Association between chronic stress and heart attacks

Association between chronic stress and heart attacks

OVERVIEW

  • Cortisol concentration in recent hair growth was measured in middle-aged people shortly after suffering a heart attack, and in people of the same age group who were in apparent good health.
  • The median concentration of cortisol in the hair of people with a myocardial infarction was 2.4 times higher than that measured in the control group.
  • The risk of myocardial infarction was approximately 5 times higher in people with high cortisol levels compared to those with normal cortisol levels.
  • These results indicate that chronic stress appears to be an important risk factor for myocardial infarction.

It is well established that acute physical and/or emotional stress (accident, anger, fear) is a risk factor for heart attack (see our article on the subject). However, it is not clear whether high levels of chronic stress also contribute to the risk of myocardial infarction. One of the reasons that little is known about this potential risk factor is that until recently, it was only possible to measure acute stress, not chronic stress. The stress response involves activation of the corticotropic axis (or hypothalamic-pituitary-adrenal axis) and the autonomic nervous system, including the secretion of cortisol, one of the main stress hormones. Chronic stress can now be objectively and conveniently assessed in people by measuring cortisol levels in hair. As the hair grows, an amount of cortisol proportional to the blood concentration is incorporated into the hair. A 1 cm hair cut at the base of the scalp will have taken 4 to 6 weeks to grow, and its cortisol content will reflect the level of chronic stress the person has experienced during that time. The last 5–10 days of hair growth is in and under the scalp.

In a retrospective study of women and men under the age of 65 in Sweden, the levels of cortisol in the hair of 174 people who had suffered a myocardial infarction were compared to those of 3156 people in apparent good health. The median concentration of cortisol in the hair of people with a myocardial infarction was 2.4 times higher (53.2 pg/mg) than that measured in the control group (22.2 pg/mg).

Analysis of the data shows a very clear dose-response relationship, i.e. that the higher the levels of cortisol detected in the participants’ hair, the greater the risk of a heart attack. This dose-effect relationship is not linear, as can be seen in Figure 1: the cortisol levels of the first 3 quintiles are not associated with a significantly higher risk of myocardial infarction, but this risk increases very significantly for cortisol levels in quintiles 4 and 5.

Figure 1. Relative risk of myocardial infarction as a function of the concentration of cortisol in the hair of the participants. *Very significant (p <0.001). From Faresjö et al., 2020.

 

This retrospective study shows an association between high cortisol levels and myocardial infarction, but this type of study does not establish a causal link. Results from other studies also suggest that cortisol may cause myocardial infarction. For example, the elevated cortisol levels seen in people with Cushing’s syndrome or in patients receiving glucocorticoid therapy are linked to an increased prevalence of cardiovascular risk factors and myocardial infarction. It is therefore plausible that increased cortisol levels cause metabolic disorders that lead to atherosclerosis and, in the long term, to coronary artery blockage and myocardial infarction. Increased blood cortisol levels also have direct effects on the cardiovascular system, including increased contractility of blood vessels, inhibition of angiogenesis, and increased platelet activation, which can lead to thrombosis.

Exposure to chronic stress is typical of our modern societies and can be the cause of many illnesses. We have to learn to manage this chronic stress, for example by practicing cardiac coherence or meditation. I encourage readers to learn more on this subject; there are many very accessible books: Christophe André: Looking at Mindfulness, Matthieu Ricard: The Art of Meditation, Jon Kabat-Zinn: Full Catastrophe Living, and Rick Hanson: Hardwiring Happiness.

The benefits of extra virgin olive oil on cardiovascular health

The benefits of extra virgin olive oil on cardiovascular health

OVERVIEW

  • In addition to being an excellent source of monounsaturated fat, olive oil is the only vegetable oil that contains a significant amount of phenolic compounds with antioxidant and anti-inflammatory properties.
  • These molecules are found in much larger quantities in extra virgin quality oils compared to refined olive oils.
  • Several studies indicate that the presence of these phenolic compounds contributes to the many positive effects of extra virgin olive oil on cardiovascular health.

The traditional Mediterranean diet has several positive effects on cardiovascular health by improving the lipid profile (cholesterol, triglycerides) and by reducing chronic inflammation, blood pressure, blood sugar and the risk of diabetes. Several studies have clearly established that these effects result in a significant reduction in the risk of cardiovascular disease.

The Mediterranean diet is characterized by the abundant consumption of plant-based foods (fruits, vegetables, whole-grain cereals, legumes, nuts, herbs), a moderate intake of fermented dairy products (yogurt, cheese), fish, seafood and red wine as well as a low consumption of red meat and added sugars. It is therefore an exemplary diet, in which complex plant sugars are the main sources of carbohydrates and where the proteins come mainly from fish and legumes instead of red meat.

Another important feature of the Mediterranean diet is the daily use of large amounts (60–80 mL) of olive oil as the main source of fat for cooking. Several studies have reported that countries that are heavy consumers of olive oil have a much lower incidence of cardiovascular disease than those that consume mainly animal fats, suggesting a positive role of olive oil in this protective effect. Traditionally, these beneficial properties of olive oil have been attributed to its very high content (around 80%) of oleic acid, a monounsaturated fatty acid that contributes to its antioxidant properties. However, and unlike most vegetable oils, olive oil also contains a host of minor compounds (1–3% of the oil) that also play very important roles in its positive effects on cardiovascular health (see below). This is particularly the case for several phenolic compounds found exclusively in olive oil, including phenolic alcohols such as hydroxytyrosol and tyrosol and polyphenols of the secoiridoid family such as oleuropein, ligstroside, oleacein and oleocanthal (Figure 1).

 

Figure 1. Molecular structures of the main phenolic compounds of olive oil.


One fruit, several types of oils
Most vegetable oils come from seeds that have been extracted with an organic solvent (e.g. hexane) and subsequently heated to a high temperature to evaporate this solvent and remove impurities that give them an undesirable smell and flavour. These drastic procedures are not necessary for olive oil as the olives are simply pressed and the oil in the pulp is extracted by mechanical pressure, without using chemical processes or excessive heat.

Olive oils are classified according to the quality of the oil that is obtained by the pressing procedure (Figure 2). Good quality oils, i.e. those with low acidity (<2% free oleic acid) and that meet certain taste, bitterness and spiciness criteria are called “virgin” olive oils or, if their acidity is less than 0.8%, “extra virgin” olive oils. These oils contain the majority of the polyphenols in the starting olives and, after centrifugation and filtration, can be consumed as is.

