The cardiovascular benefits of avocado

The cardiovascular benefits of avocado

OVERVIEW

  • Avocado is an exceptional source of monounsaturated fat, with content similar to that of olive oil.
  • These monounsaturated fats improve the lipid profile, in particular by raising HDL-cholesterol levels, a phenomenon associated with a reduced risk of cardiovascular disease.
  • A recent study confirms this cardioprotective potential of avocado, with a 20% reduction in the risk of coronary heart disease observed in regular consumers (2 or more servings per week).

There is currently a consensus in the scientific community on the importance of favouring dietary sources of unsaturated fats (especially monounsaturated and omega-3 polyunsaturated fats) to significantly reduce the risk of cardiovascular disease and premature mortality (see our article on this subject). With the exception of fatty fish rich in omega-3 (salmon, sardines, mackerel), plant-based foods are the main sources of these unsaturated fats, particularly oils (olive oil and those rich in omega-3 like canola oil), nuts, certain seeds (flax, chia, hemp) as well as fruits such as avocado. Regular consumption of these foods high in unsaturated fats has repeatedly been associated with a marked decrease in the risk of cardiovascular events, a cardioprotective effect that is particularly well documented for extra-virgin olive oil and nuts.

A unique nutritional profile
Although the impact of avocado consumption has been less studied than that of other plant sources of unsaturated fat, it has been suspected for several years that this fruit also exerts positive effects on cardiovascular health. On the one hand, avocado stands out from other fruits for its exceptionally high monounsaturated fat content, with a content (per serving) similar to that of olive oil (Table 1). On the other hand, a serving of avocado contains very high amounts of fibre (4 g), potassium (350 mg), folate (60 µg), and several other vitamins and minerals known to participate in the prevention of cardiovascular disease.

Table 1. Comparison of the lipid profile of avocado and olive oil. The data corresponds to the amount of fatty acids contained in half of a Haas avocado, the main variety consumed in the world, or olive oil (1 tablespoon or 15 mL). Taken from USDA. FoodData Central.

Fatty acidsAvocado (68 g)Olive oil (15 mL)
Total10 g12.7 g
Monounsaturated6.7 g9.4 g
Polyunsaturated1.2 g1.2 g
Saturated1.4 g2.1 g

This positive impact on the heart is also suggested by the results of intervention studies that examined the impact of avocado on certain markers of good cardiovascular health. For example, a meta-analysis of 7 studies (202 participants) indicates that the consumption of avocado is associated with an increase in HDL cholesterol and a decrease in the ratio of total cholesterol to HDL cholesterol, a parameter which is considered to be a good predictor of coronary heart disease mortality. A decrease in triglycerides, total cholesterol and LDL cholesterol levels associated with the consumption of avocado has also been reported, but is, however, not observed in all studies. Nevertheless, the increase in HDL cholesterol observed in all the studies is very encouraging and strongly suggests that avocado could contribute to the prevention of cardiovascular disease.

A cardioprotective fruit
This cardioprotective potential of avocado has just been confirmed by the results of a large-scale epidemiological studycarried out among people enrolled in two large cohorts headed by Harvard University, namely the Nurses’ Health Study (68,786 women) and the Health Professionals Follow-up Study (41,701 men). Over a period of 30 years, researchers periodically collected information on the dietary habits of participants in both studies and subsequently examined the association between avocado consumption and the risk of cardiovascular disease.

The results obtained are very interesting: compared to people who never or very rarely eat them, regular avocado consumers have a risk of coronary heart disease reduced by 16% (1 serving per week) and 21% (2 servings or more per week) (Figure 1).

Figure 1. Association between the frequency of avocado consumption and the risk of coronary heart disease. The quantities indicated refer to one serving of avocado, corresponding to approximately half of the fruit. Taken from Pacheco et al. (2022).

There are therefore only benefits to integrating avocado into our eating habits, especially if its monounsaturated fats replace other sources of fats that are less beneficial to health. According to the researchers’ calculations, replacing half a serving of foods rich in saturated fat (butter, cheese, deli meats) with an equivalent quantity of avocado would reduce the risk of cardiovascular disease by approximately 20%.

