothing of whizzing down to Sainsbury’s with my trolley bag. But despite frequent trolley dashes, there’s a big but – my big butt, in fact! I’m lucky that I’ve always been a healthy weight, but it’s starting to creep up, the muffin top is rising steadily and there’s no way I’m going to fit into my dream 40th birthday dress again, at least not the way things are going.
My fear of exercise means I’ve never liked the gym or classes. It’s the classic ‘I was always the last to be picked’ for the team at school. It’s made me a tad anxious in sporting environments.
But that all changed a few weeks ago. As part of a work feature, I tried a yoga class for the first time with my work colleagues. And I could see the attraction of exercising as a group. In fact, I rather enjoyed it. And so, Tina tries… was born. It’s a week by week log of my mission to get fit - and get me back into that party dress.
My first stop was the Health Check at Nuffield Health at their flagship centre at London’s Cannon Street (it’s really more hip hotel than soulless gym). All members go through checks before starting their fitness plan.
Nuffield Health’s senior wellbeing adviser Katarina Berceliova took me through my body MOT, checking my BMI, resting heart rate, blood glucose levels (all healthy) and quizzed me about my sleep patterns (fine) and lifestyle habits (cholesterol and alcohol quotas not so fine). Generally, at 5ft 5in and 9 stone 3lb, my BMI at 21.2 is very good and my blood pressure spot on. But I know I need to do something about my fitness levels – I’ve reached the age where you can’t take anything for granted.
I came away feeling optimistic with three main Wellbeing Action points: to monitor my blood cholesterol, up my water consumption and increase my activity and fitness levels.
Come back next week to read about my first ever session with my personal trainer. I have to admit, just those words make me nervous…
Recently two meta-analysis papers were published addressing the findings from population studies of the association between egg intake and the risk of cardiovascular disease.12 Unfortunately the authors of these two review papers reached contradictory conclusions regarding the dangers of egg intake which is likely to lead to unnecessary public confusion. The authors of the most recent meta-analysis paper reviewed studies on coronary heart disease, heart failure, diabetes and all cardiovascular diseases (CVD) combined and concluded:
Our study suggests that there is a dose-response positive association between egg consumption and the risk of CVD and diabetes.
In contrast to this conclusion, the authors of the earlier meta-analysis paper limited their review to studies that specifically addressed coronary heart disease and stroke and concluded:
Higher consumption of eggs (up to one egg per day) is not associated with increased risk of coronary heart disease or stroke. The increased risk of coronary heart disease among diabetic patients and reduced risk of hemorrhagic stroke associated with higher egg consumption in subgroup analyses warrant further studies.
The second meta-analysis paper is problematic in part because the authors failed to consider the relevant findings from dozens of rigorously controlled feeding experiments on humans and thousands of experiments on animals, including nonhuman primates that strongly support the recommendations to limit the intake of eggs and cholesterol [reviewed previously]. This paper is also problematic in part because the authors failed to consider many other relevant findings from prospective cohort studies which suggest that egg and cholesterol intake increases the risk of coronary heart disease, diabetes, heart failure, cardiovascular disease and all-cause mortality.
Firstly, the association between egg intake and the risk of cardiovascular disease is meaningless without considering suitable substitutes for eggs. As a lower intake of eggs implies a higher intake of other foods in order to maintain caloric balance, the effect that egg intake has on coronary heart disease depends on which foods eggs are substituted for. For example, data from the Nurses’ Health Study, one of the largest studies included in these meta-analyses suggested that replacing one serving of nuts, but not red meat and dairy with one serving of eggs per day is associated with a significantly increased risk of coronary heart disease.3 The authors of both meta-analyses failed to address this factor despite the fact that the importance of evaluating suitable food alternatives has been strongly emphasized by many prominent diet-heart researchers.4 The findings from these meta-analyses should therefore be interpreted with caution as eggs may have been primarily compared to processed foods and other animal foods which make up the majority of caloric intake in developed nations.45
Eggs, Cholesterol and Diabetics
The authors of the most recent meta-analysis paper found that among diabetics, frequent egg intake was associated with a 83% increased risk of cardiovascular disease, whereas the authors of the earlier meta-analysis paper found that frequent intake was associated with a 54% increased risk of coronary heart disease. The authors of the most recent meta-analysis paper excluded one, while the authors of the earlier meta-analysis paper excluded two additional cohort studies that found that among diabetics, high compared to low intake of eggs was associated with an approximately five-fold increased risk of cardiovascular disease.67 These additional studies had they been addressed by these authors would have potentially strengthened the association between egg intake and an increased risk of cardiovascular disease in diabetics.
The authors of the most recent meta-analysis found that frequent egg intake was associated with a 68% increased risk of type II diabetes, a major risk factor for cardiovascular disease. However, the authors of the earlier meta-analysis largely failed to address this evidence. A literature search I performed produced papers from 5 separate prospective cohort studies addressing egg intake and the risk of developing type II diabetes, including two additional studies that were not addressed in both meta-analyses papers.891011 In addition, I also found one additional cohort study addressing egg intake and the risk of developing gestational diabetes.12 All except one smaller cohort found a statistically significant association after adjusting for potential confounders. These cohorts also found suggestive evidence that the increased risk persisted regardless of whether eggs were consumed in the presence of a higher or lower carbohydrate diet, and that the association was even stronger when repeated measurements of egg intake were considered.9 In addition, these cohorts also found suggestive evidence that the increased risk could partly be explained by the dietary cholesterol and protein content of eggs, and that substituting eggs with carbohydrate-rich foods, especially fiber-rich bread and cereals significantly decreases the risk of developing type II diabetes.891112
In the one cohort that did not find a statistically significant association, average egg intake was relatively low and there was suggestive evidence of an increased risk when a follow-up measurement of egg intake was used to update exposure overtime.10 In addition to these findings, a paper from the Health Professionals Follow-Up Study also found suggestive evidence that egg intake is associated with an increased risk of type II diabetes.13 Furthermore, papers from an additional 5 cohort studies found that dietary cholesterol was associated with a significantly increased risk of developing either type II diabetes or gestational diabetes.141516
Overall findings from 12 prospective cohort studies with 265,675 participants and 14,497 cases of type II diabetes and gestational diabetes strongly implies that egg and cholesterol intake are significant risk factors in the development of diabetes. In addition to the findings from cohort studies, 4 cross-sectional studies found that egg or cholesterol intake was associated with between a nearly two-fold and greater than four-fold increased risk of developing type II diabetes and gestational diabetes.12171819 Also consistent with these findings, in the Adventist Health Study 2 it was observed that vegans had a lower risk of developing type II diabetes compared to lacto-ovo vegetarians, and especially non-vegetarians.20
One cohort included in these meta-analyses that used repeated egg intake measurements to update exposure over time found that in diabetics, intake of at least 7 eggs compared to less than 1 egg per week was associated with a two-fold increased risk of all-cause mortality, whereas another cohort that did not use repeated measurements found suggestive evidence of a 30% increased risk of all-cause mortality.2122 The authors of the first study stated:
…among male physicians with diabetes, any egg consumption is associated with a greater risk of all-cause mortality, and there was suggestive evidence for a greater risk of MI [heart attack] and stroke.