On the other hand, some olive varieties give an inferior quality oil due to too high acidity (> 2%) and/or an unpleasant smell and taste that does not meet the established criteria. These oils, which are unfit for consumption, are called “lampantes” (a name which comes from their ancient use as fuel in oil lamps) and must be refined as is done for other vegetable oils, i.e. using different physicochemical procedures (neutralization with soda, high temperature bleaching and deodorization, hexane extraction, etc.). These steps remove the compounds responsible for the excess acidity and the unpleasant taste of the oil and produce a “neutral” olive oil that has lost its acidity and its flaws, but that is now devoid of the smell, flavour, colour and most of the phenolic components of the starting virgin olive oil. To stabilize these oils and improve their taste, a certain proportion (15–20%) of virgin olive oil is subsequently added and the final product, which is a mixture of refined olive oil and virgin olive oil, is what is sold in grocery stores as “pure olive oil” or simply “olive oil”.

In short, there are three main types of olive oil on the market: virgin olive oil (VOO), extra virgin olive oil (EVOO), and regular olive oil (OO).

Figure 2. The different types of olive oil. From Gorzynik-Debicka et al. (2018).

 

These manufacturing differences obviously have a huge impact on the amount of polyphenols present in virgin, extra virgin, and refined oils (Table 1). For OO-type olive oils (which contain refined oils), the polyphenols come exclusively from virgin olive oil that has been added to restore a minimum of taste and colour (from yellow to greenish) to the chemically treated oil. The amount of these polyphenols is therefore necessarily less than in VOO and EVOO and, as a general rule, does not exceed 25–30% of the content of these two oils. This difference is particularly striking for certain polyphenols of the secoiridoid family (oleuropein, oleocanthal, oleacein and ligstroside) whose concentrations are 3 to 6 times greater in EVOO than in OO (Table 1). It should be noted, however, that these values ​​can vary greatly depending on the origin and cultivar of the olives; for example, some extra virgin olive oils have been found to contain up to 10 times more hydroxytyrosol and tyrosol than regular olive oils. The same goes for other polyphenols like oleocanthal: an analysis of 175 distinct extra virgin olive oils from Greece and California revealed dramatic variations between the different oils, with concentrations of the molecule ranging from 0 to 355 mg/kg.

It should also be mentioned that even if the quantities of phenolic compounds in regular olive oil are lower than those found in virgin and extra virgin oils, they nevertheless largely exceed those present in other vegetable oils (sunflower, peanut, canola, soy), which contain very little or none at all.

FamilyMoleculesOO (mg/kg)VOO (mg/kg)EVOO (mg/kg)
Secoiridoidsoleocanthal38.95 ± 9.2971.47 ± 61.85142.77 ± 73.17
oleacein57.37 ± 27.0477.83 ± 256.09251.60 ± 263.24
oleuropein (aglycone)10.90 ± 0.0095.00 ± 116.0172.20 ± 64.00
ligstroside (aglycone)15.20 ± 0.0069.00 ± 69.0038.04 ± 17.23
Phenolic alcoholshydroxytyrosol6.77 ± 8.263.53 ± 10.197.72 ± 8.81
tyrosol4.11 ± 2.245.34 ± 6.9811.32 ± 8.53
Flavonoidsluteolin1.17 ± 0.721.29 ± 1.933.60 ± 2.32
apigenin0.30 ± 0.170.97 ± 0.7111.68 ± 12.78
Phenolic acidsp-coumaric -0.24 ± 0.810.92 ± 1.03
ferulic -0.19 ± 0.500.19 ± 0.19
cinnamic - -0.17 ± 0.14
caffeic -0.21 ± 0.630.19 ± 0.45
protocatechuic -1.47 ± 0.56 -
Table 1. Comparison of the content of phenolic compounds in olive oil (OO), virgin olive oil (VOO) and extra virgin olive oil (EVOO). Please note that the large standard deviations of the mean values reflect the huge variations in polyphenol content depending on the region, cultivar, degree of fruit ripeness, and olive oil manufacturing process. Adapted from Lopes de Souza et al. (2017).

 

Anti-inflammatory spiciness
The amounts of polyphenols contained in a bottle of olive oil are not indicated on its label, but it is possible to detect their presence simply by tasting the oil. The polyphenols in olive oil are indeed essential to the organoleptic sensations so characteristic of this oil, in particular the sensation of tickling or stinging in the throat caused by good quality extra virgin oils, what connoisseurs call “ardour”. Far from being a defect, this ardour is considered by experts as a sign of a superior quality oil and, in tasting competitions, the “spiciest” oils are often those that receive the highest honours.

It is interesting to note that it is by tasting different olive oils that a scientist succeeded, by coincidence, in identifying the molecule responsible for the sensation of spiciness caused by extra virgin olive oil (see box).

Plant ibuprofen

Chance often plays a role in scientific discoveries, and this is especially true when it comes to the discovery of the molecule responsible for the typical irritation caused by olive oil. On a trip to Sicily (Italy) to attend a conference on the organoleptic properties of different foods, Dr. Gary Beauchamp and his colleagues were invited by the organizers of the event to a meal where guests were encouraged to taste extra virgin olive oil from olive trees cultivated on their estate. Even though it was the first time he had tasted this type of olive oil, Dr. Beauchamp was immediately struck by the tingling sensation in his throat, which was similar in every way to that caused by ibuprofen, and that he had experienced multiple times as part of his work to replace acetaminophen (paracetamol) with ibuprofen in cough syrups. Suspecting that olive oil contained a similar anti-inflammatory drug, Dr. Beauchamp and his team subsequently managed to isolate the molecule responsible for this irritation, a polyphenol they called “oleocanthal”. They subsequently discovered that oleocanthal had, like ibuprofen, a powerful anti-inflammatory action and that regular consumption of extra virgin olive oil, rich in oleocanthal, provided an intake equivalent to about 10 mg of ibuprofen and therefore may contribute to the well-documented anti-inflammatory effects of the Mediterranean diet. 

But why is the stinging sensation of olive oil only felt in the throat? According to work carried out by the same group, this exclusive localization is due to a specific interaction of oleocanthal (and ibuprofen, for that matter) with a subtype of heat-sensitive receptor (TRPA1). Unlike other types of heat receptors, which are evenly distributed throughout the oral cavity (the TRPV1 receptor activated by the capsaicin of chili peppers, for example, and which causes the burning sensation of some particularly hot dishes), the TRPA1 receptor is located only in the pharynx and its activation by oleocanthal causes a nerve impulse signalling the presence of an irritant only in this region. In short, the more an olive oil stings in the back of the throat, the more oleocanthal it contains and the more anti-inflammatory properties it has. As a general rule, extra virgin olive oils contain more oleocanthal (and polyphenols in general) than virgin olive oils (see Table 1) and are therefore considered superior, both in terms of taste and their positive effects on health.