Avocados are increasingly popular, especially among young people, and are even predicted to become the 2nd most traded tropical fruit by 2030 globally, just behind bananas. In light of the positive effects of these fruits on cardiovascular health, we can only welcome this new trend.

Obviously, the high demand for avocado creates strong pressures on the fruit’s production systems, particularly in terms of deforestation for the establishment of new crops and increased demand for water. However, it is important to note that the water footprint (the amount of water required for production) of avocado is much lower than that of all animal products, especially beef (Table 2). In addition, as is the case for all plants, the carbon footprint of avocado is also much lower than that of animal products, the production of an avocado generating approximately 0.2 kg of CO2-eq compared to 4 kg for beef.

Table 2. Comparison of the water footprint of avocado and different foods of animal origin. Taken from UNESCO-IHE Institute for Water Education (2010) 

FoodWater footprint
(m3/ton)
Beef15,400
Lamb and sheep10,400
Porc6,000
Chicken4,300
Eggs3,300
Avocado1,981

The influence of oral health on the risk of cardiovascular disease

The influence of oral health on the risk of cardiovascular disease

OVERVIEW

  • Periodontitis is an inflammatory reaction affecting the periodontium, i.e., all the structures responsible for anchoring the teeth (gums, ligaments, alveolar bone).
  • A very large number of studies have observed a close link between periodontitis and an increased risk of several pathologies, including myocardial infarction and stroke.
  • The expansion of health insurance to cover dental care would therefore be an important step forward for cardiovascular prevention and the prevention of several other chronic diseases.

It is now clearly established that the microbiome, the vast bacterial community that lives in symbiosis with us, plays an essential role in the functioning of the human body and the maintenance of good health. This link is particularly well documented with regard to the intestinal microbiome, that is, the hundreds of billions of bacteria that are located in the digestive system, in particular at the level of the colon. In recent years, an impressive number of studies have shown that these bacteria play a leading role in the proper functioning of the metabolism and the immune system and that imbalances in the composition of the microbiome are associated with the development of several chronic diseases.

Oral microbiome
The mouth represents another privileged site of colonization by bacteria; each mL of saliva from a healthy adult contains approximately 100 million bacterial cells, not to mention the millions of bacteria present in other areas of the oral cavity, such as dental plaque, tongue, cheeks, palate, throat and tonsils. It is therefore not surprising that a simple 10-second kiss with tongue contact and exchange of saliva (French kiss) can transfer around 80 million bacteria between partners!

On average, the human mouth contains about 250 distinct bacterial species, from the approximately 700 species of oral bacteria that have been identified so far. The composition of this bacterial community is unique to each person and is influenced by their genetics, age, place of residence, cohabitation with other people, the nature of the diet and, obviously, the frequency of oral hygiene care.

In a healthy mouth, the oral bacterial community is a balanced ecosystem that performs several beneficial functions for the host. For example, some bacteria have anti-inflammatory activity that can block the action of certain pathogens, while others reduce the acidity of dental plaque (through the production of basic compounds such as ammonia) and thus prevent the demineralization of teeth, the first step in the process of tooth decay. Oral bacteria also have the ability to convert nitrates found in fruits and vegetables into nitric oxide (NO), a vasodilator that helps control blood pressure (see our article on this subject).

Disturbed ecosystem
It is the disruption of this balance of the bacterial ecosystem (dysbiosis) that is the trigger for the two main diseases affecting the teeth, namely dental caries and periodontal disease. In the case of caries, the cause is the establishment of a bacterial community enriched in certain species (Streptococci of the mutans group, in particular), capable of fermenting dietary sugars and reducing the pH sufficiently to initiate the demineralization of the tooth. The action of these bacteria is however local, restricted to the level of tooth enamel, and therefore generally does not have a major impact on health in general.

The global repercussions associated with periodontal diseases are much more serious, and it is for this reason that these infections have attracted a great deal of interest from the scientific and medical communities in recent years. Not only with regard to the identification of the bacteria responsible for these infections and their mechanisms of action, but also, and perhaps above all, because of the close relationship observed in several epidemiological studies between periodontitis and several serious chronic diseases, including cardiovascular disease, diabetes, certain cancers and even Alzheimer’s disease.

