The old debate over whether egg consumption is detrimental to cardiovascular health has been revived since the recent publication of a study that finds a significant, albeit modest, association between egg or dietary cholesterol consumption and the incidence of cardiovascular disease (CVD) and all-cause mortality. Eggs are an important food source of cholesterol: a large egg (≈50 g) contains approximately 186 mg of cholesterol. The effect of eggs and dietary cholesterol on health has been the subject of much research over the last five decades, but recently it has been assumed that this effect is less important than previously thought. For example, the guidelines of medical and public health organizations have in recent years minimized the association between dietary cholesterol and CVD (see the 2013 AHA/ACC Lifestyle Guidelines and the 2015–2020 Dietary Guidelines for Americans). In 2010, the American guidelines recommended consuming less than 300 mg of cholesterol per day; however, the most recent recommendations (2014–2015) do not specify a daily limit. This change stems from the fact that cholesterol intake from eggs or other foods has not been shown to increase blood levels of LDL-cholesterol or the risk of CVD, as opposed to the dietary intake of saturated fat that significantly increases LDL cholesterol levels, a significant risk of CVD.
Some studies have reported that dietary cholesterol increases the risk of CVD, while others reported a decrease in risk or no effect with high cholesterol consumption. In 2015, a systematic review and meta-analysis of prospective studies was unable to draw conclusions about the risk of CVD associated with dietary cholesterol, mainly because of heterogeneity and lack of methodological rigour in the studies. The authors suggested that new carefully adjusted and rigorously conducted cohort studies would be useful in assessing the relative effects of dietary cholesterol on the risk of CVD.
What distinguishes the study recently published in JAMA from those published previously is its great methodological rigour, in particular a more rigorous categorization of the components of the diet, which makes it possible to isolateindependent relationships between the consumption of eggs or cholesterol from other sources and the incidence of CVD. The cohorts were also carefully harmonized, and several fine analyses were performed. The data came from six U.S. cohorts with a total of 29,615 participants who were followed for an average of 17.5 years.
The main finding of the study is that greater consumption of eggs or dietary cholesterol (including eggs and meat) is significantly associated with a higher risk of CVD and premature mortality. This association has a dose-response relationship: for every additional 300 mg of cholesterol consumed daily, the risk of CVD increases by 17% and that of all-cause mortality increases by 18%. Each serving of ½ egg consumed daily is associated with an increased risk of CVD of 6% and an increased risk of all-cause mortality of 8%. On average, an American consumes 295 mg of cholesterol every day, including 3 to 4 eggs per week. The model used to achieve these results took into account the following factors: age, gender, race/ethnicity, educational attainment, daily energy intake, smoking, alcohol consumption, level of physical activity, use of hormone therapy. These adjustments are very important when you consider that egg consumption is commonly associated with unhealthy behaviours such as smoking, physical inactivity and unhealthy eating. These associations remain significant after additional adjustments to account for CVD risk factors (e.g. body mass index, diabetes, blood pressure, lipidemia), consumption of fat, animal protein, fibre and sodium.
A review of this study suggests that the association between cholesterol and the incidence of CVD and mortality may be due in part to residual confounding factors. The authors of this review believe that health-conscious people reported eating fewer eggs and cholesterol-containing foods than they actually did. Future studies should include “falsification tests” to determine whether a “health consciousness” factor is the cause of the apparent association between dietary cholesterol and CVD risk.
Eggs, TMAO and atherosclerosis
A few years ago, a metabolomic approach identified a compound in the blood, trimethylamine-N-oxide (TMAO), which is associated with increased cardiovascular risks. TMAO is formed from molecules from the diet: choline, phosphatidylcholine (lecithin) and carnitine. Bacteria present in the intestinal flora convert these molecules into trimethylamine (TMA), then the TMA is oxidized to TMAO by liver enzymes called flavin monooxygenases. The main dietary sources of choline and carnitine are red meat, poultry, fish, dairy products and eggs (yolks). Eggs are an important source of choline (147 mg/large egg), an essential nutrient for the liver, muscles and normal foetal development, among others.
A prospective study indicated that elevated plasma concentrations of TMAO were associated with a risk of major cardiac events (myocardial infarction, stroke, death), independent of traditional risk factors for cardiovascular disease, markers of inflammation, and renal function. It has been proposed that TMAO promotes atherosclerosis by increasing the number of macrophage scavenger receptors, which carry oxidized LDL (LDLox) to be degraded within the cell, and by stimulating macrophage foam cells (i.e. filled with LDLox fat droplets), which would lead to increased inflammation and oxidation of cholesterol that is deposited on the atheroma plaques. A randomized controlled study indicates that the consumption of 2 or more eggs significantly increases the TMAO in blood and urine, with a choline conversion rate to TMAO of approximately 14%. However, this study found no difference in the blood levels of two markers of inflammation, LDLox and C-reactive protein (hsCRP).
Not all experts are convinced that TMAO contributes to the development of CVD. A major criticism is focused on fish and seafood, foods that may contain significant amounts of TMAO, but are associated with better cardiovascular health. For example, muscle tissue in cod contains 45–50 mmol TMAO/kg. For comparison, the levels of choline, a precursor of TMAO, are 24 mmol/kg in eggs and 10 mmol/kg in red meat. The only sources of choline that are equivalent to that in TMAO in marine species are beef and chicken liver. TMAO contained in fish and seafood is therefore significantly more important quantitatively than TMAO that can be generated by the intestinal flora from choline and carnitine from red meat and eggs. This was also measured: plasma levels of TMAO are much higher in people who have a fish-based diet (> 5000 μmol / L) than in people who eat mostly meat and eggs (139 μmol / L). In their response to this criticism, the authors of the article point out that not all fish contain the same amounts of TMAO and that many (e.g. sea bass, trout, catfish, walleye) do not contain any. Fish that contain a lot of TMAO are mainly deep-sea varieties (cod, haddock, halibut). The TMAO content of other fish, including salmon, depends on the environment and when they are caught.