An additional study found that in diabetics, an increment of one egg per day was associated with a greater than three-fold increased risk of all-cause mortality.6
According to the International Diabetes Federation, globally approximately 183 million people, or half of those who have diabetes have not been diagnosed. Even in high-income countries about one-third of people with diabetes have not been diagnosed.23 Given this data and the data that egg and cholesterol intake is associated with a significantly increased risk of developing diabetes, and that in diabetics egg intake is associated with a significantly increased risk of coronary heart disease, cardiovascular disease and all-cause mortality, there is likely a significantly greater number of people at risk than suggested by the authors of these recent meta-analyses.
Eggs, Cholesterol and Non-Diabetics
The Nurses’ Health Study found that an increment of cholesterol equivalent to one medium size egg per day was associated with a 17% increased risk of all-cause mortality, consistent with the findings from several other studies.242526 Another study included in these meta-analyses found that in non-diabetics, intake of at least 7 eggs compared to less than 1 egg per week was associated with a 22% increased risk of all-cause mortality.21 Also, another cohort from Japan found that frequent egg intake was associated with an increased risk of all-cause mortality in women, consistent with the findings from the Adventists Mortality Study.2728 In addition, a cohort of elderly found suggestive evidence that egg intake was associated with a significantly increased risk of all-cause mortality, and that substituting eggs with fruits, vegetables and grains significantly decreases risk.29
The authors of the most recent meta-analysis paper found that in largely non-diabetic populations that frequent egg intake was associated with 19% increased risk of cardiovascular disease compared to all other sources of calories combined, which is predominantly processed foods and other animal foods. The authors of the earlier meta-analysis that did not reach this conclusion suggested that their findings are relevant for total cardiovascular disease but failed to address the findings from prospective cohort studies regarding the risk for heart failure. For example, two cohort studies which were included in the most recent meta-analyses found that intake of at least 7 eggs compared to less than 1 egg per week was associated with an approximately 30% increased risk of heart failure.3031
Another potential important finding that has contributed to the knowledge of the dangers of eggs are the results from studies that were carried out on populations with a low habitual cholesterol intake, such as vegetarian populations. The authors of the most recent meta-analysis paper excluded one, while the authors of the earlier meta-analysis paper excluded two cohort studies that were carried out on largely vegetarian populations. Frequent consumption of eggs was associated with a more than 2.5 increased risk of fatal coronary heart disease in the Oxford Vegetarian Study and also an increased risk in females in the Adventists Mortality Study.2832 The characteristics of the participants in these studies differ from that of most other studies, not only because of the their lower habitual intake of dietary cholesterol, but also because of their lower rates of obesity and typically healthier overall diet. Therefore separately analyzing egg intake in this subgroup of the population may be of significant importance. The authors of a paper from the Nurses’ Health Study and the Health Professionals Follow-Up Study cited in these meta-analyses described the potential importance of addressing egg intake in people with very low habitual cholesterol intake and how their study may have been inadequate to test this hypothesis: 33
One potential alternative explanation for the null finding is that background dietary cholesterol may be so high in the usual Western diet that adding somewhat more has little further effect on blood cholesterol. In a randomized trial, Sacks et al found that adding 1 egg per day to the usual diet of 17 lactovegetarians whose habitual cholesterol intake was very low (97 mg/d) significantly increased LDL cholesterol level by 12%. In our analyses, differences in non-egg cholesterol intake did not appear to be an explanation for the null association between egg consumption and risk of CHD. However, we cannot exclude the possibility that egg consumption may increase the risk among participants with very low background cholesterol intake.
As it is well documented that cholesterol intake has a much greater effect of raising serum cholesterol when baseline intake is very low, this may in part explain why egg and cholesterol intake was more strongly associated with coronary heart disease in studies on largely vegetarian populations.3435 Another explanation for a possibly stronger association in vegetarian populations is that egg intake may have a greater effect in leaner people, and it has been well documented that vegetarians are generally leaner than their omnivorous counterparts [reviewed previously]. This hypothesis is supported by several dietary experiments which found that dietary cholesterol had a greater effect of raising serum cholesterol among leaner compared to overweight participants.3637 This hypothesis is also supported by the findings from the Chicago Western Electric Study which found that while dietary cholesterol was associated with a significantly increased risk of coronary heart disease in lean men over and above the adverse effects it has on serum cholesterol, increased intake had little appreciable effect on men with a greater BMI and body fatness.38 Another explanation for these findings is that vegetarians may choose healthier substitutes for eggs, such as nuts which was associated with a significantly lower risk of coronary heart disease compared to eggs in the Nurses’ Health Study.3
It was found in a sub-analysis based on 4 cohorts included in the earlier meta-analyses that egg intake was associated with an 18% non-significant increased risk of fatal coronary heart disease. The addition of the mortality findings from the two largely vegetarian cohorts that were excluded from this meta-analysis would have likely strengthened this association.2832 This suggests that similar to saturated fat intake, egg intake may increase the risk of fatal coronary heart disease more than non-fatal coronary heart disease [reviewed previously]. The lack of a significant association likely reflects the fact that eggs were not compared to healthy foods, and also likely due to misclassification of participants into ranges of usual dietary intake as the result of measurement error [reviewed previously].