Periodontitis
As its name suggests, periodontitis is an inflammatory reaction affecting the periodontium, i.e., all the structures responsible for anchoring the teeth (gums, ligaments, alveolar bone) (Figure 1). Periodontitis begins in the form of gingivitis, which is local inflammation of the gums caused by bacteria present in dental plaque (the bacterial biofilm that forms on the teeth). This inflammation is usually quite benign and reversible, but can progress to chronic periodontitis in some more susceptible individuals. There is then a gradual resorption of the gums, ligaments and alveolar bone, which causes the appearance of periodontal pockets around the tooth and, eventually, its fall. Periodontal disease is one of the most common chronic inflammatory diseases, affecting almost 50% of the population to varying degrees, including 10% who develop severe forms of the disease, and is one of the main causes of tooth loss.

Figure 1. Schematic illustration of the main features of periodontitis. Image from Shutterstock.

The trigger factor for periodontitis is an imbalance in the composition of the microbial community present in dental plaque that promotes the growth of pathogenic species responsible for this infection. Among the approximately 400 different species of bacteria associated with dental plaque, the presence of a complex composed of the anaerobic bacteria Porphyromonas gingivalis, Treponema denticola, and Tanneralla forsythia (known as the red complex) is closely correlated with clinical measures of periodontitis, and more particularly with advanced periodontal lesions, and could therefore play an important role in the development of these pathologies. It is also interesting to note that the analysis of human skeletons has revealed that periodontitis became more frequent around 10,000 years ago (in the Neolithic period) and that this increase coincides with the increased presence of one of these bacteria (P. gingivalis) in dental plaque. It is likely that this change in plaque microbial composition is a consequence of changes in the human diet introduced by agriculture, in particular a higher carbohydrate intake.

A disproportionate inflammatory response
It is the exaggerated inflammatory response caused by the presence of this bacterial imbalance in dental plaque that is largely responsible for the development of periodontitis (Figure 2).


Figure 2. Impact of inflammation generated by bacterial imbalance (dysbiosis) on the development of periodontitis.
In a healthy mouth (left figure), the bacterial biofilm is in balance with the host’s immune system and does not generate an inflammatory response. Disruption of this balance (by poor dental hygiene or smoking, for example) can cause gingivitis, which is a mild inflammation of the gums characterized by the formation of a slight gingival crevice (≤ 3 mm deep), but without bone damage. Gingivitis can progress to periodontitis when the bacterial imbalance of the biofilm induces a strong inflammatory reaction that destroys the tissues surrounding the tooth to form deeper periodontal pockets (≥ 4 mm) and the destruction of the alveolar bone. From Hajishengallis (2015).

When they manage to colonize the subgingival space, pathogenic bacteria such as P. gingivalis secrete numerous virulence factors (proteases, hemolytic factors, etc.) that degrade the tissues present at the site of infection and generate the essential elements for the growth of these bacteria. The bleeding gums caused by this infection is particularly beneficial for P. gingivalis since the growth of this bacterium requires a high supply of iron, present in the heme group of the hemoglobin of red blood cells.

The immune system obviously reacts strongly to this microbial invasion (which can reach several hundred million bacteria in certain deep periodontal pockets) by recruiting at the site of infection the first-line innate immunity (neutrophils, macrophages), specialized in the rapid response to the presence of pathogens. There is then massive production of cytokines, prostaglandins, and matrix metalloproteinases by these immune cells which, collectively, create a high-intensity inflammation intended to eliminate the bacteria present in the periodontal tissues.

However, this inflammatory response does not have the expected effects at all. On the one hand, periodontal bacteria have developed several subterfuges to escape the immune response and are therefore little affected by the host response; on the other hand, the continuous presence of an inflammatory microenvironment causes considerable damage to the periodontal tissues, which accelerates their destruction and the resorption of the gums, ligaments and bone characteristic of periodontitis. This inflammatory attack on the periodontium also has the perverse effect of generating several essential nutrients for bacterial growth, which further amplifies the infection and accelerates the degradation of the tissues surrounding the tooth. In other words, periodontitis is the result of a vicious circle in which the bacterial imbalance associated with dental plaque provokes a strong inflammatory immune response, with this inflammation leading to the destruction of the periodontal tissues, which in turn promotes the growth of these bacteria (Figure 3).