Other experts believe this could be a case of reverse causality: the reduction in renal function associated with atherosclerosis could lead to an accumulation of TMAO, which would mean that this metabolite is a marker and not the cause of atherosclerosis. To which the authors of the hypothesis counter that the high concentration of TMAO is associated with a higher risk of cardiovascular events even when people have completely normal kidney function.
Diabetes and insulin resistance
People who are overweight (BMI> 25) and obese (BMI> 50) are at higher risk of becoming insulin resistant and having type 2 diabetes and metabolic syndrome, conditions that can, independently or in combination, lead to the development of cardiovascular disease. There is evidence that dietary cholesterol may be more harmful to diabetics. Intestinal absorption of cholesterol is impaired in diabetics, i.e. it is increased. However, in a randomized controlled trial, when diabetic patients consumed 2 eggs per day, 6 times per week, their lipid profile was not altered when their diet contained mono- and polyunsaturated fatty acids. Other studies (mostly subsidized by the egg industry) suggest that eggs are safe for diabetics.
Dr. J. David Spence of the Stroke Prevention & Atherosclerosis Research Center believes that people at risk for CVD, including diabetics, should avoid eating eggs (see also this more detailed article). This expert in prevention argues that it is the effects of lipids after a meal that matter, not fasting lipid levels. Four hours after a meal high in fat and cholesterol, harmful phenomena such as endothelial dysfunction, vascular inflammation and oxidative stress are observed. While egg whites are unquestionably a source of high-quality protein, egg yolks should not be eaten by people with cardiovascular risks or genetic predispositions to heart disease.
The association between the consumption of eggs or foods containing cholesterol and the risk of CVD is modest. But since this risk increases with the amount consumed, people who eat a lot of eggs or foods containing cholesterol have a significant risk of harming their cardiovascular health. For example, according to the study published in JAMA, people who consume two eggs per day instead of 3 or 4 per week have a 27% higher risk of CVD and a 34% higher risk of premature mortality. It is therefore prudent to minimize the consumption of eggs (less than 3 or 4 eggs per week) and meat in order to limit the high intake of cholesterol and choline and avoid promoting atherosclerosis.
So-called “sugary drinks” generally refer to beverages containing added sugars (sucrose, corn syrup, juice concentrates or other sweeteners) such as soft drinks, fruit punches, energy drinks or even sports drinks. These beverages are the main source of simple sugar in the diet of North Americans and a significant proportion of calories consumed daily, especially among teenagers and young adults. In the United States, for example, sugary drinks account for an average of 9.3% of calories among young men and 8.2% among young women. This is huge, especially considering that the World Health Organization recommends limiting the total daily energy intake of added sugars to a maximum of 10% of calories, or 50 g of sugar.
This 10% limit is based on a large number of studies showing that a high intake of added sugars promotes overweight and increases the risk of type 2 diabetes, coronary heart disease and stroke. The negative impact on cardiovascular health is of particular concern, as a recent study has shown that regular consumption of soft drinks for several years is associated with an increased risk of premature mortality of around 20%, mainly as a result of cardiovascular disease.
Traditionally, 100% pure fruit juices are not included in the sugary drinks category as the sugar they contain is of natural origin and not artificially added. However, fruit juice sugar is identical to that of artificially sweetened drinks (glucose and fructose) and is present in quite comparable amounts (Figure 1). It is therefore possible that fruit juices, even when 100% pure, may cause the same adverse effects as other sugary drinks when consumed in large quantities.
Figure 1. Comparison of the sugar content of different fruit juices and beverages containing added sugars. Adapted from Gill and Sattar (2014).
This possibility has recently been explored by an analysis of the link between the consumption of sugary drinks and pure fruit juice and the risk of premature death. Looking at the eating habits of 13,440 participants, the researchers found that people who drank a lot of sugary drinks including pure fruit juice (10% or more of daily calories) were 44% more likely to die prematurely from coronary artery disease compared to people who limit the consumption of these drinks to less than 5% of daily calories. When the types of sugary drinks were analyzed separately, the increased risk of coronary death is 11% for each serving of 355 mL of sweetened beverages and 24% for each 355 mL of pure juice consumed. It should be noted, however, that the small number of deaths associated with coronary heart disease in the study does not support the conclusion that fruit juices are more harmful than other sugary drinks at these levels. Certainly, however, it seems that pure juices, when consumed in large quantities, can greatly contribute to the rise in premature death caused by sugary drinks. These results strengthen the case of the growing number of people (see here and here, for example) for whom fruit juices, even when 100% pure, are sugary drinks in the same category as the others and should therefore be totally eliminated from the diet.
A question of quantity
However, it should be noted that the negative effect of fruit juices on the risk of premature mortality is observed for fairly large quantities of juice, well above the quantities that are generally recommended (150 mL per day). At these more moderate amounts, the effect of fruit juice on health is much more nuanced: a review of the studies carried out to date shows that the consumption of reasonable quantities of fruit juice, i.e., a serving of 150–240 mL a day, has little effect on weight gain, both in adults (gain of about 0.2 kg over 3–4 years) and children (very slight increase in the BMI-z score, i.e., the body mass index of children adjusted for sex and age) (Table 1). These increases are significantly lower than those observed for sugary drinks such as soft drinks: for example, a study showed that each serving of soft drink consumed daily causes an increase in body weight of about 1 kg over a period of 4 years, three times more than the one associated with the consumption of a daily serving of pure fruit juice (0.3 kg).
Table 1. Health effects of consumption of pure fruit juices. Adapted from Auerbach et al. (2018).