The superiority of extra virgin olive oil
Several studies have shown that the higher polyphenol content in extra virgin olive oil is correlated with a greater positive effect on several parameters of cardiovascular health than that observed for regular olive oil (see Table 2). For example, epidemiological studies carried out in Spain have reported a decrease of about 10–14% in the risk of cardiovascular disease among regular consumers of extra virgin olive oil, while regular consumption of olive oil had no significant effect. A role of phenolic compounds is also suggested by the EUROLIVE study where the effect of daily ingestion, over a period of 3 weeks, of 25 mL of olive oils containing small (2.7 mg/kg), medium (164 mg/kg), or high (366 mg/kg) amounts of polyphenols was compared. The results show that an increased intake of polyphenols is associated with an improvement in two important risk factors for cardiovascular disease: an increase in the concentration of HDL cholesterol and a decrease in oxidized LDL cholesterol levels. Collectively, the data gathered from the intervention studies indicate that the polyphenols found in extra virgin olive oil play an extremely important role in olive oil’s positive effects on cardiovascular health.

Measured parameterResultsSources
Incidence of cardiovascular disease10% reduction in risk for every 10 g/day of EVOO. No effect of regular OO.Guasch-Ferré et al. (2014)
14% reduction in risk for each 10 g/day of EVOO. No effect of regular OO.Buckland et al. (2012)
Lipid profileLinear increase in HDL cholesterol as a function of the amount of polyphenols.Covas et al. (2006)
Increase in HDL cholesterol only observed with EVOO.Estruch et al. (2006)
Blood glucoseEVOO improves postprandial glycemic profile (decrease in glucose levels and increased insulin).Violo et al. (2015)
Polyphenol-rich EVOO reduces fasting blood glucose and glycated hemoglobin (HbA1c) levels in diabetic patients.Santagelo et al. (2016)
InflammationEVOO, but not OO, induces a decrease in inflammatory markers (TXB(2) and LTB(4)).Bogani et al. (2017)
EVOO, but not OO, induces a decrease in IL-6 and CRP.Fitó et al. (2007)
EVOO, but not OO, decreases the expression of several inflammatory genes.Camargo et al. (2010)
EVOO, but not OO, decreases levels of inflammatory markers sICAM-1 and sVCAM-1.Pacheco et al. (2007)
Oxidative stressStrong in vitro antioxidant activity of phenolic compounds of olive oil.Owen et al. (2000)
Linear decrease in oxidized LDL levels as a function of the amount of polyphenols.Covas et al. (2006)
Lower levels of oxidized LDL after ingestion of EVOO compared to OO.Ramirez-Tortosa et al. (1999)
EVOO phenolic compounds bind to LDL particles and protect them from oxidation.de la Torre-Carbot et al. (2010)
EVOO induces the production of neutralizing antibodies against oxidized LDL.Castañer et al. (2011)
EVOO decreases urinary levels of 8-isoprostane, a marker of oxidative stress.Visioli et al. (2000)
EVOO positively influences the oxidative/antioxidant status of blood plasma.Weinbrenner et al. (2004)
Blood pressureEVOO causes a decrease in systolic and diastolic pressures in hypertensive women.Ruíz-Gutiérrez et al. (1996)
EVOO, but not OO, causes a decrease in systolic pressure in hypertensive coronary patients.Fitó et al. (2005)
EVOO improves postprandial endothelial dilation.Ruano et al. (2005)
EVOO increases the NO vasodilator and decreases systolic and diastolic pressures.Medina-Remón et al. (2015)
EVOO, but not OO, improves vessel dilation in pre-diabetic patients.Njike et al. (2021)
EVOO, but not OO, decreases systolic pressure by 2.5 mmHg in healthy volunteers.Sarapis et al. (2020)
Table 2. Examples of studies comparing the effect of EVOO and OO on several cardiovascular health parameters.

 

In addition to its multiple direct actions on the heart and vessels, it should also be noted that extra virgin olive oil could also exert an indirect beneficial effect, by blocking the formation of the metabolite trimethylamine N-oxide (TMAO) by intestinal bacteria. Several studies have shown that TMAO accelerates the development of atherosclerosis in animal models and is associated with an increased risk of cardiovascular events in clinical studies. Extra virgin olive oils (but not regular olive oils) contain 3,3-dimethyl-1-butanol (DMB), a molecule that blocks a key enzyme involved in TMAO production and prevents development of atherosclerosis in animal models fed a diet rich in animal protein. Taken together, these observations show that there are only advantages to favouring the use of extra virgin olive oil, both for its superior taste and its positive effects on cardiovascular health.

Some people may dislike the slightly peppery taste that extra virgin olive oil leaves in the back of the throat, but interestingly, this irritation is greatly reduced when the oil is mixed with other foods. According to a recent study, this attenuation of the pungent taste is due to the interaction of the polyphenols in the oil with the proteins in food, which blocks the activation of the heat receptors that are normally activated by these polyphenols. People who hesitate to use extra virgin olive oil because of its irritant side can therefore get around this problem and still enjoy the benefits of these oils simply by using it as the main fat when preparing a meal.

Why do the Japanese have the highest life expectancy in the world?

Why do the Japanese have the highest life expectancy in the world?

OVERVIEW

  • The Japanese have the highest life expectancy at birth among the G7 countries.
  • The higher life expectancy of the Japanese is mainly due to fewer deaths from ischemic heart disease, including myocardial infarction, and cancer (especially breast and prostate).
  • This exceptional longevity is explained by a low rate of obesity and a unique diet, characterized by a low consumption of red meat and a high consumption of fish and plant foods such as soybeans and tea.

Several diets are conducive to the maintenance of good health and to the prevention of cardiovascular disease, for example, the Mediterranean diet, the DASH diet (Dietary Approaches to Stop Hypertension), the vegetarian diet, and the Japanese diet. We often refer to the Mediterranean Diet in these pages, because it is well established scientifically that this diet is particularly beneficial for cardiovascular health. Knowing that the Japanese have the highest life expectancy among the G7 countries, the special diet in Japan has also captured the attention of experts and an informed public in recent years.

Japanese life expectancy
Among the G7 countries, Japan has the highest life expectancy at birth according to 2016 OECD data, particularly for women. Japanese men have a slightly higher life expectancy (81.1 years) than that of Canadian men (80.9 years), while the life expectancy of Japanese women (87.1 years) is significantly higher (2.4 years) than that of Canadian women (84.7 years). The healthy life expectancy of the Japanese, 74.8 years, is also higher than in Canada (73.2 years).

