A large number of studies indicate that there is a positive association between exercise and good health, particularly good cardiovascular health. Researchers are now focusing their efforts on identifying the physiological and molecular mechanisms underlying these beneficial effects.
A study conducted among 580 young Finnish men shows that aerobic fitness (also known as cardiorespiratory capacity) is associated with levels of several metabolites that are beneficial to health. The approach used in this study is referred to as “metabolomics”, i.e. an approach that aims to identify metabolic differences, for example in the blood of people with a disease (diabetes, cancer) compared to people in good health. Most of the metabolomic studies conducted to date have focused on diseases, but this approach has also been applied recently to determine which metabolites are indicative of good health, particularly with regard to exercise.
Of the 66 metabolites selected in the Finnish study, 48 were at different levels between the group of participants who had the highest aerobic fitness and the one with the lowest aerobic fitness (see Figure 2 and Figure 3 of the original article). These differences include a 44% lower concentration of low-density lipoprotein (LDL, the “bad cholesterol”), an 81% higher concentration of high-density lipoprotein (HDL, the “good” cholesterol), a 52% lower total of triglycerides (Figure 1 below, orange bars). On the other hand, greater muscular strength of the participants was not associated with favourable levels for these same metabolites (Figure 1 below, blue bars).
Figure 1. Main differences in blood metabolites between the participants who had the highest aerobic fitness and those who had the lowest (orange bars) or between the participants who had the highest muscular strength and those who had the lowest (blue bars). * Significant difference (P <0.001 or P <0.002); NS: Not significant difference. From Kujala et al., 2019.
The more detailed analysis (see Figure 2 in the original article) shows that all LDL and VLDL particles of different sizes (small, medium, large, very large, extremely large) are present in lower concentrations in the blood of participants who have a good aerobic capacity than in participants who have a lower aerobic capacity. On the contrary, all HDL particles (very large, large, or medium-sized), except for small ones, are present in higher concentrations in the group with the highest aerobic fitness. Large-size HDLs are particularly beneficial for good cardiovascular health.
Participants with good cardiorespiratory capacity had 80% less apolipoprotein B (ApoB) in their blood than those who were less fit. ApoB is a protein found in very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL). The measurement of the ApoB makes it possible to estimate the number of particles of cholesterol, which is a good indication of the risk of developing cardiovascular disease. High blood levels of ApoB are therefore a risk marker for cardiovascular disease, independently of the level of LDL-cholesterol.
A high concentration of triglycerides in the blood is a risk marker for coronary heart disease and is associated with obesity and type 2 diabetes. Excessive consumption of sugars and alcohol (not fat) is generally the cause of a high level of triglycerides in the blood.
Other important metabolites that are present in lower concentrations in individuals with good aerobic capacity include total fatty acids (-60%), glycerol (-64%), lactate (-34%), pyruvate (-36%), branched-chain amino acids (BCAA) isoleucine (-37%) and leucine (-55%), and amino acids phenylalanine (-54%) and tyrosine (-55%). Interestingly, theunsaturation degree of fatty acid of participants in better aerobic fitness was 59% higher than in less fit participants; asituation conducive to good cardiovascular health knowing that it is saturated fatty acids that, in excess, increase theconcentration of LDL-cholesterol and are atherogenic.
High levels of BCAA, phenylalanine and tyrosine are found in obese people and they have been associated with a 5-fold increased risk of developing type 2 diabetes in two separate cohorts. Lower levels of glycerol and ketone bodies (acetylacetate, 3-hydroxybutyrate) in individuals with a high aerobic capacity suggest an increase in fat degradation.
Several metabolites (19) remain associated with a high aerobic fitness after adjustments to account for age and percentageof body fat. After making the same adjustments, muscular strength was associated with only 8 measures of the “metabolome” and none of these associations related to cholesterol or other blood lipids.
This study found more favourable associations between aerobic fitness and certain metabolites that are risk factors for cardiovascular disease than for high muscular strength. It should not be concluded, however, that muscular endurance exercises are useless, quite the contrary. Indeed, muscle training increases aerobic fitness and is an important component of maintaining and improving the condition of people with chronic diseases and the elderly. It is therefore necessary to combine aerobic and muscular exercises to optimize the benefits for cardiovascular health and overall well-being.
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.
Numerous epidemiological studies carried out over the last decades have shown a link between exposure to cardiovascular risk factors early in life and cardiovascular events at a later age. High blood pressure and high cholesterol are important modifiable risk factors for cardiovascular disease (CVD) and major components of risk prediction algorithms.