Figure 3. Amplification of the inflammatory response is responsible for the development of periodontitis. The imbalance of the microbiome of dental plaque (dysbiosis) leads to the activation of the immune defences (mainly the complement system and the Toll-like receptors (TLR)) and the triggering of an inflammatory response. This inflammation causes the destruction of the tissues surrounding the tooth, including the alveolar bone, which generates several nutrients that support the proliferation of pathogenic bacteria, adapted to grow in these inflammatory conditions. An amplification loop is therefore created in which inflammation promotes bacterial growth and vice versa, which supports the progression of periodontitis.

The mechanisms involved in this “immunodestruction” are extraordinarily complex and will not be described in detail here, but let us only mention that the sustained presence of periodontal bacteria activates certain defence systems specialized in the rapid response to infections (Toll-like receptors and complement system) present on the surface of immune cells, which activates the production of inflammatory molecules that are very irritating to the surrounding tissues. In the alveolar bone, for example, the production of cytokines (interleukin-17, in particular) stimulates the cells involved in the breakdown of bone tissue (osteoclasts) and leads to bone resorption.

It is important to mention that even if the initiation of periodontitis depends on the presence of pathogenic bacteria in dental plaque, the evolution of the disease remains strongly influenced by several factors, both genetic and associated with lifestyle. For example, there is a strong genetic predisposition to periodontal disease, with an estimated heritability of 50%: some people do not develop periodontitis despite a massive build-up of tartar (and bacteria) around the teeth, while others will be affected by the disease despite a small amount of dental plaque. These differences in susceptibility to periodontitis are thought to be caused by the presence of variations (polymorphisms) in certain genes involved in the inflammatory response.

In terms of lifestyle habits, the nature of the diet, certain metabolic diseases such as obesity and type 2 diabetes, stress and smoking are well-documented aggravating factors for periodontitis. This influence is particularly dramatic for smoking, which has catastrophic effects on the onset, progression and severity of periodontitis, with an increase in the risk of the disease that can reach more than 25 times (see Table 3). It should be noted that a common point to all of these risk factors is that they all influence in one way or another the degree of inflammation, which highlights to what extent the development of periodontitis depends on the intensity of the host’s inflammatory response in reaction to the presence of pathogenic bacteria in dental plaque.

Periodontitis and cardiovascular disease
Although the damage caused by this disproportionate inflammatory response is first and foremost local, at the level of the tissues surrounding the tooth, the fact remains that the inflammatory molecules that are generated at the site of infection are in close contact with the bloodstream and can therefore diffuse into the blood and affect the whole body. The impact of this systemic inflammation is probably very important, as numerous studies have reported that the incidence of periodontitis is strongly correlated with the presence of several other diseases (comorbidities) whose development is influenced by chronic inflammation, in particular cardiovascular disease, diabetes, certain cancers and arthritis (Table 1).

Table 1. Association of periodontitis with different pathologies.

Comorbidities of periodontitisObserved phenomenaSources
Cardiovascular diseasePeriodontitis is associated with an increased risk of heart attack and stroke.See Table 2 references.
Diabetes (types 1 and 2)Chronic inflammation associated with diabetes accelerates the destruction of periodontal tissues.Lalla and Papapanou (2011)
This association between the two diseases is bidirectional, as the chronic inflammation generated by periodontitis increases insulin resistance and in turn disrupts blood sugar control.
Alzheimer'sSeveral epidemiological studies have reported an association between periodontitis and the risk of developing Alzheimer’s disease.Dioguardi et al. (2020)
The periodontal bacterium P. gingivalis (DNA, proteases) has been detected in the brains of patients who have died of Alzheimer’s disease as well as in the cerebrospinal fluid of people suffering from the disease. Dominy et al. (2019)
The risk of mortality from Alzheimer’s disease is correlated with antibody levels to a group of periodontal bacteria, including P. gingivalis, Campylobacter rectus, and Prevotella melaninogenica.Beydoun et al. (2020)
Rheumatoid arthritisSeveral epidemiological studies have observed an association between periodontitis and rheumatoid arthritis.Sher et al. (2014)
The inflammation caused by periodontitis stimulates the production of cells that increase bone resorption in the joints.Zhao et al. (2020)
CancerThe incidence of colorectal cancer is 50% higher in individuals with a history of periodontitis.Janati et al. (2022)
A periodontal bacterium (Fusobacterium nucleatum) has been repeatedly observed in colorectal cancers. Castellarin et al. (2011)
High levels of P. gingivalis have been detected in oral cancers.Katz et al. (2011)
High levels of antibodies against P. gingivalis are associated with a 2-fold higher risk of pancreatic cancer. Michaud et al. (2013)
Liver diseasesPeriodontitis is correlated with an increased incidence of liver disease.Helenius-Hietala et al. (2019)
In patients with fatty liver disease or non-alcoholic steatohepatitis, treatment of periodontitis decreases blood levels of markers of liver damage.Yoneda et al. (2012)
Intestinal diseasesChronic inflammatory bowel disease is associated with an increased risk of periodontitis.Papageorgiou et al. (2017)
This relationship is bidirectional, as periodontal bacteria ingested via saliva contribute to intestinal inflammation and disrupt the microbiome and intestinal barrier.Kitamoto et al. (2020)
Pregnancy complicationsMaternal periodontitis is associated with a higher risk of undesirable pregnancy outcomes such as miscarriages, premature deliveries, and low birth weight.Madianos et al. (2013)
Periodontal bacteria (P. gingivalis, F. nucleatum) have been observed in the placenta and clinical studies have reported a link between the presence of these bacteria and pregnancy complications.Han and Wang (2013)