* 240 mL serving; ** “BMI-z” (Body mass index z-score) is a relative measure of weight, adjusted for age and sex of the child.
|Outcome|| ||Population||Subjects||Amounts consumed||Results||Study
|Tooth decay||Children||1,919||≥1 serving*/d vs. ≤1 serving/week||20% increase in risk||Salas et al. (2015)
|Weight gain||Adults||108,708||Each additional serving/day||Gain of 0.22 kg over 4 years||Hebden et al. (2015)
|Children||20,639||Consumption vs. no consumption||No association||O’Neil and Nicklas (2008)
|Children||34,470||Each additional serving/day||BMI z score** change of 0.09 U over 1 year (0.03, 0.17 U) in children 1–6 y and no change in children 7–18 y||Auerbach et al. (2017)
|Adults||49,108||For each serving/day||Gain of 0.18 kg over 3 years||Auerbach et al. (2018)
|Cardiovascular diseases||Adults||114,279||Each additional serving/d of 100% citrus juice||28% decrease in risk of ischemic stroke||Joshipura et al. (2009)
|Adults||54,383||Highest vs. lowest consumers||15% decrease in the risk of acute coronary syndromes||Hansen et al. (2010)
|Adults||109,635||For each serving/day (citrus juice)||No significant effect||Hung et al. (2004)
|Adults||34,560||1–7 servings (150 mL)/week||17% decrease in risk of cardiovascular disease (24% risk of stroke)||Scheffers et al. (2019)
|Type 2 diabetes||Adults||137,663||Highest vs. lowest consumers||3% increase in risk||Xi et al. (2014)
|Adults||440,937||Each additional serving/day||7% increase in risk||Imamura et al. (2015)
|Adults||120,877||≥1 serving/day vs. ≤1 serving/month||No effect||Schulze et al. (2004)
A marked difference in the risk of developing type 2 diabetes has also been observed between artificially sweetened beverages and pure fruit juices. For example, one study found that daily consumption of soft drinks or fruit punches with added sugars caused an approximately two-fold increase in the risk of diabetes, while that of fruit juice had no impact (Figure 2). A meta-analysis of 4 studies reported similar results, i.e., fruit drinks containing added sugars increased the risk of diabetes while consumption of pure fruit juices had no effect. It should be noted, however, that other studies have reported a slight increase in the risk of diabetes in people consuming 240 mL and more per day of fruit juice (see Table 1).
Figure 2. Comparison of the increased risk of type 2 diabetes associated with the consumption of soft drinks, fruit juices containing added sugars, and 100% pure fruit juices. From Schulze et al. (2004).
The effect of moderate amounts of pure fruit juice is particularly interesting with regard to cardiovascular health. It has long been known that people who eat a lot of fruits are less likely to be affected by cardiovascular disease. These benefits are due, at least in part, to the high fruit content of polyphenols (including flavonoids) that prevent the oxidation of LDL cholesterol and prevent the development of atherosclerotic plaques. Since these polyphenols are extracted during fruit pressing and are therefore present in pure fruit juices, it is possible that these juices may also have positive effects on cardiovascular health. This has recently been highlighted by a study in the Netherlands among 34,560 participants aged 20 to 69 (EPIC-NL study). The researchers found that people who regularly consumed small amounts of pure fruit juice (150 mL daily, 7 days a week) were 17% less likely to be affected by cardiovascular disease, especially stroke (24% less risk). However, these protective effects disappeared at higher amounts of juice (> 8 glasses of pure juice per week), suggesting that the window of consumption associated with these preventive effects is relatively narrow. Decreases in the risk of ischemic stroke and acute coronary events following consumption of pure fruit juice have also been reported. It is also interesting to note that a study recently reported that people who consumed 150 mL of orange juice every day had half the risk of cognitive decline compared to those who rarely consumed it (once a month).
It is therefore possible that the different molecules present in fruit juices (vitamins, minerals, polyphenols) in some way counteract the negative effects of high amounts of sugar by reducing oxidative stress and chronic inflammation, two phenomena involved in the development of cardiovascular and neurodegenerative diseases. In any event, these observations suggest that it is clearly an exaggeration to say that pure fruit juices, in small quantities, are as harmful to health as beverages containing added sugars. It is only in high quantities that pure fruit juice becomes a sugary drink like any other and can cause the many health problems that are associated with excess sugar.
That being said, everyone agrees that the best way to consume fruits is in their whole form. In addition to the different bioactive compounds that are present in juices, whole fruits also contain fibres that increase the feeling of satiety (which reduces the amount of sugar ingested), prevent excessive fluctuations in blood sugar, and contribute to the maintenance of a diversified intestinal microbiome. Ideally, we should therefore favour the consumption of fresh fruits and drink water rather than juice to quench our thirst.
However, for people who may have difficult access to fresh fruit or prefer to consume it in a liquid form, the studies mentioned earlier suggest that pure fruit juice may be a valid alternative, but only when consumed in moderate amounts, around a small glass (150 mL) a day. At these amounts, juices significantly contribute to the daily intake of vitamins and minerals, and studies to date suggest a positive impact on the prevention of cardiovascular disease, especially stroke. It also appears that a moderate intake of pure juices does not have a major impact on the risk of overweight and diabetes, including in young children, confirming the validity of the recommendations of the American Academy of Pediatrics to limit the consumption of pure juice to 150 mL per day.