In the video below Dr. Michael Gregor addresses recent research on choline when consumed from eggs and other animal foods and the risk of cardiovascular disease and cancer.
Carnitine, Choline, Cancer and Cholesterol: The TMAO Connection
Egg Intake and Stroke
In regards to a sub-group analysis of 5 cohort studies, the authors of the earlier meta-analysis suggested that egg intake was associated with a lower risk of hemorrhagic stroke. The authors suggested that the inverse association between egg intake and hemorrhagic stroke is supported by findings of an inverse association between serum cholesterol and hemorrhagic stroke in several cohort studies. However, in the largest cohort study the authors cited, the inverse association was confined to participants with elevated blood pressure.39 A similar interaction between blood pressure and serum cholesterol and hemorrhagic stroke was observed in much larger cohort studies in both Asian and Western populations that the authors of this meta-analysis conveniently failed to cite.4041 In a meta-analysis of 61 cohort studies it was found that among participants with near optimal systolic blood pressure (<125 mmHg), lower serum cholesterol was actually associated with a significantly lower risk of hemorrhagic, ischemic and total stroke mortality [reviewed previously]. Furthermore, most mammalian species have very low LDL levels (mean value of 42 mg/dl in 18 species), and there is very scant evidence that these animals are at high risk of having a stroke.42
This data demonstrates that continued emphasis should be placed on lowering both LDL cholesterol and blood pressure which have been proven in hundreds of randomized controlled trials to lower not only the risk of cardiovascular disease, but also all-cause mortality.4344 Increasing the intake of eggs after achieving a near optimal blood pressure is unlikely to reduce the risk of hemorrhagic stroke and will likely increase the risk of dying of any cause.
Unwarranted Mediocre Health Recommendations
The conclusions of the earlier meta-analysis are misleading and inconsistent with the body of literature. What is more concerning is that these findings will likely be used in marketing campaigns to confuse the general population, of which the great majority are already at risk of cardiovascular disease. The most recent meta-analysis paper while being overall informative and more clearly demonstrating the dangers of eggs for both diabetics and non-diabetics, the authors still failed to address many important findings that have been addressed in this series of posts. A greater emphasis on the effects of replacing eggs with other suitable foods is required, and the available evidence suggests a significant benefit of replacing eggs with whole plant foods, including fruits, vegetables, whole grains and nuts.31129 As Spence and colleagues pointed out in regards to recent controversy surrounding dietary cholesterol and eggs:45
…the only ones who could eat egg yolk regularly with impunity would be those who expect to die prematurely from nonvascular causes.
A recent publication from the EPIC-Oxford cohort with 15,000 vegetarians and 30,000 non-vegetarians found that the vegetarians had a 32% lower risk of hospitalization or death from coronary heart disease.1 These findings are consistent with a previous meta-analysis of 5 cohort studies with 48,000 non-vegetarians and 28,000 vegetarians which found that lacto-ovo vegetarians had a 34% lower risk of fatal coronary heart disease compared to regular meat eaters.2 These findings remained significant even after adjusting for non-dietary factors and alcohol intake. In addition, in each of these 6 cohort studies, vegetarians and non-vegetarians shared a similar interest in healthy lifestyles or were of a similar religious background, therefore limiting the number of potential confounders that could have obscured these findings.
This review will focus on the evidence from randomized controlled trials and long-term prospective cohort studies addressing the influence of vegetarian dietary patterns on the risk of coronary heart disease, and how these findings have contributed to the current understanding of the diet-heart hypothesis. This review will also consider the question as to whether the simple definition of a vegetarian diet is meaningful in the context of a healthy diet to reduce the risk of coronary heart disease. Regarding cohort studies, this review will primarily consider the influence of lacto-ovo vegetarian diets on the risk of coronary heart disease due to limited evidence from these studies addressing the long-term adherence to other types of vegetarian diets. A more informative analysis maybe possible after a longer follow-up of the on-going and largest cohort of vegetarians, the Adventist Health Study 2, which has observed more favorable cardiovascular risk factors within different vegetarian subgroups, particularly vegans.3
Skeptics of the diet-heart hypothesis often suggest that there are no plausible mechanisms in which a vegetarian dietary pattern can lower the risk of coronary heart disease, and often ascribe the observed benefits of vegetarianism to factors other than the avoidance of animal foods. Typically either ignored or downplayed by these skeptics is the convincing evidence that vegetarian dietary patterns can lower LDL cholesterol, which is an established risk factor for coronary heart disease.456
Establishing Causation
In the 6 cohorts described, a sizable portion of the non-vegetarians consumed significantly less meat than the general population. For example, in the EPIC-Oxford cohort, most participants were either occasional meat eaters, or affiliated with vegetarians or with vegetarian societies. Also, a potential problem in these cohorts is that measurement error of usual dietary intake of meat may have resulted in misclassifying a sizable portion of non-vegetarians as vegetarians. For example, in the Health Food Shoppers Study included among these cohorts, a validity assessment of the survey used to classify the participants vegetarian status suggested that 34% of the participants classified as vegetarians actually consumed meat. This data strongly suggests a much smaller than otherwise expected difference in dietary intake between the groups classified as vegetarians and non-vegetarians, potentially masking a stronger protective effect of a vegetarian dietary pattern.7
Another potential problem in these cohorts is the possibility that a sizable portion of participants classified as vegetarians stopped consuming meat or other animal foods in response to deteriorating health or unfavorable risk factors that would ultimately become life-threatening. This has been referred to as the ‘sick quitter effect’, which is known to mask the protective effect of smoking cessation in studies due to participants quitting in response to deteriorating health.8 In regards to diet, it has been documented that people tend to lower intake of saturated fat and cholesterol in response to unfavorable serum cholesterol levels, which has actually been shown to bias the association between diet and serum cholesterol in the opposite direction than expected [reviewed previously]. This bias is known as reverse causation, and may explain why in the Adventist studies that participants with short-term adherence (less than 5 years) to a vegetarian diet experienced an increased risk of mortality, while participants with long-term adherence (more than 17 years) to a vegetarian diet experienced a significantly lower risk of mortality compared to non-vegetarians (Fig. 1).8
Figure 1. Life expediencies for long-term vegetarians and short-term vegetarians in the Adventist Health Study and Adventist Mortality Study*
These factors should be taken into account when testing for causality as failing to do so may mask a protective effect of a vegetarian dietary pattern. One of the most important factors in order to establish causality is to address whether the association is biologically plausible, which in this case requires examining how vegetarian dietary patterns can influence cardiovascular risk factors.