The link between periodontitis and cardiovascular disease has been particularly studied because it is clearly established that inflammation participates in all stages of the development of atherosclerosis, from the appearance of the first lesions caused by the infiltration of white blood cells which store cholesterol, until the formation of clots that block blood circulation and cause heart attack and stroke. These inflammatory conditions are usually a consequence of certain lifestyle factors (smoking, poor diet, stress, physical inactivity), but can also be created by acute infections (influenza and COVID-19, for example) or chronic infections (Chlamydia pneumoniae, Helicobacter pylori, human immunodeficiency virus). Since all of these infections increase the risk of cardiovascular disease, it is therefore possible that a similar phenomenon exists for the chronic inflammation that results from periodontitis.

The first clue to the existence of a link between periodontitis and the risk of cardiovascular disease comes from a study published in 1989, where it was observed that a group of patients who had suffered a myocardial infarction had poorer oral health (more cavities, gingivitis, periodontitis) than a control group. Since then, hundreds of studies examining the issue have confirmed this association and shown that the presence of oral health problems, periodontitis in particular, is very often correlated with an increased risk of heart attack and stroke (Table 2).

 

Table 2. Summary of the main studies reporting an association between periodontitis and the risk of heart attack and stroke.

Measured parameterObserved phenomenonSources
Coronary artery diseasePeriodontitis is associated with an increased risk of heart attack (men < 50 years).DeStefano et al. (1993)