Although regular physical activity is associated with a marked decrease in the risk of several chronic diseases and premature mortality, the proportion of sedentary people, i.e. who do not reach the minimum of 150 minutes of physical activity recommended per week, continues to increase worldwide. According to recent estimates, a sedentary lifestyle is directly responsible for about 10% of premature deaths worldwide, a negative impact similar to that of smoking and obesity. Several factors contribute to this decline in the level of physical activity, the most important of which are probably the major social transformations that accompanied industrialization and, more recently, the technological revolution: motorized transport modes make it possible to travel great distances easily, computing is at the centre of many professions, and the constant arrival of new electronic devices continues to reduce the energy costs of most of our activities, both at work and at home. While this progress can generally be viewed as positive in terms of improving quality of life, it is important to remain aware that the resulting decrease in physical activity can be detrimental to health.
Canada is not immune to this trend, as studies that have measured physical activity levels accurately (using an accelerometer) show that only 15% of adults are active enough to reach the minimum of 150 minutes of physical activity per week. This is very little, and although lack of time is the main reason given by sedentary people for their low participation in physical activity, this excuse does not really hold up: 29% of Canadian adults spend 15 hours or more per week (more than two hours a day) in front of the TV and 15% are frequent computer users (11 hours or more per week) during leisure time. There is therefore a window of time available to reduce the sedentary lifestyle, especially since it is possible to be more active without having to dedicate a specific period of the day to exercise: several studies show that the simple fact of integrating light or moderate physical activities in our daily routine, whether walking, gardening or doing housework, is enough to enjoy the benefits of exercise on health (see our article on this subject).
The time spent commuting to and from work represents another interesting opportunity to increase the level of physical activity. In Canada, the use of motorized means of transportation to get to work is widespread, with 8 out of 10 workers using a motor vehicle for daily commuting (75% as drivers, 5% as passengers) (Figure 1). Conversely, active modes of transport such as walking and cycling are used by only 8% of workers, a proportion that is much lower than in most European countries: in Holland for example, no less than 50% of all daily trips are made by walking and cycling, while in all Nordic countries (Denmark, Sweden, Norway and Finland) this proportion is around 30%.
Figure 1. Distribution of the modes of transportation used by Canadians to get to work. From Statistics Canada (2013).
This low use of active transportation in North America likely contributes to the negative impacts of a sedentary lifestyle, particularly with respect to the high proportion of people who are overweight. It has been estimated that each hour spent in a car is associated with a 6% increase in the risk of obesity, while every kilometre walked is associated with a 5% reduction in the risk of being overweight. For example, an Australian study that followed 822 people over 4 years found that those who travelled every day by car tended to have greater weight gain (2.18 kg) than those who did not use a car (0.46 kg). This is in agreement with the results of a British study showing that people who stopped using their car to get to work and replaced it with active transportation or public transit lost weight (- 0.30 kg/m2). Conversely, those who stopped using active modes of transportation and instead opted for the car saw their body mass index significantly increase (+ 0.32 kg/m2).
In addition to promoting the maintenance of a healthy weight, several studies have shown that active transportation also has several positive effects on health, particularly in terms of prevention of cardiovascular disease, type 2 diabetes and premature mortality. One of the best examples is a large study of 263,540 participants living in 22 communities in the United Kingdom. By analyzing the modes of transportation used by this population to get to work, the researchers found that cyclists had a 41% lower risk of premature mortality than those who used motorized transport (public or cars). A positive effect was also observed for walkers, with a 27% reduction in the risk of myocardial infarction and a 36% reduction in the risk of dying from a cardiovascular event. Overall, a meta-analysis of 23 prospective studies that examined this issue (531,333 participants in total) shows that commuters who use active transportation (cycling, walking) have a significantly lower risk of cardiovascular disease (9%), type 2 diabetes (30%), and premature mortality (8%). As with any form of physical activity, these benefits associated with active transportation come from the many positive effects of this type of exercise on all cardiovascular risk factors, including hypertension, dyslipidemia, diabetes and obesity (Table 1).
Table 1. Major cardiovascular risk factors influenced by active transportation.
The benefits of cycling
The positive impacts of active transportation are particularly striking for those who travel by bicycle, with higher reductions in the risk of several chronic diseases and premature mortality than those who walk (Figure 2). These benefits associated with regular cycling are in line with Danish and British studies indicating that premature mortality rates are about 30% lower for cyclists compared to non-cyclists. This superiority of cycling over walking is probably due to the fact that cyclists in these studies showed a higher level of overall physical activity than walkers, with 90% of the people travelling by bicycle who reached the minimum recommended activity against 54% for those who travel on foot.
Figure 2. Reduced risk of several chronic diseases depending on the mode of active transportation. Adapted from Dinu et al. (2019).
Intervention studies carried out among sedentary people show that the positive effects of active bicycle transportation on health can be observed in the first six months following the adoption of this mode of transport. For example, people who cycle 20 minutes daily to commute to work for 8 weeks already show a noticeable improvement in their maximum aerobic fitness (VO2max), one of the best markers of good health. More recently, a British study showed that only 6 months of active bicycle transportation resulted in abdominal fat loss and significant improvement in insulin sensitivity in a group of sedentary people who were overweight or obese. The positive impact of active transportation is therefore very rapid, and these modes of transport can really contribute to improving the health of sedentary people.
It is also interesting to note that the benefits of active bicycle transportation on the reduction of all-cause mortality and type 2 diabetes are similar to those observed among people who cycle in their leisure time (Figure 3). For people who lack the time to exercise during the week or the weekend, riding a bike to work compensates for this lack of time by integrating physical activity into their daily routine. Not to mention that some studies suggest that the bicycle is the mode of transport that makes you happiest!
Figure 3. Risk of premature death for people who use bicycles in leisure time or as an active means of transportation. Adapted from Østergaard et al. (2018).