The higher life expectancy of Japanese people is mainly due to fewer deaths from ischemic heart disease and cancers, particularly breast and prostate cancer. This low mortality is mainly attributable to a low rate of obesity, low consumption of red meat, and high consumption of fish and plant foods such as soybeans and tea. In Japan, the obesity rate is low (4.8% for men and 3.7% for women). By comparison, in Canada 24.6% of adult men and 26.2% of adult women were obese (BMI ≥ 30) in 2016. Obesity is an important risk factor for both ischemic heart disease and several types of cancers.

Yet in the early 1960s, Japanese life expectancy was the lowest of any G7 country, mainly due to high mortality from cerebrovascular disease and stomach cancer. The decrease in salt and salty food intake is partly responsible for the decrease in mortality from cerebrovascular disease and stomach cancer. The Japanese consumed an average of 14.5 g of salt/day in 1973 and probably more before that. They eat less salt these days (9.5 g/day in 2017), but it’s still too much. Canadians now consume on average about 7 g of salt/day (2.76 g of sodium/day), almost double the intake recommended by Health Canada.

The Japanese diet
Compared to Canadians, the French, Italians and Americans, the Japanese consume much less meat (especially beef), dairy products, sugar and sweeteners, fruits and potatoes, but much more fish and seafood, rice, soybeans and tea (Table 1). In 2017, the Japanese consumed an average of 2,697 kilocalories per day according to the FAO, significantly less than in Canada (3492 kcal per day), France (3558 kcal per day), Italy (3522 kcal per day), and the United States (3766 kcal per day).

Table 1. Food supply quantity (kg/capita/year) in selected countries in 2013a.

              aAdapted from Tsugane, 2020. FAO data: FAOSTAT (Food and agriculture data) (http://www.fao.org/).

Less red meat, more fish and seafood
The Japanese eat on average almost half as much meat as Canadians (46% less), but twice as much fish and seafood. This considerable difference translates into a reduced dietary intake of saturated fatty acids, which is associated with a lower risk of ischemic heart disease, but an increased risk of stroke. On the contrary, dietary intake of omega-3 fatty acids found in fish and seafood is associated with a reduced risk of ischemic heart disease. The lower consumption of red meat and higher consumption of fish and seafood by the Japanese could therefore explain the lower mortality from ischemic heart disease and the higher mortality from cerebrovascular disease in Japan. Experts believe that the decline in death from cerebrovascular disease is associated with changes in the Japanese diet, specifically increased consumption of animal products and dairy products, and consequently of saturated fat and calcium (a consumption which remains moderate), combined with a decrease in salt consumption. Indeed, contrary to what is observed in the West, the consumption of saturated fat in Japan is associated with a reduction in the risk of hemorrhagic stroke and to a lesser extent of ischemic stroke, according to a meta-analysis of prospective studies. The cause of this difference is not known, but it could be attributable to genetic susceptibility or confounding factors according to the authors of the meta-analysis.

Soybeans
Soy is a food mainly consumed in Asia, including Japan where it is consumed as is after cooking (edamame) and especially in processed form, by fermentation (soy sauce, miso paste, nattō) or by coagulation of soy milk (tofu). It is an important source of isoflavones, molecules that have anticancer properties and are beneficial for good cardiovascular health. Consumption of isoflavones by Asians has been linked to a lower risk of breast and prostate cancer (see our article on the subject).

Sugar
The Japanese consume relatively few sugars and starches, which partly explains the low prevalence of obesity-associated diseases such as ischemic heart disease and breast cancer.

Green tea
The Japanese generally consume green tea with no added sugar. Prospective studies from Japan show that green tea consumption is associated with a lower risk of all-cause mortality and cardiac death.

Westernization of Japanese eating habits
The westernization of the Japanese diet after World War II allowed the inhabitants of this country to be healthier and to reduce mortality caused by infectious diseases, pneumonia and cerebrovascular diseases, thereby considerably increasing their life expectancy. A survey of the eating habits of 88,527 Japanese from 2003 to 2015 indicates that this westernization continues. Based on the daily consumption of 31 food groups, the researchers identified three main types of eating habits:

1- Plant foods and fish
High intakes of vegetables, fruits, legumes, potatoes, mushrooms, seaweed, pickled vegetables, rice, fish, sugar, salt-based seasonings and tea.

2- Bread and dairy
High intakes of bread, dairy products, fruits and sugar. Low intake of rice.

3- Animal foods and oils
High intakes of red and processed meat, eggs, vegetable oils.

A downward trend in the “plant foods and fish” group (the staple of the traditional Japanese diet or washoku) was observed in all age groups. An increase in the “bread and dairy” group was observed in the 50–64 and ≥65 years age groups, but not among the youngest. For the “animal foods and oils” group, an increasing trend was observed during the thirteen years of the study in all age groups except the youngest (20–34 years). The Japanese are eating more and more like Westerners. Will this have an adverse effect on their health and life expectancy? It is too early to know, only the next few decades will tell.

Contribution of genes and lifestyle to the health of the Japanese
Some risk factors for cardiovascular disease and cancer are hereditary, while others are associated with lifestyle (diet, smoking, exercise, etc.). At the turn of the 20th century, there was significant Japanese immigration to the United States (especially California and Hawaii) and South America (Brazil, Peru). After a few generations, the descendants of Japanese migrants adopted the way of life of the host countries. While Japan has one of the lowest incidences of cardiovascular disease in the world, this incidence doubled among the Japanese who migrated to Hawaii and quadrupled among those who chose to live in California according to a 1975 study. What is surprising is that this increase has been observed regardless of blood pressure or cholesterol levels, and seems rather directly related to the abandonment of the traditional Japanese way of life by migrants.

Since the 1970s, the average cholesterol level of the Japanese has nonetheless increased, but despite this and the high rate of smoking in this country, the incidence of coronary heart disease remains substantially lower in Japan than in the West. To better understand these differences, a 2003 study compared the risk factors and diets of Japanese living in Japan with third- and fourth-generation Japanese migrants living in Hawaii in the United States. Men’s blood pressure was significantly higher among Japanese than among Japanese-Americans, while there was no significant difference for women. Far fewer Japanese were treated for hypertension than in Hawaii. More Japanese people (especially men) smoked than Japanese-Americans. Body mass index, blood levels of LDL cholesterol, total cholesterol, glycated hemoglobin (an indicator for diabetes), and fibrinogen (a marker of inflammation) were significantly lower in Japan than in Hawaii. HDL cholesterol (the “good” cholesterol) was higher in the Japanese than in the Japanese-Americans. The dietary intake of total fat and saturated fatty acids (harmful to cardiovascular health) was lower in Japan than in Hawaii. In contrast, the intake of polyunsaturated fatty acids and omega-3 fatty acids (beneficial for good cardiovascular health) was higher in Japan than in Hawaii. These differences may partly explain the lower incidence of coronary heart disease in Japan than in Western industrialized countries.