Poor oral health (caries, periodontitis) is associated with an increased risk of heart attack and sudden death in coronary patients.Mattila et al. (1995)
Tooth loss caused by periodontitis is associated with an increased risk of heart attack and sudden death.Joshipura et al. (1996)
Bone loss caused by periodontitis is associated with an increased risk of heart attack, fatal and non-fatal.Beck et al. (1996)
The severity of periodontitis (bone loss) is associated with an increased risk of heart attack.Arbes et al. (1999)
Periodontitis is associated with an increased risk of fatal infarction.Morrison et al. (1999)
Periodontitis is associated with a slight (non-significant) increase in the risk of coronary heart attacks.Hujoel et al. (2000)
Periodontitis is associated with a slight (non-significant) increase in the risk of heart attack.Howell et al. (2001)
Bleeding gums are correlated with a higher risk of heart attack.Buhlin et al. (2002)
Periodontitis is associated with a higher risk of hospitalization for heart attack, angina or unstable angina.López et al. (2002)
High levels of antibodies against two pathogens responsible for periodontitis (A. actinomycetemcomitans and P. gingivalis) are associated with an increased risk of coronary heart disease.Pussinen et al. (2003)
Coronary patients more often experience poor oral health and an increase in inflammatory markers.Meurman et al. (2003)
Periodontitis is associated with an increased risk of mortality from coronary heart disease.Ajwani et al. (2003)
High levels of antibodies against a bacterium responsible for periodontitis (P. gingivalis) are associated with an increased risk of heart attack.Pussinen et al. (2004)
Periodontitis is associated with an increase (15%) in the risk of coronary heart disease (meta-analysis).Khader et al. (2004)
Periodontitis, combined with tooth loss, is associated with an increased risk of coronary heart disease.Elter et al. (2004)
Oral pathologies are more common in coronary patients.Janket et al. (2004)
Periodontitis is more common in coronary patients.Geerts et al. (2004)
High levels of antibodies against the bacteria responsible for periodontitis are associated with an increased risk of coronary heart disease in both smokers and non-smokers.Beck et al. (2005)
Higher levels of antibodies to bacteria involved in periodontitis (P. gingivalis and A. actinomycetemcomitans) are associated with an increased risk of coronary heart disease.Pussinen et al. (2005)
The presence of deep periodontal pockets is more common in women with coronary artery disease.Buhlin et al. (2005)
Periodontitis is associated with a higher risk of acute infarction.Cueto et al. (2005)
Periodontitis and levels of pathogenic bacteria (A. actinomycetemcomitans in particular) in the subgingival biofilm are associated with an increased risk of coronary heart disease.Spahr et al. (2006)
Periodontitis is more common in patients with coronary artery disease.Geismar et al. (2006)
Poor periodontal health is associated with an increased risk of coronary heart disease.Briggs et al. (2006)
Gingivitis, cavities and tooth loss are all associated with an increased risk of angina.Ylostalo et al. (2006)
Patients with acute coronary syndrome are at greater risk of being affected by periodontitis simultaneously.Accarini and de Godoy (2006)
The severity of periodontitis (bone loss) is associated with an increased risk of heart attack in 40-60 year-olds.Holmlund et al. (2006)
Patients affected by periodontitis have an increased risk (15%) of coronary heart disease (meta-analysis).Bahekar et al. (2007)
Periodontitis is associated with an increased risk of acute coronary syndrome.Rech et al. (2007)
Patients with acute coronary syndrome are more likely to have oral microbial flora enriched with periodontitis-causing bacteria.Rubenfire et al. (2007)
Periodontitis is associated with an increased risk of heart attack in both men and women.Andriankaja et al. (2007)
Coronary patients have deeper periodontal pockets and higher levels of a bacterium (Prevotella intermidia) involved in periodontitis.Nonnenmacher et al. (2007)
Men and women with < 10 teeth have a higher risk of coronary heart disease than those with > 25 teeth.Hung et al. (2007)
The severity of coronary artery disease (number of vessels affected) is correlated with the severity of periodontal disease.Gotsman et al. (2007)
Severe periodontitis is more common in patients with coronary artery disease.Starkhammar Johansson et al. (2008)
Chronic periodontitis is associated with an increased risk of coronary heart disease in men < 60 years of age.Dietrich et al. (2008)
Periodontitis is associated with an increased risk of angina and heart attack in both men and women.Senba et al. (2008)
Higher levels of antibodies to bacteria involved in periodontitis (P. gingivalis, A. actinomycetemcomitans, T. forsythia, and T. denticola) are associated with an increased risk of heart attack.Lund Håheim et al. (2008)