Walking or cycling to work is obviously not within everyone’s reach, especially for people who have to travel long distances from home to their workplace (in Canada, for example, over half of workers live more than 8 km from their work). On the other hand, even without completely replacing the use of motorized vehicles, it is still possible to be more physically active by walking or cycling for a portion of the journey (using bicycle-sharing systems), for example by parking the car at a certain distance from work or by getting off the bus or the metro a few stops earlier. For commuters using motorized transportation, the mere fact of walking the last kilometre (about 10 minutes) to and from work is equivalent to 100 minutes of physical activity per work week, a good proportion of the minimum recommended exercise. This is a worthwhile investment of time: in the British study mentioned earlier, even if the maximum protection (41%) is observed among commuters who make the entire trip by bike, people who used this mode of transportation for only part of the journey still had a 24% lower risk of premature mortality compared to those who travelled exclusively by motorized transport.
In North America, land use planning is unfortunately not very favourable to active transportation. In most cases, the cities developed after the invention of the automobile, which resulted in the construction of infrastructure focused mainly on the use of the car as a means of transport and therefore favoured urban sprawl. In Europe, the cities are older and were built before the advent of motorized transport, leaving in place infrastructure more conducive to non-motorized travel. For example, the proportion of workers who use bicycles as a means of transportation to work is 10 times higher in some European cities such as Copenhagen and Amsterdam than in North America (Figure 4).
Figure 4. Comparison of active bicycle transportation in various international cities. Adapted from Buehler and Pucher (2012). It should be noted that the data for Montréal are from 2006, so before the implementation of the bike-sharing system (Bixi). The proportion of bike users has increased since then to 3.2% in 2011, and Montréal is now ranked 18th cycling metropolis in the world.
To promote active transportation, we must therefore rethink what is called the “built environment”, i.e. the overall infrastructure that is part of our daily life, such as buildings, parks, schools, the road network, food sources (grocery stores, restaurants) or recreational facilities. Several studies have shown that people who live in cities where distances are reduced, streets are well connected, shops easily accessible and where areas for walking and cycling are well demarcated and safe are more physically active and in better cardiovascular health. It is therefore to be hoped that this type of built environment will become the norm in the near future.
The role of dietary fat in the development of obesity, cardiovascular disease and type 2 diabetes has been the subject of vigorous scientific debate for several years. In an article recently published in the prestigious Science, four experts on dietary fat and carbohydrate with very different perspectives on the issue (David Ludwig, Jeff Volek, Walter Willett, and Marian Neuhouser) identified 5 basic principles widely accepted in the scientific community and that can be of great help for non-specialists trying to navigate this issue.
This summary is important as the public is constantly bombarded with contradictory claims about the benefits and harmful effects of dietary fat. Two great, but diametrically opposed currents have emerged over the last few decades:
- The classic low-fat position, i.e., reducing fat intake, adopted since the 1980s by most governments and medical organizations. This approach is based on the fact that fats are twice as caloric as carbohydrates (and therefore more obesigenic) and that saturated fats increase LDL cholesterol levels, a major risk factor for cardiovascular disease. As a result, the main goal of healthy eating should be to reduce the total fat intake (especially saturated fat) and replace it with carbohydrate sources (vegetables, bread, cereals, rice and pasta). An argument in favour of this type of diet is that many cultures that have a low-fat diet (Okinawa’s inhabitants, for example) have exceptional longevity.
- The low-carb position, currently very popular as evidenced by the ketogenic diet, advocates exactly the opposite, i.e., reducing carbohydrate intake and increasing fat intake. This approach is based on several observations showing that increased carbohydrate consumption in recent years coincides with a phenomenal increase in the incidence of obesity in North America, suggesting that it is sugars and not fats that are responsible for excess weight and the resulting chronic diseases (cardiovascular disease, type 2 diabetes, some cancers). One argument in favour of this position is that an increase in insulin in response to carbohydrate consumption can actually promote fat accumulation and that low-carb diets are generally more effective at promoting weight loss, at least in the short term.
Reaching a consensus from two such extreme positions is not easy! Nevertheless, when we look at different forms of carbohydrates and fat in our diet, the reality is much more nuanced, and it becomes possible to see that a number of points are common to both approaches. By critically analyzing the data currently available, the authors have managed to identify at least five major principles they all agree on:
1) Eating unprocessed foods of good nutritional quality helps to stay healthy without having to worry about the amount of fat or carbohydrate consumed.
A common point of the low-fat and low-carb approaches is that each one is convinced it represents the optimal diet for health. In fact, a simple observation of food traditions around the world shows that there are several food combinations that allow you to live longer and be healthy. For example, Japan, France and Israel are the industrialized countries with the two lowest mortality rates from cardiovascular disease (110, 126 and 132 deaths per 100,000, respectively) despite considerable differences in the proportion of carbohydrates and fat from their diet.
It is the massive influx of ultra-processed industrial foods high in fat, sugar and salt that is the major cause of the obesity epidemic currently affecting the world’s population. All countries, without exception, that have shifted their traditional consumption of natural foods to processed foods have seen the incidence of obesity, type 2 diabetes, and cardiovascular disease affecting their population increase dramatically. The first step in combating diet-related chronic diseases is therefore not so much to count the amount of carbohydrate or fat consumed, but rather to eat “real” unprocessed foods. The best way to do this is simply to focus on plant-based foods such as fruits, vegetables, legumes and whole-grain cereals, while reducing those of animal origin and minimizing processed industrial foods such as deli meats, sugary drinks, and other junk food products.
2) Replace saturated fat with unsaturated fat.
The Seven Countries Study showed that the incidence of cardiovascular disease was closely correlated with saturated fat intake (mainly found in foods of animal origin such as meats and dairy products). A large number of studies have shown that replacing these saturated fats with unsaturated fats (e.g., vegetable oils) is associated with a significant reduction in the risk of cardiovascular events and premature mortality. A reduction in saturated fat intake, combined with an increased intake of high quality unsaturated fat (particularly monounsaturated and omega-3 polyunsaturated), is the optimal combination to prevent cardiovascular disease and reduce the risk of premature mortality.