In other words, even if these migrants have the same basic risk as their compatriots who have remained in the country of origin (age, sex and heredity), the simple fact of adopting the lifestyle of their host country is enough to significantly increase their risk of cardiovascular disease.

Although the Japanese diet is different from those of Western countries, it has similar characteristics to the Mediterranean diet. Why not prepare delicious Japanese soy dishes from time to time (for example, tofu, edamame, miso soup), drink green tea, eat less meat, sugar and starch and more fish? Not only will your meals be more varied, but you could enjoy the health benefits of the Japanese diet.

Reducing calorie intake by eating more plants

Reducing calorie intake by eating more plants

OVERVIEW

  • Twenty volunteers were fed a low-fat or low-carbohydrate diet in turn for two weeks.
  • Participants on the low-fat diet consumed an average of nearly 700 fewer calories per day than with the low-carbohydrate diet, a decrease correlated with a greater loss of body fat.
  • Compared to the low-carbohydrate diet, the low-fat diet also led to lower cholesterol levels, reduced chronic inflammation, and lowered heart rate and blood pressure.
  • Overall, these results suggest that a diet mainly composed of plants and low in fat is optimal for cardiovascular health, both for its superiority in reducing calorie intake and for its positive impact on several risk factors for cardiovascular disease.

It is estimated that there are currently around 2 billion overweight people in the world, including 600 million who are obese. These statistics are truly alarming because it is clearly established that excess fat promotes the development of several diseases that decrease healthy life expectancy, including cardiovascular disease, type 2 diabetes, and several types of cancer. Identifying the factors responsible for this high prevalence of overweight and the possible ways to reverse this trend as quickly as possible is therefore essential to improve the health of the population and avoid unsustainable pressures on public health systems in the near future.

Energy imbalance
The root cause of overweight, and obesity in particular, is a calorie intake that exceeds the body’s energy needs. To lose weight, therefore, it is essentially a matter of restoring the balance between the calories ingested and the calories expended.

It might seem simple in theory, but in practice most people find it extremely difficult to lose weight. On the one hand, it is much easier to gain weight than to lose weight. During evolution, we have had to deal with periods of prolonged food shortages (and even starvation, in some cases) and our metabolism has adapted to these deficiencies by becoming extremely efficient at accumulating and conserving energy in the form of fat. On the other hand, the environment in which we currently live strongly encourages overconsumption of food. We are literally overwhelmed by an endless variety of attractive food products, which are often inexpensive, easily accessible, and promoted by very aggressive marketing that encourages their consumption. The current epidemic of overweight and obesity thus reflects our biological predisposition to accumulate reserves in the form of fat, a predisposition that is exacerbated by the obesogenic environment that surrounds us.

Eating less to restore balance
The body’s innate tendency to keep energy stored in reserve as fat makes it extremely difficult to lose weight by “burning” those excess calories by increasing the level of physical activity. For example, a person who eats a simple piece of sugar pie (400 calories) will have to walk about 6.5 km to completely burn off those calories, which, of course, is difficult to do on a daily basis. This does not mean that exercise is completely useless for weight loss. Research in recent years shows that exercise can specifically target certain fat stores, especially in the abdominal area. Studies also show that regular physical activity is very important for long-term maintenance of the weight lost from a low-calorie diet. However, there is no doubt that it is first and foremost the calories consumed that are the determining factors in weight gain. Moreover, contrary to what one might think, levels of physical activity have hardly changed for the last thirty years in industrialized countries, and the phenomenal increase in the number of overweight people is therefore mainly a consequence of overconsumption of food. Exercise is essential for the prevention of all chronic diseases and for the maintenance of general good health, but its role in weight loss is relatively minor. For overweight people, the only realistic way to lose weight significantly, and especially to maintain these losses over prolonged periods, is thus to reduce calorie intake.

Less sugar or less fat?
How do we get there? First, it’s important to realize that the surge in the number of overweight people has coincided with a greater availability of foods high in sugar or fat (and sometimes both). All countries in the world, without exception, that have adopted this type of diet have seen their overweight rates skyrocket, so it is likely that this change in eating habits plays a major role in the current obesity epidemic.

However, the respective contributions of sugar and fat to this increase in caloric intake and overweight are still the subjectof vigorous debate:

1) On the one hand, it has been proposed that foods high in fat are particularly obesogenic, since fats are twice as high in calories as carbohydrates, are less effective in causing a feeling of satiety, and improve the organoleptic properties of foods, which generally encourages (often unconscious) overconsumption of food. Therefore, the best way to avoid overeating and becoming overweight would be to reduce the total fat intake (especially saturated fat due to its negative impact on LDL-cholesterol levels) and replace it with complex carbohydrates (vegetables, legumes, whole-grain cereals). This is colloquially called the low-fat approach, advocated for example by the Ornish diet.

2) On the other hand, the exact opposite is proposed, i.e. that it would be mainly carbohydrates that would contribute to overconsumption of food and to the increase in the incidence of obesity. According to this model, carbohydrates in foods in the form of free sugars or refined flours cause insulin levels to rise markedly, causing massive energy storage in adipose tissue. As a result, fewer calories remain available in the circulation for use by the rest of the body, causing increased appetite and overeating to compensate for this lack. In other words, it wouldn’t be because we eat too much that we get fat, but rather because we are too fat we eat too much.

3) By preventing excessive fluctuations in insulin levels, a diet low in carbohydrates would thus limit the anabolic effect of this hormone and, therefore, prevent overeating and the accumulation of excess fat.

Less fat on the menu, fewer calories ingested
To compare the impact of low-carb and low-fat diets on calorie intake, Dr. Kevin Hall’s group (NIH) recruited 20 volunteers who were fed each of these diets in turn for two weeks. The strength of this type of cross-study is that each participant consumes both types of diets and that their effects can therefore be compared directly on the same person.