Higher levels of antibodies to bacteria involved in periodontitis (P. gingivalis and A. actinomycetemcomitans) are associated with increased coronary artery calcification in type 1 diabetics.Colhoun et al. (2008)
The severity of periodontitis is correlated with greater blockage of the coronary arteries.Amabile et al. (2008)
The risk of coronary injury is higher (34%) in patients with periodontitis (meta-analysis).Blaizot et al. (2009)
Periodontitis is associated with a 24-35% increase in the risk of coronary heart disease (meta-analysis).Sanz et al. (2010)
Mortality from coronary heart disease is 7 times higher in patients with < 10 teeth compared to those with > 25 teeth.Holmlund et al. (2010)
High levels of two bacteria involved in periodontitis (Tannerella forsythensis and Prevotella intermedia) are correlated with an increased risk of heart attack.Andriankaja et al. (2011)
Periodontitis is associated with a higher risk of heart attack, regardless of smoking and diabetes.Rydén et al. (2016)
Periodontitis is associated with a twice as high risk of a heart attack (meta-analysis).Shi et al. (2016)
Patients with periodontitis are at higher risk of heart attack, cardiovascular mortality and all-cause mortality.Hansen et al. (2016)
Periodontitis doubles the risk of a heart attack (meta-analysis).Xu et al. (2017)
Oral infections in childhood (including cavities and periodontitis) are associated with the thickening of the carotid wall in adulthood.Pussinen et al. (2019)
Periodontitis and tooth loss are associated with a higher risk of coronary heart disease (meta-analysis).Gao et al. (2021)
Inflammation caused by periodontitis is associated with an increased risk of cardiovascular events.Van Dyke et al. (2021)
People affected by periodontitis have an increased risk of coronary heart attacks and premature mortality.Bengtsson et al. (2021)
StrokeBone loss caused by periodontitis is associated with an increased risk of stroke.Beck et al. (1996)
Poor oral health is associated with an increased risk of stroke in men > 60 years of age.Loesche et al. (1998)
Severe gingivitis, periodontitis and tooth loss are associated with an increased risk of fatal stroke.Morrison et al. (1999)
Periodontitis is associated with an increased risk of stroke (non-hemorrhagic).Wu et al. (2000)
Periodontitis is associated with a slight (non-significant) increase in the risk of stroke.Howell et al. (2001)
Bleeding gums are associated with a higher risk of stroke.Buhlin et al. (2002)
Periodontitis and tooth loss (< 24 teeth) are associated with an increased risk of stroke.Joshipura et al. (2003)
The risk of stroke associated with periodontitis is 2 times higher than the risk of coronary heart disease (2.85 vs 1.44)Janket et al. (2003)
Severe periodontitis (bone loss) is associated with an increased risk of stroke.Elter et al. (2003)
Severe periodontitis is associated with an increased risk of stroke.Dorfer et al. (2004)
High levels of antibodies against two pathogens responsible for periodontitis (A. actinomycetemcomitans and P. gingivalis) are associated with an increased risk of stroke (primary and secondary).Pussinen et al. (2004)
Periodontitis is associated with an increased risk of stroke in men < 60 years of age.Grau et al. (2004)
Higher-than-normal tooth loss is associated with a higher risk of stroke-related mortality and all-cause mortality.Abnet et al. (2005)
Poor periodontal health is associated with an increased risk of stroke.Lee et al. (2006)
Higher levels of antibodies to a bacterium involved in periodontitis (P. gingivalis) are associated with an increased risk of stroke.Pussinen et al. (2007)
Loss of > 9 teeth is associated with an increased risk of stroke.Tu et al. (2007)
Periodontitis is associated with an increased risk of stroke in 60-year-old and normotensive men.Sim et al. (2008)
The loss of > 7 teeth is associated with an increased risk of stroke (ischemic and hemorrhagic).Choe et al. (2009)
Bone loss caused by periodontitis is associated with a higher risk of stroke, especially in men < 65 years of age.Jimenez et al. (2009)
The loss of > 17 teeth is associated with an increase in inflammatory markers and an increased risk of stroke.You et al. (2009)
Periodontitis is associated with an increased risk of fatal stroke.Holmlund et al. (2010)
Periodontitis (periodontal pocket > 4.5 mm) is associated with an increased risk of stroke.Pradeep et al. (2010)
Periodontitis is associated with an increased risk of hemorrhagic stroke in obese men.Kim et al. (2010)
Patients with periodontitis are at greater risk of stroke, cardiovascular mortality and all-cause mortality.Hansen et al. (2016)
Periodontitis is associated with an increased risk of carotid atherosclerosis (meta-analysis)Zeng et al. (2016)
The severity of periodontitis is associated with an increased risk of stroke. Conversely, regular dental care is associated with a decreased risk.Sen et al. (2018)
Periodontitis is associated with an increased risk of stroke affecting the major arteries.Mascari et al. (2021)