These benefits can be explained by the many negative effects of an excess of saturated fat on health. In addition to increasing LDL cholesterol levels, an important risk factor for cardiovascular disease, a high intake of saturated fat causes an increase in the production of inflammatory molecules, an alteration of the function of the mitochondria (the power plants of the cell), and a disturbance of the normal composition of the intestinal microbiome. Not to mention that the organoleptic properties of a diet rich in saturated fats reduce the feeling of satiety and encourage overconsumption of food and accumulation of excess fat, a major risk factor for cardiovascular disease, type 2 diabetes and some cancers.
3) Replace refined carbohydrates with complex carbohydrates.
The big mistake of the “anti-fat crusade” of the ’80s and ’90s was to believe that any carbohydrate source, even the sugars found in processed industrial foods (refined flours, added sugars), was preferable to saturated fats. This belief was unjustified, as subsequent studies have demonstrated beyond a doubt that these refined sugars promote atherosclerosis and can even triple the risk of cardiovascular mortality when consumed in large quantities. In other words, any benefit that can come from reducing saturated fat intake is immediately countered by the negative effect of refined sugars on the cardiovascular system. On the other hand, when saturated fats are replaced by complex carbohydrates (whole grains, for example), there is actually a significant decrease in the risk of cardiovascular events.
Another reason to avoid foods containing refined or added sugars is that they have low nutritional value and cause significant variations in blood glucose and insulin secretion. These metabolic disturbances promote excess weight and the development of insulin resistance and dyslipidemia, conditions that significantly increase the risk of cardiovascular events. Conversely, increased intake of complex carbohydrates in whole-grain cereals, legumes, and other vegetables helps keep blood glucose and insulin levels stable. In addition, unrefined plant foods represent an exceptional source of vitamins, minerals and antioxidant phytochemicals essential for maintaining health. Their high fibre content also allows the establishment of a diverse intestinal microbiome, whose fermentation activity generates short-chain fatty acids with anti-inflammatory and anticancer properties.
4) A high-fat low-carb diet may be beneficial for people who have disorders of carbohydrate metabolism.
In recent years, research has shown that people who have normal sugar metabolism may tolerate a higher proportion of carbohydrates, while those with glucose intolerance or insulin resistance may benefit from adopting a low-carb diet richer in fat. This seems particularly true for people with diabetes and prediabetes. For example, an Italian study of people with type 2 diabetes showed that a diet high in monounsaturated fat (42% of total calories) was more effective in reducing the accumulation of fat in the liver (a major contributor to the development of type 2 diabetes) than a diet low in fat (28% of total calories).
These benefits seem even more pronounced for the ketogenic diet, in which the consumption of carbohydrates is reduced to a minimum (<50 g per day). Studies show that in people with a metabolic syndrome, this type of diet can generate a fat loss (total and abdominal) greater than a hypocaloric diet low in fat, as well as a higher reduction of blood triglycerides and several markers of inflammation. In people with type 2 diabetes, a recent study shows that in the majority of patients, the ketogenic diet is able to reduce the levels of glycated haemoglobin (a marker of chronic hyperglycaemia) to a normal level, and this without drugs other than metformin. Even people with type 1 diabetes can benefit considerably from a ketogenic diet: a study of 316 children and adults with this disease shows that the adoption of a ketogenic diet allows an exceptional control of glycemia and the maintenance of excellent metabolic health over a 2-year period.
5) A low-carb or ketogenic diet does not require a high intake of proteins and fats of animal origin.
Several forms of low carbohydrate or ketogenic diets recommend a high intake of animal foods (butter, meat, charcuteries, etc.) high in saturated fats. As mentioned above, these saturated fats have several negative effects (increase of LDL, inflammation, etc.), and one can therefore question the long-term impact of this type of low-carb diet on the risk of cardiovascular disease. Moreover, a study recently published in The Lancet indicates that people who consume little carbohydrates (<40% of calories), but a lot of fat and protein of animal origin, have a significantly increased risk of premature death. For those wishing to adopt a ketogenic diet, it is therefore important to realize that it is quite possible to reduce the proportion of carbohydrates in the diet by substituting cereals and other carbohydrate sources with foods rich in unsaturated fats like vegetable oils, vegetables rich in fat (nuts, seeds, avocado, olives) as well as fatty fish.
In short, the current debate about the merits of low-fat and low-carb diets is not really relevant: for the vast majority of the population, several combinations of fat and carbohydrate make it possible to remain in good health and at low risk of chronic diseases, provided that these fats and carbohydrates come from foods of good nutritional quality. It is the overconsumption of ultra-processed foods, high in fat and refined sugars, which is responsible for the dramatic rise in food-related diseases, particularly obesity and type 2 diabetes. Restricting the consumption of these industrial foods and replacing them with “natural” foods, especially those of plant origin, remains the best way to reduce the risk of developing these diseases. On the other hand, for overweight individuals with metabolic syndrome or type 2 diabetes, currently available scientific evidence suggests that a reduction in carbohydrate intake by adopting low-carb and ketogenic diets could be beneficial.
Updated on January 24, 2019
It is well established that aspirin is beneficial in secondary prevention, that is, for patients who have already suffered a myocardial infarction or stroke or who have a condition such as angina, acute coronary syndrome, or myocardial ischemia, and for those who have undergone coronary artery bypass grafting or coronary angioplasty. It has been suggested that aspirin may also be beneficial in primary prevention, i.e., to prevent cardiovascular events in those who have never had one, but are at risk. For the last few decades, aspirin has been used at low doses to prevent myocardial infarction and stroke; however, a recent study indicates that this drug does not prevent a first heart attack or stroke in people with moderate cardiovascular risk. In another study, this time of people with type 2 diabetes, taking aspirin modestly reduced the risk of cardiovascular events, but increased the risk of serious bleeding.