As shown in Figure 1, the two diets studied were completely opposite of each other, with 75% of the calories in the low-fat (LF) diet coming from carbohydrates versus only 10% from fat, while in the low-carb (LC) diet, 75% of calories were in the form of fat, compared to only 10% from carbohydrates. The LF diet under study consisted exclusively of foods of plant origin (fruits, vegetables, legumes, root vegetables, soy products, whole grains, etc.), while the LC diet contained mainly (82%) animal foods (meat, poultry, fish, eggs, dairy products).

Figure 1. Comparison of the amounts of carbohydrates, fats and proteins present in the low-carbohydrate (LC) and low-fat (LF) diets consumed by study participants. Adapted from Hall et al. (2021).

The study shows that there is indeed a big difference between the two types of diets in the number of calories consumed by participants (Figure 2). Over a two-week period, participants who ate an LF (low-fat) diet consumed an average of nearly 700 calories (kcal) per day less than an LC (low-carbohydrate) diet. This difference in calorie intake is observed for all meals, both at breakfast (240 calories less for the LF diet), at lunch (143 calories less), at dinner (195 calories less), and during snacks taken between meals (128 calories less). This decrease is not caused by a difference in the appreciation of the two diets by the participants, as parallel analyses did not find any difference in the level of appetite of the participants, nor in the degree of satiety and satisfaction generated by the consumption of either diet. However, the LF diet was composed exclusively of plant-based foods and therefore much richer in non-digestible fibres (60 g per day compared to only 20 g for the LC diet), which greatly reduce the energy density of meals (quantity of calories per g of food) compared to the high-fat LC diet. It is therefore very likely that this difference in energy density contributes to the lower calorie intake observed for the low-fat diet.

Overall, these results indicate that a diet consisting of plants, and thus low in fat and high in complex carbohydrates, is more effective than a diet consisting mainly of animal products, high in fat and low in carbohydrates, to limit calorie intake.

Figure 2. Comparison of the daily calorie intake of participants on a low-carbohydrate (LC) or low-fat (LF) diet. From Hall et al. (2021).

Weight loss
Despite the significant difference in calorie intake observed between the two diets, their respective impact on short-term weight loss is more nuanced. At first glance, the LC diet appeared to be more effective than the LF diet in causing rapid weight loss, with about 1 kg lost on average in the first week and almost 2 kg after two weeks, compared to only 1 kg after two weeks of the LF diet (Figure 3). However, further analysis revealed that the weight loss caused by the LC diet was mainly in the form of lean mass (protein, water, glycogen), while this diet had no significant impact on fat loss during this period. Conversely, the LF diet had no effect on this lean body mass, but did cause a significant decrease in body fat, to around 1 kg after two weeks. In other words, only the LF diet caused a loss of body fat during the study period, which strongly suggests that the decrease in calorie intake made possible by this type of diet may facilitate the maintenance of astable body weight and could even promote weight loss in overweight people.

Figure 3. Comparison of changes in body weight (top), lean mass (middle), and body fat (bottom) caused by low-carbohydrate and low-fat diets. From Hall et al. (2021).

Cardiovascular risk factors
In addition to promoting lower calorie intake and fat loss, the LF diet also appears to be superior to the LC diet in terms of its impact on several cardiovascular risk factors (Table 1):

Cholesterol. It is well established that LDL cholesterol levels increase in response to a high intake of saturated fat (see our article on the issue). It is therefore not surprising that the LF diet, which contains only 2% of all calories as saturated fat, causes a significant decrease in cholesterol, both in terms of total cholesterol and LDL cholesterol. At first glance, the high-fat LC diet (containing 30% of the daily calorie intake as saturated fat) does not appear to have a major effect on LDL cholesterol; however, it should be noted that this diet significantly modifies the distribution of LDL cholesterol particles, in particular with a significant increase in small and dense LDL particles. Several studies have reported that these small, dense LDL particles infiltrate artery walls more easily and also appear to oxidize more easily, two key events in the development and progression of atherosclerosis. In sum, just two weeks of a high-fat LC diet was enough to significantly (and negatively) alter the atherogenic profile of participants, which may raise doubts about the long-term effects of this type of diet on cardiovascular health.

Table 1. Variations in certain risk factors for cardiovascular disease following a diet low in carbohydrates or low in fat. From Hall et al. (2021).

Branched-chain amino acids. Several recent studies have shown a very clear association between blood levels of branched-chain amino acids (leucine, isoleucine and valine) and an increased risk of metabolic syndrome and type 2 diabetes, two very important risk factors for cardiovascular diseases. In this sense, it is very interesting to note that the levels of these amino acids are almost twice as high after two weeks of the LC diet compared to the LF diet, suggesting a positive effect of a diet rich in plants and poor in fats in the prevention of these disorders.

Inflammation. Chronic inflammation is actively involved in the formation and progression of plaques that form on the lining of the arteries and can lead to the development of cardiovascular events such as myocardial infarction and stroke. Clinically, this level of inflammation is often determined by measuring levels of high-sensitivity C-reactive protein (hsCRP), a protein made by the liver and released into the blood in response to inflammatory conditions. As shown in Table 1, the LF diet significantly decreases the levels of this inflammatory marker, another positive effect that argues in favour of a plant-rich diet for the prevention of cardiovascular disease.

In addition to these laboratory data, the researchers noted that participants who were fed the LF diet had a slower heart rate (73 vs. 77 beats/min) as well as lower blood pressure (112/67 vs. 116/69 mm Hg) than observed following the LC diet. In the latter case, this difference could be related, at least in part, to the much higher sodium consumption in the LC diet compared to the LF diet (5938 vs. 3725 mg/day).

All of these results confirm the superiority of a diet mainly composed of plants on all the factors involved in cardiovascular health, whether in terms of lipid profile, chronic inflammation, or adequate control of calorie intake necessary to maintain body weight.

Electronic cigarettes cause much less inflammation than tobacco

Electronic cigarettes cause much less inflammation than tobacco

OVERVIEW

  • Cigarette smoke causes chronic inflammation that significantly increases the risk of lung and cardiovascular disease.
  • Two recent studies show that this inflammation can be considerably reduced by replacing cigarettes with e-cigarettes.
  • Smokers can therefore drastically reduce the damage caused by cigarette smoke and the risk of smoking-related illnesses by using e-cigarettes as a source of nicotine.

It is now well established that smokers have a reduced life expectancy of around 10 years compared to non-smokers. This dramatic increase in the risk of premature mortality is due to the repeated exposure of smokers to the thousands of toxic and carcinogenic substances that are generated during the combustion of tobacco leaves (polycyclic aromatic hydrocarbons and nitrosamines, among others). For example, it is estimated that each pack of cigarettes contains enough carcinogenic compounds to cause two mutations in the DNA of lung cells, so decades of smoking results in the accumulation of several thousand of these mutations and dramatically increases (about 40 times) the risk of lung cancer.