In prospective studies, childhood obesity, which subsides in adulthood, appears to cause only a slight increase in the risk of developing cardiovascular disease (CVD) over the course of life. Similarly, a few years after quitting smoking, the cardiovascular risk associated with smoking seems very low, even if smoking is stopped in adulthood. The same is not true for hypertension and hypercholesterolemia. Treatment of hypertension with medication does not reverse the damage done earlier in life, mainly to the heart, blood vessels and kidneys. For example, people who are hypertensive, but whose blood pressure is normalized by medication, have an increased risk of CVD after age 40. Treatment of familial hypercholesterolemia by statins significantly reduces the risk of CVD in young adults, but these people have more atherosclerotic CVD.
Until recently, we did not know whether exposure to these risk factors in early adulthood independently contributed to the risk of CVD, i.e. regardless of exposure to these same risk factors later in life. A study on the long-term effects of hypercholesterolemia and hypertension experienced at a young age, including a large amount of data and therefore of great statistical power, was recently published in the Journal of the American College of Cardiology (JACC). The data included in this study came from 6 U.S. cohorts, including 36,030 participants, who were followed for an average of 17 years.
The study found a strong association between having high blood pressure (BP) or high LDL-cholesterol at a young age (18–39 years), and the development of cardiovascular disease later in life (≥40 years). Specifically, young adults with LDL-cholesterol> 2.6 mmol/L had a 64% higher risk of coronary heart disease than those with a level of <2.6 mmol/L, regardless of cholesterol-LDL levels later in life. Similarly, young adults with systolic BP ≥130 mmHg had a 37% higher risk of heart failure than those with systolic BP <120 mmHg, and young adults with diastolic BP ≥80 mmHg had a 21% higher risk of heart failure than those with diastolic BP <80 mmHg. With respect to the risk of stroke after age 40, they are not affected by elevated cholesterol levels or increased systolic or diastolic BP at a younger age (18–39 years).
Even slightly elevated LDL-cholesterol levels of 2.6-3.3 mmol/L during early adulthood significantly increase the risk of coronary heart disease (28%) compared to <2.6 mmol / L. However, LDL cholesterol levels of 2.6-3.3 mmol/L are generally considered acceptable for healthy individuals who have no known CVD or other cardiovascular risk factors.
In an editorial published in the same journal, Gidding and Robinson suggest that the impacts of high cholesterol and hypertension in young people on cardiovascular risks later in life could be underestimated since: 1) the data from this study come from old cohorts, and we know that today’s young adults are more likely to be obese and have diabetes at a younger age; 2) there is probably a “survivor bias” in this type of study, i.e. it is possible that some young adults with particularly high blood pressure or cholesterol may have had a cardiovascular accident (an exclusion criteria) or that they have died before reaching the age at which the participants in these studies are recruited.
The increase in cardiovascular accidents before the age of 65 and the results of the study described above make it urgentto take action on prevention. Young adults, particularly women and non-Caucasians, did not benefit from the overall reduction of cardiovascular disease rates in the general population. This is probably due to three factors: the epidemic of obesity and diabetes; the lack of treatment for young adults who would benefit; the lack of clinical trials focusing on this age group, which would lead to better guidelines.
Drs. Gidding and Robinson believe that the first response of the medical community to the results of the study recently published in JACC and other similar analyses should be to become aware and recognize that there is a prevention deficit among young adults. In the United States, less than one third of adults under the age of 50 who should be treated for hypertension according to the guidelines receive treatment, and less than half of the participants in the NHANES study (National Health and Nutrition Examination Survey) who had a diagnostic criterion for familial hypercholesterolemia were treated with a statin.
The current trend is to treat hypercholesterolemia at a later age when the burden of the disease is already high and only a modest reduction in cardiovascular risk has been demonstrated. However, by lowering cholesterol earlier in life, mainly through a change in lifestyle, it is possible to avoid cardiovascular events in old age. By focusing more on young adults with less advanced disease and therefore more likely to be treated successfully, prevention and future clinical trials will reduce the burden of cardiovascular disease for future generations.
It is well established that regular physical exercise improves lipid levels, glucose tolerance, and insulin sensitivity, all of which are cardiovascular risk factors. One question researchers have been asking in recent years is whether a single exercise session can, after a period of prolonged physical inactivity, have a positive impact on the risk factors associated with a sedentary lifestyle. This is an important issue as more and more workers are sitting for long hours at the office or in their car, and many of them do not have time to exercise more than once a week.
In a randomized controlled trial published in 2019 in the Journal of Applied Physiology, participants (n = 10) first spent four days without exercise, sitting for much of the day (≈13.5 hours/day). At the end of the fourth day, half of the participants did one hour of intense treadmill exercise (60–65% VO2max) and the other half remained inactive. On the morning of the fifth day, after fasting for 12 hours, all participants consumed a meal high in fat and glucose. Blood samples were taken before and every hour (up to 6 h) after the meal, and triglycerides, glucose and insulin were measured. After a rest period of several days, the experiment was repeated by swapping the groups (crossover study design).