Primary prevention in people at moderate risk
Low-dose aspirin (100 mg/day) does not prevent a first heart attack or stroke in people at moderate risk of developing cardiovascular disease according to the ARRIVE study (Aspirin to Reduce Risk of Initial Vascular Events), published in The Lancet in August 2018. Aspirin has been tested in primary prevention over an average of 5 years, with 12,546 people living in the United Kingdom, Poland, Germany, Italy, Ireland, Spain and the USA. During these years, participants who took 100 mg of aspirin daily did not have significantly fewer vascular events than those who took a placebo [269 participants (4.3%) vs. 281 (4.5%); p=0.6038]. There were fewer vascular events than expected in this study, suggesting that participants had low cardiovascular risk rather than moderate risk. Gastrointestinal bleeding, which was mostly mild, was significantly higher in the aspirin group than in the placebo group [61 participants (0.97%) vs. 29 (0.46%); p=0007].
The authors of the ARRIVE study conclude that “The use of aspirin remains a decision that should involve a thoughtful discussion between a clinician and a patient, given the need to weigh cardiovascular and possible cancer prevention benefits against the bleeding risks, patient preferences, cost, and other factors. The ARRIVE data must be interpreted and used in the context of other studies, which have tended to show a reduction primarily in myocardial infarction, with less of an effect on total stroke (including both ischaemic and haemorrhagic stroke).”
Primary prevention in people with diabetes
Aspirin has been tested for primary prevention in 15,480 people with type 2 diabetes, who are therefore at increased risk of developing or dying from cardiovascular disease. During the seven years of the randomized study, people who took 100 mg of aspirin daily had significantly fewer serious vascular events than those who took a placebo [658 participants (8.5%) vs. 743 (9.6%)]. In contrast, major bleeding was greater in the aspirin group than in the placebo group [314 participants (4.1%) vs. 245 (3.2%)]. There was no significant difference between the group that took aspirin and the placebo group for gastrointestinal cancer incidence [157 participants (2.0%) vs. 158 (2.0%)] or any type of cancer [897 participants (11.6%) vs. 887 (11.5%)]. The authors of this study conclude that the benefits of aspirin for people with diabetes are largely outweighed by the risk of bleeding.
Aspirin for prevention in the elderly
The effects of daily low-dose aspirin were evaluated specifically in the elderly in the ASPREE study (Aspirin in Reducing Events in the Elderly), the results of which were published as three articles in the New England Journal Of Medicine (see here, here, and here). The study enlisted 19,114 Australians and Americans aged 70 or older who did not have cardiovascular disease, dementia, or physical disability. Participants were randomly assigned to take a 100 mg enteric-coated aspirin or placebo tablet daily for 5 years. The primary endpoint was a composite endpoint including death, dementia, and persistent physical disability. Secondary endpoints included severe bleeding and cardiovascular disease (nonfatal myocardial infarction, fatal coronary heart disease, fatal or nonfatal stroke, hospitalization for heart failure).
Aspirin did not prolong disability-free survival in the elderly and did not decrease the risk of cardiovascular disease, but it increased the rate of serious bleeding compared with placebo. The composite rate of mortality, dementia, and persistent physical disability was 21.5 and 21.2 events per 1,000 person-years in the group who took aspirin and in the placebo group, respectively. The rates of cardiovascular events were 10.7 and 11.3 events per 1,000 person-years in the aspirin group and the placebo group, respectively. The rate of serious bleeding was significantly higher (P <0.001) in the aspirin group (8.6 events per 1,000 person-years) than in the placebo group (6.2 events per 1,000 person-years). Finally, the all-cause mortality rate was higher in the aspirin group than in the placebo group, a result mainly attributable to deaths from cancer. Since an increase in mortality has not been observed in previous studies on aspirin used for prevention, this unexpected result should be interpreted with caution according to the authors.
Systematic review and meta-analysis
A synthesis of 13 randomized controlled trials of aspirin for primary prevention of cardiovascular disease, including the 3 major trials in 2018, was published in January 2019 in JAMA. All studies included 164,225 participants aged 53 to 74 and a follow-up of 1,050,511 person-years. This meta-analysis confirms that aspirin is associated with a decreased risk of cardiovascular events (cardiovascular mortality, nonfatal myocardial infarction, nonfatal stroke) and an increased risk of major bleeding. Aspirin was associated with an 11% reduction in relative risk (absolute risk reduction of 0.38%) of cardiovascular events and a 43% greater relative risk of major bleeding (absolute risk increase of 0.47%). As a result, 265 people will need to be treated with aspirin for 5 years to prevent a cardiovascular event, but one in 210 treated people will experience major bleeding. Because of the unfavourable benefit-to-disadvantage ratio, the European guidelines do not recommend taking aspirin until cardiovascular disease occurs (secondary prevention), i.e., at a time when the benefits outweigh the risks of adverse effects. On the other hand, the US Preventive Services Task Force (USPSTF) recommends improving the benefit-harm ratio for aspirin in primary prevention by estimating the risks of cardiovascular events and bleeding for each patient, considering the potential longer-term benefits of aspirin for the prevention of colorectal cancer, and carefully discussing with patients the balance between the risks of vascular and haemorrhagic events.
Heat waves are sporadic events of high temperatures, which can have serious consequences on human life. More than 70,000 people died during the heat wave that hit Europe in 2003, and another 10,860 died during a heat wave in Russia in 2010. The criteria for defining a heat wave vary from country to country. In Canada, a heat wave occurs when it is 30°C or higher for at least three consecutive days. It has been estimated that the average temperature of our planet will increase by 1°C by 2100 if we reduce greenhouse gas (GHG) emissions or 3.7°C if we do not. In 2000, about 30% of the world’s population was exposed to heat waves for at least 20 days a year. By 2100, it is expected that this proportion will increase to about 48% if we drastically reduce GHG emissions and 74% if we continue to increase GHG emissions.