Serum Lipids
In 1922, de Langen published what was perhaps the first study that provided strong evidence that a vegetarian dietary pattern favorably effects serum cholesterol when he placed five native Indonesians consuming a rice-based vegetarian diet into a metabolic ward and shifted the diet to one rich in meat, butter and egg fats, resulting in significant elevations in serum cholesterol [reviewed previously]. In 1954, Hardinge and Stare published what was perhaps the first observational study comparing the serum lipids of vegetarians to non-vegetarians in an affluent population. Lacto-ovo vegetarians and especially vegans had significantly lower serum cholesterol concentrations despite relatively high intakes of saturated fat.910 In 2009, Ferdowsian and Barnard published a systematic review of 27 randomized controlled trials and observational studies on either vegetarian or predominantly plant-based diets, and found that certain plant-based dietary patterns can lower LDL cholesterol by up to 35%, independent of changes to body weight (Figs 2, 3).4
Figure 2. Effects of plant-based diets in normolipidemic individuals: Randomized controlled trials*
Figure 3. Effects of plant-based diets in hyperlipidemic individuals: randomized controlled trials*
In the Lifestyle Heart Trial lead by Dr. Dean Ornish, intensive lifestyle changes including a vegetarian diet that allowed a small amount of non-fat dairy foods successfully reduced LDL by 37.2%, angina episodes by 91% and regressed coronary atherosclerosis in the experimental group after 1 year. In both the experimental and control group LDL and total cholesterol was correlated with changes in coronary atherosclerosis.11
A recent meta-analysis of statin based randomized controlled trials found that lowering LDL cholesterol to less than 100 mg/dl was associated with regression of coronary atherosclerosis in participants with coronary heart disease.12 Similarly, a recent mendelian randomization study of over 100,000 individuals found that genetically-predicted higher LDL cholesterol was associated with greater carotid atherosclerosis, but there was no causal association for HDL cholesterol and triglycerides.13 Consistent with these lines of evidence, it has been consistently demonstrated in experiments on non-human primates that coronary atherosclerosis induced by feeding of dietary cholesterol and saturated fat can be reversed by a cholesterol lowering diet [reviewed previously]. Therefore the preponderance of evidence strongly suggests that the findings from the Lifestyle Heart Trial of a correlation between lower LDL cholesterol and regression of coronary atherosclerosis was causal, and can at least partly be explained by the intervention of a cholesterol lowering vegetarian diet. In the meta-analysis of 5 cohorts it was found that in a sample of participants from 3 of the cohorts that serum cholesterol ranged from between 13 mg/dl to 23 mg/dl lower in the vegetarians compared to non-vegetarians. The researchers suggested that the difference in serum cholesterol could have largely explained the difference in fatal coronary heart disease between these groups.2 In the EPIC-Oxford cohort, serum lipids and blood cholesterol were measured in a sample of the participants. Non-HDL cholesterol was 17 mg/dl lower and systolic blood pressure was 3.3 mmHg lower in the vegetarians compared to the non-vegetarians. The researchers calculated that the differences between these two risk factors alone would expect to lower the risk of coronary heart disease by 24%, which is less than the observed 32% lower risk.1
The researchers from the EPIC-Oxford cohort suggested that the high ratio of polyunsaturated fat to saturated fat largely explained the difference in non-HDL cholesterol between groups, but failed to mention that a number of other plant based nutrients may have also contributed to this difference.1 It has been repeatedly demonstrated in randomized controlled trials that intake of plant protein, particularly from soy, plant sterols, and dietary fiber can also lower LDL cholesterol.141516 In fact in many of the interventions with the greatest diet induced decrease in LDL cholesterol, the decrease could not be explained by changes in dietary fat and cholesterol intake alone, but also likely due to the additive effects of a number of plant based nutrients.171819
It is clear that the LDL cholesterol levels of the vegetarians in these cohort studies far exceeded optimal levels, likely due to a diet deficient in whole plant foods and still relatively rich in animal foods. If these vegetarians had adhered to a much more phytonutrient rich cholesterol lowering diet such as that used in the aggressive dietary experiments, an even significantly lower risk of coronary heart disease may have been observed.Plant Positive recently referred to this informative statement made by Michael Brown and Joseph Goldstein the year before they were awarded the Nobel Prize for their research on the LDL-receptor:20
If the LDL-receptor hypothesis is correct, the human receptor system is designed to function in the presence of an exceedingly low LDL level. The kind of diet necessary to maintain such a level would be markedly different from the customary diet in Western industrial countries (and much more stringent than moderate low-cholesterol diets of the kind recommended by the American Heart Association). It would call for the total elimination of dairy products as well as eggs, and for a severely limited intake of meat and other sources of saturated fat.
Evidence from over one hundred randomized controlled trials has proven beyond plausible doubt that changing from a diet rich in animal foods to a dieter richer in certain whole plant foods significantly lowers LDL cholesterol.41415162122 Similarly, evidence from over one hundred randomized controlled trials has proven beyond plausible doubt that lowering LDL cholesterol decreases the risk of coronary heart disease and all-cause mortality.56 Therefore consistent with the diet-heart hypothesis, there is convincing evidence that an appropriately designed vegetarian diet would reduce the risk of coronary heart disease, and that this reduction can at least be partly explained by lower LDL cholesterol.