Pro-inflammatory smoke
Another factor that contributes to the harmfulness of tobacco is the chronic inflammation caused by the many toxic compounds found in cigarette smoke. Locally, this inflammation damages cells in the airways and greatly increases the risk of developing chronic obstructive pulmonary disease (e.g. emphysema). But the damage caused by this inflammation is not limited to the lungs. Following inhalation of cigarette smoke, the toxic compounds rapidly diffuse into the pulmonary capillaries and can then spread throughout the body via the bloodstream. A climate of generalized chronic inflammation is then created, characterized by an increase in several inflammatory markers (IL-6, CRP, ICAM) and the recruitment of immune cells to the surface of blood vessels, two phenomena that contribute to the development of atherosclerosis.

The blood vessels that supply the heart (coronary arteries) are particularly vulnerable to this inflammation. Since the heart is closely associated with the lungs, it is the first organ to receive blood that has been in contact with cigarette smoke and is therefore necessarily exposed to higher concentrations of toxic compounds.

The consequences of this proximity are disastrous. Studies show that people who smoke a pack a day have a 5 times higher risk of myocardial infarction compared to those who have never smoked, and smoking is estimated to be responsible for about 20% of all coronary heart disease deaths. So, even though we mainly talk about the major impact of tobacco on the risk of suffering from lung cancer, we must not forget that cardiovascular diseases remain the main cause of death associated with smoking. Of all the actions a person can take to improve their cardiovascular health (and overall health), quitting smoking is by far the most important.

Reversible damage
The good news is that this damage of smoking on cardiovascular health can be reversed by quitting. Studies show that former smokers see their risk of cardiovascular accident decrease by 40% in the first five years after quitting and becomes similar to that of non-smokers after 10–15 years. Smoking cessation is beneficial at any age, but is particularly effective before the age of 40, with a 90% reduction in the risk of premature death from smoking.

Quitting smoking is difficult, with only 5% of people able to remain smoke-free after one year. However, several recent data show that this smoking cessation success rate can be considerably increased among smokers who opt for e-cigarettes. For example, a randomized clinical trial recently showed that e-cigarettes can double the effectiveness of smoking cessation compared to traditional approaches based on nicotine replacement therapy. A Cochrane review of 50 studies (including 26 randomized trials) with a total of 12,430 participants comes to a similar conclusion.

Reducing damage
In addition to facilitating smoking cessation in the longer term, adopting e-cigarettes also has the advantage of immediately reducing the damage caused by tobacco. Remember that in an e-cigarette, a nicotine solution is heated to 80°C (compared to temperatures around 900°C in a cigarette), and therefore the vapour generated does not contain carbon monoxide, nor the thousands of toxic combustion products found in cigarette smoke. According to a recent study by the Institut Pasteur, the vapour emanating from e-cigarettes contains less than 1% of the toxins present in cigarette smoke, and consequently substantially reduce smokers’ exposure to these toxic compounds (see our article on this subject).

Two recent studies show that this drastic decrease in the amount of toxic compounds in e-cigarette vapour correlates with a significant decrease in inflammation normally observed in response to cigarette smoke. In the first of these studies, the researchers compared the levels of different inflammatory markers (hsCRP, IL-6, sICAM) or oxidative stress (urinary 8-isoprostane) present in non-smokers, vapers, cigarette smokers, and mixed users (vapers and smokers). As shown in Figure 1, while smoking causes a significant increase in the levels of all markers examined, these increases are much smaller, and in some cases (IL-6) even completely abolished, among exclusive e-cigarette users. Replacing tobacco cigarettes with an e-cigarette can therefore substantially decrease the inflammatory response and, in turn, reduce the risk of cardiovascular disease. However, the study clearly shows that this reduction in inflammation is not at all observed in vapers who continue to smoke cigarettes at the same time. To truly reduce the damage caused by smoking, e-cigarettes must therefore completely replace cigarettes and not simply serve to reduce the number of cigarettes smoked in a day.

Figure 1. Change in the levels of different markers of inflammation and oxidative stress in vapers and smokers. From Stokes et al. (2020). hsCRP: high sensitivity C-reactive protein; IL-6: interleukin-6; sICAM: soluble intercellular adhesion molecule.

The other study looked at the impact of e-cigarettes on the expression of inflammatory proteins by monocytes, a class of white blood cells involved in the innate immune response. Over-activation of these cells (by toxic compounds like cigarette smoke, for example) has been shown to trigger an inflammatory response that plays an important role in the initiation and progression of atherosclerosis.

Using blood samples taken from non-smokers, smokers, and vapers, the researchers examined by flow cytometry the profiles of inflammatory proteins (caspase-1, IL-6 receptor, TLR4) present in circulating monocytes in each category of volunteers. Unsurprisingly, they noted that the expression of all of these inflammatory proteins was higher in smokers, about 4 times higher on average than in non-smokers. However, this inflammatory signature was completely absent in vapers, suggesting once again that the elimination of cigarettes in favour of e-cigarettes leads to concrete health benefits for smokers. This is consistent with a recent randomized controlled trial that showed that the transition of smokers to e-cigarettes is accompanied by a rapid improvement (in just 1 month) in the health of the blood vessels.

This study shows once again how e-cigarettes allow smokers to significantly reduce their exposure to the many toxic substances in cigarette smoke and are therefore an extremely useful tool in the fight against diseases caused by smoking.

Effects of cold on cardiovascular health

Effects of cold on cardiovascular health

OVERVIEW

  • Exposure to cold causes a contraction of blood vessels as well as an increase in blood pressure, heart rate, and the work of the heart muscle.
  • The combination of cold and exercise further increases stress on the cardiovascular system.
  • Cold temperatures are associated with increased cardiac symptoms (angina, arrhythmias) and an increased incidence of myocardial infarction and sudden cardiac death.
  • Patients with coronary artery disease should limit exposure to cold and dress warmly and cover their face when exercising.

Can the sometimes biting cold of our winters affect our overall health and our cardiovascular health in particular? For an exhaustive review of the literature on the effects of cold on health in general, see the summary report (in French only) recently published by the Institut national de santé publique du Québec (INSPQ). In this article, we will focus on the main effects of cold on the cardiovascular system and more specifically on the health of people with cardiovascular disease.