When it is very hot, humid or both, the excess heat absorbed by the body must be dissipated by the skin and the respiratory system in order to maintain body temperature at 37°C: this is the thermoregulation process. The hypothalamus initiates a cardiovascular response by dilating blood vessels to redistribute blood to the body surface (the skin) where heat can be dissipated into the environment. Sweating is activated, allowing heat to dissipate by evaporation (600 kcal/hour). When it is very hot and humid, the evaporation of sweat is greatly reduced and the body struggles to maintain an adequate temperature. Heat stroke is a serious and life-threatening condition, which is defined as a body temperature above 40°C, accompanied by neurological signs such as confusion, seizures or loss of consciousness. The main risk factors for heat stroke are shown in Table 1.
Table 1. Risk factors for heat stroke. From Yeo, 2004.
|Extremes of age (younger than 15, older than 65)
|Skin-altering conditions (psoriasis, eczema, burns)
|Lack of air conditioning in home
|Living in a multi-storey building
|Low socioeconomic status
|Occupations with prolonged exertion and environmental exposure to temperature extremes (e.g., athletes, military workers, miners, steel workers, firefighters, factory workers, rescue workers)
· Impaired thermoregulation (diuretics, beta blockers, anticholinergics, phenothiazines, alcohol, butyrophenones)
· Increased metabolic heat production (benzotropin, trifluoperazine, ephedra containing dietary supplements, diet pills, amphetamines, cocaine, ecstasy)
|Previous history of heat-related illness
|Prolonged sun exposure
|Wearing heavy or excessive clothing
In a review of the literature on the causes of death during heat waves, 5 physiological mechanisms disrupting 7 vital organs have been identified (brain, heart, intestines, kidneys, liver, lungs, pancreas). The authors have identified 27 different ways in which heat-activated physiological mechanisms can lead to organ failure and ultimately death.
1- Ischemia. When the human body is exposed to heat, the hypothalamus initiates a cardiovascular response by dilating the blood vessels to redistribute blood to the body surface (the skin) where heat can be dissipated into the environment. This compensatory process can lead to an insufficient supply of blood to the internal organs (ischemia) and consequently to a lack of oxygen (hypoxia).
2- Toxicity due to thermal shock. High body temperature causes stress the body reacts to by producing stress proteins and free radicals that damage cells. This damage, combined with that caused by ischemia, affects the functioning of several organs.
3- Inflammatory response. Erosion of the intestinal mucosa allows bacteria and endotoxins to enter the bloodstream, leading to sepsis and activation of a systemic inflammatory response. If hyperthermia persists, the exaggerated inflammatory response causes damage to various organs.
4- Disseminated intravascular coagulation. Systemic inflammation and damage to the vascular endothelium caused by ischemia and heat shock can initiate this harmful mechanism. The proteins responsible for the control of coagulation become overactive and this can lead to the formation of clots that block the blood supply to vital organs. Depletion of blood clotting proteins can lead to subsequent bleeding (even in the absence of injury), which can be fatal.
5- Rhabdomyolysis. This is the rapid degradation of skeletal muscle cells caused by heat shock and ischemia. Muscle proteins such as myoglobin are released into the bloodstream and are toxic to the kidneys and can lead to kidney failure.
The heart is hit hard
In the heart, the combination of ischemia, heat shock cytotoxicity, and hypokalemia (potassium deficiency caused by excessive sweating) can lead to cardiac muscle breakdown. This myocardial injury increases the risk of cardiac arrest due to loss of myofibrils and reduced efficiency of the body in controlling heart rate and blood pressure. Stress on the heart can be exacerbated by dehydration, which thickens the blood and causes vasoconstriction, increasing the risk of coronary thrombosis and stroke. In the pancreas, erosion of the endothelial lining allows leukocytes to infiltrate the tissue, exacerbating inflammation. In the brain, the permeability of the blood-brain barrier allows toxins and pathogens to enter, increasing the risk of neuronal damage. All these physiological responses are interconnected in such a way that the failure of one organ can lead to negative effects on others, initiating a vicious cycle of deterioration that often leads to permanent damage, long-term recovery, or death.
To prevent heat stroke (according to Peiris et al., JAMA, 2014):
- Schedule outdoor activities during cool times of the day.
- Drink plenty of fluids. Avoid drinks with too much sugar or alcohol, which can cause dehydration.
- Wear loose-fitting, light-coloured clothing.
- Acclimate to new hot environments, over many days if possible.
- Be aware of medication side effects. If taking medications, be aware of those that may cause fluid losses, decrease sweating, or slow the heart rate. Common medications include those used for depression, blood pressure and heart disease, and coughs and colds.
- Never leave an impaired adult or a child in a car unattended.
What to do if you suspect a heat stroke
Call 911 if you notice these signs of heat stroke: body temperature over 40°C; accelerated heart rate; accelerated breathing; hot and red skin; nausea or vomiting; change of mental state (confusion, headache, difficulty in articulating words, convulsions or coma).
What to do while you wait for help:
- Move the individual out of the heat.
- Remove clothing to promote cooling.
- Position the person on his or her side to minimize aspiration.
- Immerse the individual in cold water or apply cold, wet cloths or ice packs to the skin (neck, armpits, and groin areas, where large blood vessels are located) to lower the body temperature.
- Continue cooling the individual until the body temperature reaches 38.4°C to 39°C (101°F to 102°F).
- Do not give any fluids to the person because it is not safe to drink during an altered level of consciousness. If the person is alert and requests water, give small sips.
- Avoid aspirin and acetaminophen; they do not help with cooling.