Beyond Cholesterol
There are likely a number of dietary related factors that contribute to the lower risk of coronary heart disease observed in people with vegetarian dietary patterns that cannot entirely be explained by lower LDL cholesterol. For example, it has been shown in randomized controlled trials that a number of plant based nutrients can lower blood pressure, which may explain the lower blood pressure observed in vegetarians in a number of observation and intervention studies [reviewed previously]. Furthermore, appropriately designed vegetarian diets likely reduce the risk of being overweight and developing type II diabetes.2324252627 Other factors such as reduced oxidation of LDL and changes in blood clotting have also been suggested as explanations for the lower risk of coronary heart disease observed in vegetarians.2829
Perhaps the main concern with an inappropriately designed vegetarian diet is that it may result in elevated homocysteine due to an inadequate intake of vitamin B12, suggested to be a risk factor for coronary heart disease. Although deficiency of vitamin B12 is rarely observed in some populations in the developed world consuming a predominantly plant based diet, perhaps due to regular contact with vitamin B12 producing bacteria, health authorities strongly recommended that vegetarians diets be supplemented regularly with a bioavailable source of vitamin B12.3031 Jack Norris, RD regularly posts informative reviews on the latest research on vitamin B12 intake and homocysteine, and updates his recommendations for vitamin B12 supplementation in response to new findings.
In all of the cohort studies, and perhaps most intervention studies carried out on vegetarians, there is little doubt that only very few vegetarians were actually consuming a diet predominantly based on whole plant foods, and as expected although these vegetarians experienced a significantly lower risk of coronary heart disease than their omnivorous counterparts, they still experienced a substantial residual risk of coronary heart disease.32 In Dr. Caldwell Esselstyn’s more recent decade long study (pending publication) of around 200 patients that were advised to consume a whole foods, plant-based diet, it was found that recurrent cardiac events only occurred in 0.5% of adherent participants. This is an approximately 40 fold lower risk than achieved in other dietary or statin based trials, strongly suggesting that these results can only partially be explained by the use of LDL cholesterol lowering medication [reviewed previously]. This is an excellent example of how a whole foods, plant-based diet can confer significant benefit over-and-above favorable changes to traditional risk factors.
Caldwell Esselstyn on making heart attacks history
The definition of a vegetarian diet typically only defines which type of animal foods are restricted and not the quantity and quality of plant foods consumed. As all vegetarian diets are not created equal, studies on vegetarians may only provide limited information of the influence a more nutrient dense vegetarian dietary pattern on the risk of coronary heart disease.33 The restriction of certain animal foods however may encourage at least a modest increase of intake of high quality plant matter, including fruits, vegetables, whole grains, legumes and nuts in order to make up for calories and certain nutrients otherwise consumed from animal foods. Nevertheless, even the studies examining less than optimal vegetarian diets may contribute more to the knowledge of optimal dietary patterns than many studies on homogenous populations due to greater differences in intake of specific foods and nutrients. Vegetarian diets should be designed according to not only which animal foods are restrict, but also the quality of plant foods consumed in order to minimize and preferably eliminate the risk of developing coronary heart disease. There is very strong evidence that such a diet would also lower the risk of numerous other chronic and degenerative diseases.
In 2010, Jeremiah Stamler published the editorial Diet-heart: a problematic revisit in the American Journal of Clinical Nutrition addressing a number of very serious flaws in a meta-analysis paper supported by the National Dairy Council and authored by Siri-Tarino et al. that concluded that there was insufficient evidence from prospective cohort studies to suggest that the intake of saturated fat increases the risk of coronary heart disease and cardiovascular disease.1 A number of researchers including Stamler, who has played a prominent role in the diet-heart hypothesis for over 60 years found that a number of serious flaws in this meta-analysis would have likely biased the association between saturated fat and coronary heart disease towards null.123
In the editorial Stamler produced a meta-analysis based on the same papers included in the Siri-Tarino et al. meta-analysis and calculated that saturated fat was associated with a 32% increased risk of fatal coronary heart disease, an end point ignored, perhaps intentionally by the authors of the original meta-analysis.1 It would seem almost implausible for anyone citing the Siri-Tarino et al. meta-analysis with an interest in saving lives to fail to mention the findings for this fatal end point, the single most leading cause of death in the world.4 Perhaps the cholesterol skeptics do not share Stamler’s interest of saving lives, explaining why they have chosen to refrain from informing their audience of Stamler’s findings.
Another shortcoming of the Siri-Tarino et al. meta-analysis paper was the lack of acknowledgement in the assessments and conclusions that major cross-population studies with a prospective (future looking) design, such as the Seven Countries Study found that saturated fat was associated with a significantly increased risk of fatal coronary heart disease (Fig. 1).15 Consistent with the trend of the findings from the Seven Countries Studies, the nomadic Kirghiz plainsmen who subsist on a diet of enormous amounts of organic grass-fed milk and meat experience severe vascular disease at a very young age [reviewed previously].
Figure 1. Saturated fat as % of calories and fatal coronary heart disease in 16 cohorts from the Seven Countries Study
In this series of posts I will review the diet-heart hypothesis and the arguments against the hypothesis raised by known cholesterol skeptics. Note that in this review the diet-heart hypothesis refers to the hypothesis that dietary change, such as the substitution of individual dietary fats for carbohydrate influences serum (blood) lipids (including serum total and LDL cholesterol), and therefore at the very least indirectly influences the risk of developing coronary heart disease.
Stephan Guyenet, the author of the Whole Health Source blog has produced some very informative posts dispelling Gary Taubes’s misleading claims regarding carbohydrate metabolism, insulin and obesity.6 Unfortunately, like Taubes rather than embracing the preponderance of evidence that has established the diet-heart hypothesis, Guyenet has chosen to confuse the subject in a series of blog posts. I have previously commented on Guyenet’s blog regarding one such concerning post in May 2011 where I raised my concerns regarding Guyenet’s arguments against the evidence that saturated fat raises serum cholesterol, and increases the risk of coronary heart disease.7
One of my main concerns I presented in my comments on Guyenet’s blog was his lack of acknowledgement that saturated fat was associated with an increased risk of fatal coronary heart disease in the Health Professional’s Follow-up Study and in Stamler’s meta-analysis. Guyenet was less than appreciative of these comments, stating:
I find it disturbing that you continue to cite the Health Professionals follow-up study to support your position despite the fact that there was no statistically significant association between SFA intake and any measure of CHD after maximum adjustment. If there were really a relationship between the two factors, you wouldn't have to cite non-significant findings to support your position.