Brief and prolonged exposure to cold both affect the cardiovascular system, and exercise in cold weather further increases stress on the heart and arteries. Numerous epidemiological studies have shown that cardiovascular disease and mortality increase when the ambient temperature is cold and during cold spells. The winter season is associated with a greater number of cardiac symptoms (angina, arrhythmias) and cardiovascular events such as hypertensive crisis, deep venous thrombosis, pulmonary embolism, aortic ruptures and dissections, stroke, intracerebral hemorrhage, heart failure, atrial fibrillation, ventricular arrhythmia, angina pectoris, acute myocardial infarction, and sudden cardiac death.

Mortality from cold
Globally, more temperature-related deaths were caused by cold (7.29%) than heat (0.42%). For Canada, 4.46% of deaths were attributable to cold (2.54% for Montreal), and 0.54% to heat (0.68% for Montreal).

Intuition may lead us to believe that it is during periods of extreme cold that more adverse health effects occur, but the reality is quite different. According to a study that analyzed 74,225,200 deaths that occurred between 1985 and 2012 in 13 large countries on 5 continents, extreme temperatures (cold or hot) accounted for only 0.86% of all deaths, while the majority of cold-related deaths occurred at moderately cold temperatures (6.66%).

Acute effects of cold on the cardiovascular system of healthy people

Blood pressure. The drop in skin temperature upon exposure to cold is detected by skin thermoreceptors that stimulate the sympathetic nervous system and induce a vasoconstriction reflex (decrease in the diameter of the blood vessels). This peripheral vasoconstriction prevents heat loss from the surface of the body and has the effect of increasing systolic (5–30 mmHg) and diastolic (5–15 mmHg) blood pressure.

Heart rate. It is not greatly affected by exposure of the body to cold air, but it increases rapidly when, for example, the hand is dipped in ice water (“cold test” used to make certain diagnoses, such as Raynaud’s disease) or when very cold air is inhaled. Cold air usually causes a slight increase in heart rate in the range of 5 to 10 beats per minute.

Risk of atheromatous plaque rupture?
Post-mortem studies have shown that rupture of atheroma plaques (deposits of lipids on the lining of the arteries) is the immediate cause of over 75% of acute myocardial infarctions. Could cold stress promote the rupture of atheromatous plaques? In a laboratory study, mice exposed to cold in a cold room (4°C) for 8 weeks saw their blood LDL cholesterol level and the number of plaques increase compared to mice in the control group (room at 30°C). Furthermore, it is known that exposure to cold induces aggregation of platelets in vitro and increases coagulation factors in vivo in patients during colder days (< 20°C) compared to warmer days (> 20°C). Combined, these cold effects could help promote plaque rupture, but to date no study has been able to demonstrate this.

Risk of cardiac arrhythmias
Arrhythmias are a common cause of sudden cardiac death. Even in healthy volunteers, the simple act of dipping a hand in cold water while holding the breath can cause cardiac arrhythmias (nodal and supraventricular tachycardias). Could cold promote sudden death in people at risk for or with heart disease? Since arrhythmias cannot be detected post-mortem, it is very difficult to prove such a hypothesis. If it turns out that exposure to cold air can promote arrhythmias, people with coronary artery disease may be vulnerable to the cold since the arrhythmia would amplify the oxygenated blood deficit that reaches the heart muscle.

Effects of cold combined with exercise
Both cold and exercise individually increase the heart’s demand for oxygen, and the combination of the two stresses has an additive effect on this demand (see these two review articles, here and here). Exercising in the cold therefore results in an increase in systolic and diastolic blood pressure as well as in the “double product” (heart rate x blood pressure), a marker of cardiac work. The increased demand for oxygen by the heart muscle caused by cold weather and exercise increases blood flow to the coronary arteries that supply the heart. The rate of coronary blood flow increases in response to cold and exercise combined compared to exercise alone, but this increase is mitigated, especially in older people. Therefore, it appears that cold causes a relative lag between the oxygen demand from the myocardium and the oxygenated blood supply during exercise.

In a study carried out by our research team, we exposed 24 coronary patients with stable angina to various experimental conditions in a cold room at – 8°C, specifically a stress test with electrocardiogram (ECG) in cold without antianginal medication and an ECG at + 20°C. We then repeated these two ECGs after taking one drug (propranolol) that slows the heart rate, and then another drug (diltiazem) that causes dilation of the coronary arteries. The results showed that the cold caused mild to moderate ischemia (lack of blood supply) to the myocardium in only 1/3 of the patients. When ECG was done with medication, this effect was completely reversed. The two drugs have been shown to be equally effective in reversing this ischemia. The conclusion: cold had only a modest effect in 1/3 of patients and antianginal drugs are as effective in cold (- 8°C) as at + 20°C.

In another study in the same type of patients, we compared the effects of an ECG at – 20°C with an ECG at + 20°C. The results showed that at this very cold temperature, all patients presented with angina and earlier ischemia.

Hypertension
The prevalence of hypertension is higher in cold regions or during winter. Cold winters increase the severity of hypertension and the risk of cardiovascular events such as myocardial infarction and stroke in people with hypertension.

Heart failure
The heart of patients with heart failure is not able to pump enough blood to maintain the blood flow necessary to meet the body’s needs. Only a few studies have looked at the effects of cold on heart failure. Patients with heart failure do not have much leeway when the heart’s workload increases in cold weather or when they need to exert sustained physical effort. Cold combined with exercise further decreases the performance of people with heart failure. For example, in a study we conducted at the Montreal Heart Institute, cold reduced exercise time by 21% in people with heart failure. In the same study, the use of beta-blocker class antihypertensive drugs (metoprolol or carvedilol) significantly increased exercise time and reduced the impact of cold exposure on the functional capacity of patients. Another of our studies indicates that treatment with an antihypertensive drug from the class of angiotensin converting enzyme inhibitors, lisinopril, also mitigates the impact of cold on the ability to exercise in patients with heart failure.

Cold, exercise and coronary heart disease
It is rather unlikely that the cold alone could cause an increase in the work of the heart muscle large enough to cause a heart attack. Cold stress increases the work of the heart muscle and therefore the blood supply to the heart in healthy people, but in coronary patients there is usually a reduction in blood flow to the coronary arteries. The combination of cold and exercise puts coronary patients at risk of cardiac ischemia (lack of oxygen to the heart) much earlier in their workout than in warm or temperate weather. For this reason, people with coronary artery disease should limit exposure to cold and wear clothes that keep them warm and cover their face (significant heat loss in this part of the body) when working out outdoors in cold weather. In addition, the exercise tolerance of people with coronary heart disease will be reduced in cold weather. It is strongly recommended that coronary heart patients do indoor warm-up exercises before going out to exercise outdoors in cold weather.