No significant differences in plasma levels of triglycerides, glucose or insulin were found between the two groups. The authors conclude that prolonged physical inactivity (e.g., sitting about 13.5 hours/day and walking fewer than 4,000 steps/day) creates conditions where people become “resistant” to the metabolic improvements that are normally achieved after an aerobic exercise session. It is therefore important to develop good habits at work and at home (take active breaks, work standing, etc.), in order to fully benefit from the positive effects of exercise during leisure time.
A similar study published in 2016 came to comparable conclusions. The researchers randomized the participants into three groups: 1) sitting >14 h/day and a high-calorie diet; 2) sitting >14 h/day and a balanced diet; 3) active: standing, walking, sitting 8.4 h/day and a balanced diet. In addition to being randomized, the study had a crossover design, i.e., subjects participated in three five-day interventions (one week of rest between each intervention), changing groups each time. On the evening of the fourth day, the participants did treadmill running for 1 hour (67% VO2max). On the third and fifth day, participants consumed a high-fat meal (high-fat tolerance test) and blood tests were taken before and every hour (up to 6 hours) after the meal. Triglycerides, free fatty acids, glucose, and insulin were subsequently assayed in the plasma of the various samples collected.
After two days of sitting for long hours, participants had 27% higher triglyceride levels after consuming a high-fat meal, compared to participants who were more active. In participants who spent four days sitting for more than 14 hours, the 1-hour aerobic exercise did not decrease triglyceride levels in the blood or increase fat oxidation. On the other hand, in participants who were active during the previous four days, aerobic exercise decreased triglycerides by 14% (a non-significant decrease, p = 0.079) and significantly increased fat oxidation (p <0.05). The authors concluded that sitting for a good part of the day for 2 to 4 days was sufficient to increase postprandial triglyceride levels (after a meal) and that this increase cannot be reduced by sustained exercise.
A meta-analysis of 13 population studies assessed the ability of physical activity to eliminate or reduce the association between sitting time and all-cause mortality. These studies were conducted with more than 1 million people who were followed from 2 to 18.1 years. The results (Figure 1) show a very clear dose-effect relationship between the amount of exercise and the reduction in the relative risk of mortality associated with sitting or watching television. High levels of moderate physical activity (i.e., approximately 60–75 min/day) appear to eliminate the increased risk of mortality associated with long periods of sitting (Figure 1A). However, high levels of physical activity significantly alleviate, but do not eliminate the risk of mortality associated with long periods (> 5 h) spent watching television (Figure 1B).
Figure 1. Meta-analyses of joint associations of sitting time and amount of physical activity with all-cause mortality (A) and television-viewing time and amount of physical activity with all-cause mortality (B). 2.5 MET-h/week is equivalent to about 5 minutes of moderate activity per day; 16 MET-h/week is equivalent to 25–35 minutes of moderate activity per day; 30 MET-h/week is equivalent to 50–65 minutes of moderate activity per day, and 35.5 MET-h/week is equivalent to 60–75 minutes of moderate activity per day. From Ekelund et al., 2016.
The amount of physical activity in the highest quartile (> 35.5 MET-h/week) is equivalent to approximately 60–75 minutes of moderate-intensity exercise per day. This is much more than the minimum recommended by public health organizations (150 min/week). However, among those who do 16 MET-h/week, which is equivalent to 25–35 minutes of moderate-intensity physical activity, the increased risk of mortality associated with long periods of sitting (> 8 h/day) is less marked than for people in the least active group (<2.5 MET-h/week, equivalent to about 5 min of exercise per day). The increased risk of mortality (58%) for those who are less active and who sit more than 8 hours a day is similar to that associated with other risk factors such as smoking and obesity.
Why are the results for sitting time and television-viewing time different? This may be due in part to differences in the accuracy with which these behaviours are reported, but the authors of the study propose other plausible explanations: 1) people usually watch television in the evening, normally after dinner, and a prolonged sedentary episode after a meal could be particularly harmful to the metabolism of lipids and glucose; 2) people likely take more active breaks during work than during the viewing of TV programs, and it appears that these breaks are beneficial in reducing several cardiometabolic risk factors; 3) It is also plausible that people who watch television consume more “snacks” or obesogenic food.
Spending long periods of time in a sitting position is very common in our modern societies and this will only increase with future technological and social innovations. In addition to promoting regular physical exercise, public health organizations will likely also need to include a reduction in sedentary time in their guidelines and emphasize the importance of taking “active” breaks. Taking short active breaks may mean walking for a minute, drinking water, and getting up when talking on the phone. We must develop strategies to avoid sitting for long periods of time. In addition, we need to find the time to do at least 150 minutes of moderate exercise a week, up to 300 minutes a week to get maximum health benefits.
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.
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.