In the paper from the Health Professional’s Follow-up Study cited by Guyenet, for men in the top verses the lowest fifth of saturated fat intake the relative risk for fatal coronary heart disease was 1.72 (95% confidence interval 1.01 to 2.90) after maximum adjustment.8 In other words this study found that saturated fat intake was associated with a statistically significant 72% increased risk of fatal coronary heart disease for high compared to low intake. Guyenet avoided directly responding to my comments regarding the finding in Stamler’s meta-analysis for fatal coronary heart disease, and simply referred back to the Siri-Tarino et al. meta-analysis which failed to address this fatal end point.
In this particular post that I commented on, Guyenet made several misleading statements in reference to the findings from the Siri-Tarino et al. meta-analysis:
Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk. So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks?
Apart from the failure to acknowledge that Stamler demonstrated that the cohort studies included in this meta-analysis found that saturated fat intake was actually associated with an increased risk of fatal coronary heart disease, there are several other points in this statement that are problematic that will be addressed separately.
The Problem of Overadjustment
Guyenet’s suggestion that the Siri-Tarino et al. meta-analysis should have found a positive association between saturated fat and coronary heart disease if saturated fat raises serum cholesterol and serum cholesterol increases the risk of coronary heart disease is misleading. One of the most serious flaws in this meta-analysis was the inclusion of overadjustments for serum lipids and dietary lipids, which would have obscured this diet-cholesterol-heart relationship that Guyenet referred to. Stamler addressed this flaw in the editorial:1
…the issue of whether SFA relates to CHD in univariate analyses is relevant. If findings on this subject are positive but the association is markedly reduced or ceases in multivariate analyses, this may be due to confounding (eg, by dietary cholesterol) and/or overadjustment (eg, by inclusion in analyses of serum total or LDL cholesterol, a major CHD risk factor influenced by SFA intake)… Of 15 studies that unequivocally concern the SFA-CHD relation, 4 did not include other dietary lipids or serum lipids among covariates. Their CHD relative risks (RRs) ranged from 1.22 to 2.77—ie, >1.07, which was the estimated CHD RR in the meta-analysis. Do these larger RRs reflect freedom from confounding and overadjustment?
As Stamler demonstrated, the studies that that did not include overadjustments for dietary and serum lipids were more likely to find a positive association between saturated fat and coronary heart disease, reaffirming that the influence that saturated fat has on coronary heart disease is partly dependent on serum lipids.
The Problem of Dietary Assessment Methods
Guyenet’s suggestion that the Siri-Tarino et al. meta-analysis found that the majority of high-quality prospective studies failed to find an association between saturated fat and heart disease is also misleading. Another serious flaw in the meta-analysis was the overreliance on poor quality dietary assessment methods, which was addressed by Katan et al.:2
A major weakness of the meta-analysis is the imprecision of dietary assessment methods used in the underlying studies. About half of the studies used 1-d dietary assessments or some other unvalidated method. Food intake varies from day to day, and there is a substantial literature showing that a single 24-h recall provides a poor estimation of the usual dietary intake of an individual. Such methods cannot reliably rank individuals by their long-term intake, especially within populations with a uniformly high saturated fat intake. Such imprecision in the assessment of disease determinants systematically reduces the strength of association of determinants with the disease. This is referred to as attenuation or regression dilution bias.
Stamler noted that the studies included in the Siri-Tarino et al. meta-analysis that used more precise dietary assessment methods were more likely to find a positive association between saturated fat and coronary heart disease:1
...the meta-analysis reported its findings as independent of a quality score including diet assessment. Of the 16 CHD studies, 4 relied on one 24-h dietary recall; the SFA-CHD RR was >1.00 for only one of these studies. Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies. Five used dietary history or multiday food record; the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids. These facts, which were unnoted in the meta-analysis, prompt the question: Did low-level reliability (reproducibility) of dietary SFA data drive RR values toward 1.00 (the regression-dilution bias problem)? No data on SFA reliability are given
It could actually be concluded from this data that the majority of the cohort studies that used ‘high-quality’ dietary assessment methods, in particular those that did not include overadjustments for dietary and serum lipids found that saturated fat was associated with an increased risk of coronary heart disease.
In the Seven Countries Study dietary intake was measured with high quality assessment methods including a seven day food record and for a subsample of participants the diets were also chemically analyzed.5 Another strength of the Seven Countries Study is that dietary intake was assessed between groups of individuals which has been shown to result in less measurement error than assessing dietary intakes between individuals as was done in the cohort studies included in the Siri-Tarino et al. meta-analysis.9 A further strength of the Seven Countries Study was that saturated fat intake ranged from 3% to about 22% of calories, a far greater range than the studies on mostly homogeneous populations included in the Siri-Tarino et al. meta-analysis, providing greater statistical power to detect a significant relationship.
The Problem of Dietary Modification
Stamler also addressed the problem related to participants making voluntary dietary changes, including the reduction of saturated fat intake in response to elevated serum cholesterol that could have also obscured the findings of the Siri-Tarnio et al. meta-analysis:1
Also, the meta-analysis says nothing about the problem for the 16 studies of possible bias in SFA-CHD findings due to dietary change (eg, reduced SFA intake) in people with higher serum total cholesterol seeking to lower total cholesterol/CHD risk (as occurred for the earliest of the 16 studies).
Even over 50 years ago in the Chicago Western Electric Company study, the earliest of the studies included in the Siri-Tarino et al. meta-analysis, participants were reducing intake of saturated fat and dietary cholesterol in response to unfavourable serum cholesterol concentrations.10 In studies where participants measured their lipid profile and subsequently lowered saturated fat intake in response to unfavourable results before entering the study, the saturated fat intake of these potentially high risk participants measured during the study could have been significantly lower than their lifetime averages. This could have resulted in an artificial increase in number of coronary events in the groups of participants classified as having a low intake of saturated fat. Similarly, the participants who lowered saturated fat intake in response to unfavourable serum lipids after completing their dietary assessment for the study may have artificially lowered the number of coronary events in the groups of participants classified as having high intake.
Few studies included in the Siri-Tarino et al. meta-analysis adequately addressed this problem, with the Health Professionals Follow-up Study perhaps being one of these few.8 In addition to the problem of imprecise dietary assessment methods, this problem further obscures the classification of the participants ranges of usual saturated fat intake potentially biasing the findings further towards null.11 Another problem that could have potentially obscured the findings in these studies, especially those that lasted into the statin era is that participants with higher serum cholesterol as a result of a high saturated fat intake maybe more likely to have received aggressive medical intervention in order to prevent cardiovascular disease. It should be emphasized here that Stamler found in a meta-analysis that saturated fat was associated with a 32% increased risk of fatal coronary heart disease despite such problems.1
The Problem of the Comparison Group
Guyenet’s suggestion that the Siri-Tarino et al. meta-analysis addressed the ‘association’ between saturated fat and coronary heart disease independent of other caloric sources is also misleading, a point that was addressed by Katan et al.:2
First, the notion that there exists such a thing as “the effect of saturated fat” is flawed. A lower intake of saturated fat implies an increased intake of some other source of calories to maintain caloric balance. Different substitutions for saturated fat have different effects on risk of coronary heart disease (CHD) and need to be discussed separately.
One of the greatest contributors to unnecessary confusion in nutritional research has resulted from studies that failed to compare foods or macronutrients with other suitable sources of energy. The majority of participants studied in developed nations typically consume only negligible amounts of whole plant foods, and therefore a lower intake of one particular food typically results in a higher intake of other processed or animal foods.12 Without giving this important fact careful consideration most foods that are less than optimal for human health will appear harmless in studies as they are typically compared with other unhealthy foods. This problem was elaborated on in a research panel including Ronald Krauss, the senior researcher of the Siri-Tarino et al. meta-analysis:13
For example, it may not be useful, as is usually done, to compare a specific food to all other sources of energy, which are usually mainly refined starches, sugars, red meat, and fat-rich dairy products in typical Western diets.
Hu FB and Sun Q, two of the authors of the Siri-Tarino et al. meta-analysis also addressed this shortcoming of the meta-analysis in a paper they co-authored, describing what sources of energy saturated fat was substituted for:14
…however, in this meta-analysis saturated fat was compared with other calorie sources, primarily refined carbohydrates, and high intake of refined carbohydrates has been associated with a high risk of CHD.
As the Siri-Tarino et al. meta-analysis failed to find a lower risk of saturated fat compared primarily to foods rich in refined carbohydrates even after adjusting for serum lipids, these findings hardly justify increasing the intake of saturated fat any more than they do to increasing the intake of refined carbohydrates. As expected from these findings, meta-analysis and systematic reviews that compare foods to all other sources of energy combined have also failed to find a clear association between refined grains and cardiovascular disease and all-cause mortality, even without the inclusion of such significant overadjustments.1516 If Guyenet and the other cholesterol skeptics applied the same methodology they use to judge the health properties of saturated fat to all foods, they would not be able to justify their recommendation of limiting intake of refined grains in order to reduce the risk of cardiovascular disease and other non-communicable diseases.
In Guyenet’s post I commented in regards to a pooled analysis of 11 large prospective cohort studies which found that replacing 5% of energy from saturated fat with an equivalent of polyunsaturated fat was associated with a 26% decreased risk of coronary heart disease mortality.17 Here again Guyenet was less than appreciative of such comments, stating:
That's not how epidemiology works. What you do is you examine if people who eat more SFA have more heart attacks than people who eat less, while controlling for other variables-- and the studies have nearly all found no association. That's how epi works in other disciplines. Moving the goalposts to Keys score, SFA/PUFA ratios and using fancy math to model nutrient substitutions will only fool people who don't know any better or are desperate to believe that there's an association.
It appears that Guyenet is either desperately trying to confuse his audience or is suggesting that a change in saturated fat intake in the general population will not influence the intake of any other sources of energy for which he has provided no evidence for. Examining saturated fat intake is meaningless without considering what sources of energy it is replacing, which is why models of macronutrients substitution is preferred. The study of nutrition epidemiology is different than the study of other exposures such as tobacco smoke in the respect that energy is required in order to maintain life, and therefore it essential in nutrition science to compare one source of calories with suitable alternatives.
Additional Findings from Observational Studies
Even if one were to judge the health properties of saturated fat on the basis of findings from prospective cohort studies that compared saturated fat intake with all other sources of energy combined, it would still be implausible to conclude that saturated fat is not disease promoting. The finding from Stamler’s meta-analysis that saturated fat intake was associated with a 32% increased risk of fatal coronary heart disease by itself is a cause for concern, however other findings from cohort studies also raise significant concern. A meta-analysis of 12 cohort studies of 418,816 women found that saturated fat intake was associated with an increased risk of breast cancer, consistent with the findings from more recent cohort studies of 319,826 and 188,736 women.181920 In addition, a pooled-analysis of 12 cohort studies of 523,217 women found that a high intake of saturated fat was associated with an increased risk of ovarian cancer.21 Furthermore, a large cohort of 525,473 men and women found that saturated fat intake, especially that from animal sources increased the risk of pancreatic cancer and a cohort of 494,000 men and women found that saturated fat intake was associated with a greatly increased risk of small intentional cancer.2223 Another cohort study of 137,486 women found that saturated fat intake was associated with an increased risk of hip fracture, consistent with other lines of evidence [reviewed previously].24
Siri-Tarino et al. excluded cohort studies of type II diabetics patients from the meta-analysis which should be addressed. Two such studies found a very strong association between saturated fat and cardiovascular disease, including the Nurses’ Health Study which also found a significant association for dietary cholesterol and the Keys score.2526 Furthermore, although typically considered lower in the hierarchy of evidence than prospective cohort studies, a number of case-control studies have also found a positive association between saturated fat and coronary heart disease.27282930
In regards to the association between saturated fat intake and the risk of stroke, the Siri-Tarino et al. meta-analysis failed to address the possible influence that blood pressure has on the association between saturated fat and the risk of stroke despite finds from large cohort studies including the Nurses’ Health Study that suggest the association is dependent on blood pressure. Without consideration of these important details the Siri-Tarino et al. meta-analysis should not be considered as providing a clear interpretation of the association between saturated fat intake and the risk of stroke. I have addressed this matter in further detail in Part I and Part II of a review addressing blood pressure, blood cholesterol, diet and the risk of stroke, which also addresses the Northern Manhattan Study which found that saturated fat was associated with a trend towards an increased risk of ischemic stroke that was excluded from the Siri-Tarino et al. meta-analysis despite apparently meeting the requirements for the inclusion criteria.31
The Problem of Reductionism
The disease promoting properties of saturated animal fat cannot be ascribed purely to the substitution of saturated fat for other macronutrients, but also to other nutritional factors including the content of dietary cholesterol, ruminant trans-fat and the lack of dietary fiber and other phytonutrients. For example, a study on an apparently health conscious population included in the Siri-Tarino meta-analysis found that while saturated fat was associated with 2.77 fold increased risk of coronary heart disease which was the value used in the meta-analysis, the association for animal fat was even stronger, a 3.29 fold increased risk.32
In the pooled analysis of 11 large cohort studies, compared to saturated fat, monounsaturated fats which was predominantly derived from animal fat was associated with the greatest increased risk of coronary events out of all the studied macronutrients. Furthermore this pooled analysis adjusted for dietary fiber, dietary cholesterol and possibly ruminant trans-fat, which also needs to be taken into consideration as this could have potentially underestimated the adverse effects of increasing saturated animal fat intake at the expense of whole plant foods.33 As foods contain not only macronutrients but also tens of thousands of different bioactive constituents which can potentially influence health, it would therefore be more informative to compare the effect of substituting different foods rather than isolated macronutrients on disease outcomes.3435 Arguably the highest quality prospective cohort study to have published a paper addressing the substitution of foods on the risk of coronary heart disease was the Nurses’ Health Study (Fig. 2).14 As suggested by this study, the benefits of replacing animal foods with whole plant foods to lower the risk of coronary heart disease can be explained partly but not entirely by the displacement of saturated fat with other macronutrients.
Figure 2. Coronary heart disease associated with replacement of a major dietary protein source with another in the Nurses' Health Study
Another paper that also addressed the substitution of foods on the risk of coronary heart disease was from the Iowa Women’s Health Study, which found that substituting foods rich in refined carbohydrates with dairy was associated with a increased the risk of fatal coronary heart disease and substitution with red meat was associated with a increased risk of both fatal coronary heart disease and all-cause mortality.36 These findings raise significant doubt towards the cholesterol skeptics claims that certain animal foods appear disease promoting in studies only because they act as a marker of refined food intake. This study actually found that dairy and red meat are disease promoting even when compared to foods rich in refined carbohydrates.
The Problem of Conflicts of Interests
It is well documented that the conclusions of studies that receive industry funding, including from the dairy, soda and tobacco industries are far more likely to bias in favor of the invested industry than studies without apparent industry funding.37 The Siri-Tarino et al. meta-analysis was funded by the National Dairy Council and the senior researcher, Ronald Krauss has reported receiving grants from the National Dairy Council, the National Cattleman’s Beef Association and the Robert C. and Veronica Atkins Foundation. Although such conflicts of interests do not necessarily prove that the meta-analysis is flawed, it does at the very least suggest however that the author’s lack of acknowledgement of the positive association between saturated fat and fatal coronary heart disease and of the very serious flaws in the meta-analysis may have been intentional.
Like diet, it is notoriously difficult to accurately measure environmental tobacco smoke exposure which has obscured the findings for passive smoking and smoking related diseases in observational studies. In a similar fashion as the dairy industry has done to downplay and distort the relationship between saturated fat and cardiovascular disease, the tobacco industry has taken advantage of measurement error in order to scrutinize the association between passive smoking and lung cancer in part due to the fact that the majority of observational studies failed to find a statistically significant association.38 However, it is clear that when all of the evidence is considered there is convincing evidence that passive smoking increases the risk of lung cancer, just as the substitution of whole plant foods with saturated animal fat increases the risk cardiovascular disease.39 In 2003, tobacco affiliated researchers Enstrom and Kobat published findings from a 39 year follow-up of a prospective cohort study in the British Medical Journal and concluded that exposure to environmental tobacco smoke does not likely significantly influence the development of lung cancer and coronary heart disease. This paper received a lot of attention from the mass media, including the Wall Street Journal, and was used by the tobacco industry to criticize government sponsored ‘junk science’.40 This study was criticized by a number of researchers and by the American Cancer Society which addressed a number of the very serious flaws in the study.4142 The prominent flaw that was emphasized was the lack of a suitable comparison group. The analysis only took into account whether never smokers who had a smoking spouse were more likely to develop lung cancer and coronary heart disease compared to never smokers without a smoking spouse, and did not account other forms of environmental tobacco smoke. This was an issue because in 1959 when the participants were enrolled there was tobacco smoke virtually everywhere leaving no group unexposed. Furthermore this study only measured the spouses smoking status at study baseline and did not account for whether the spouse quit smoking, ended the marriage or died during the follow-up period. To summarize some of the shortcomings of this tobacco industry influenced study, it suffered from a lack of suitable comparison group, lack of high quality assessment methods to precisely measure exposure, and the lack of assessment of changes to exposure during the follow-up period. These shortcomings remarkably resemble those of the Siri-Tarino et al. meta-analysis. This paper has even been cited in a lawsuit against tobacco companies by the US District Court as ‘a prime example of how nine tobacco companies engaged in criminal racketeering and fraud to hide the dangers of tobacco smoke.’43 This was unfortunately not the last time that the researchers of an industry influenced study would publish a paper that has the potential to jeopardize the health of so many. What is also unfortunate is that many cholesterol skeptics have also chosen to exploit these findings in an attempt to advocate disease promoting diets to an uninformed audience. Follow-up posts in this series will critically examine other lines of evidence of the diet-heart hypothesis that cholesterol skeptics have chosen to misinterpret and exploit in an attempt to confuse the general population.