 

Bacterial invasion
In addition to the chronic inflammation generated by gum infection, it has also been proposed that damage to periodontal tissues may provide bacteria with an entry point into the circulation, a phenomenon similar to that frequently observed for many pathogen agents (about 50 bacterial species and many viruses). One of the best examples is arguably endocarditis, an infection that occurs when bacteria from dental plaque enter the bloodstream through the gums and attach themselves to the inner walls of the heart chambers and valves. It is for this reason that patients who need to undergo surgery to treat valvular heart conditions (the replacement or repair of heart valves) and who have dental problems are referred to their dentist to treat these conditions before the operation to prevent postoperative valve infection. In addition, patients with prosthetic heart valves or valvular pathologies are prescribed antibiotics before dental procedures to prevent endocarditis (bacterial infection of a heart valve).

Bacteremia (presence of bacteria in the blood) associated with periodontitis also allows pathogens to come into contact with the wall of blood vessels and penetrate the endothelial and muscle cells of these vessels, including at the level of atherosclerotic plaques. In this sense, it should be noted that infection with the main periodontal bacterium (P. gingivalis) is associated with an acceleration of the development of atherosclerosis in animal models, possibly in response to the innate inflammatory immune response directed against the bacterium at the vessel level. In sum, the link between periodontitis and cardiovascular disease is biologically plausible, whether due to the diffusion of inflammatory molecules that diffuse into the circulation or the presence of bacteria in the vessels.

Common risk factors
As a statement from the American Heart Association on the matter points out, however, it is difficult to demonstrate that these associations are causal, i.e., that periodontitis is directly responsible for the increased risk of CVD observed in these studies. This difficulty is largely due to the fact that the risk factors for periodontitis are very similar to those responsible for CV diseases (which are called in epidemiology confounding factors, i.e., variables that may influence both the risk factor and the disease being studied) (Table 3). The best example is undoubtedly smoking, which is both the most important risk factor for cardiovascular disease and periodontitis, but this similarity is also observed for all the “classic” cardiovascular risk factors, whether hypertension, diabetes, obesity, hypercholesterolemia or poor diet. In other words, what increases the risk of periodontitis also increases the risk of cardiovascular disease and vice versa, which makes it very difficult to establish a causal link between the two diseases.

Table 3. Similarity between risk factors for cardiovascular disease and periodontitis.

Cardiovascular risk factorsImpact on the risk of periodontitisSources
SmokingCompared to non-smokers, the risk of periodontitis is 18 times higher in smokers aged 20–49 and 25 times higher in smokers aged 50 and over.Hyman and Reid (2003)
HypertensionPeriodontitis, especially severe forms of the disease, is associated with higher systolic and diastolic pressures and an increased risk of hypertension (≥140 mmHg systolic, ≥90 mmHg diastolic).Aguilera et al. (2020)
DyslipidemiasPeriodontitis is associated with higher levels of LDL cholesterol and triglycerides, as well as lower levels of HDL cholesterol.Nepomuceno et al. (2017)
Diabetes (types 1 and 2)See Table 1
ObesityObesity, especially at the abdominal level, is associated with a higher prevalence of periodontitis in young adults. Al-Zahrani et al. (2003)
Diet quality
Fruit and vegetable deficiencyA diet rich in fruits and vegetables is associated with a decreased risk of periodontitis.Dodington et al. (2015)
Fibre and whole-grain deficiencyHigh fibre intake is associated with lower prevalence and severity of periodontitis. Nielsen et al. (2016)
The protective effect of fibre contributes to the decrease in the risk of periodontitis associated with a high intake of whole grains.Merchant et al. (2006)
High intake of simple carbohydrates Consumption of added sugars is associated with an increase of about 50% in the prevalence of periodontitis (and caries).Lula et al. (2014)
High intake of saturated fatsA greater portion of energy intake in the form of saturated fats is associated with an increased risk of periodontitis, possibly due to the pro-inflammatory action of these fatty acids.Iwasaki et al. (2011)

That being said, some studies have tried to establish this link by adjusting the risk of periodontitis to take into account the impact of these confounding factors. For example, the Swedish PAROKRANK study reported a significant increase (28%) in the risk of a first heart attack in people affected by periodontitis, even after subtracting the contribution of the main cardiovascular risk factors. According to the currently available clinical data, it is estimated that periodontitis could be an independent risk factor for cardiovascular disease, with an increase of about 10–15% in risk.

Beneficial treatment
A causal link between periodontitis and cardiovascular disease is also suggested by certain studies showing that periodontal treatments (scaling and root planing) are associated with an improvement in certain cardiovascular health parameters and/or a decrease in cardiovascular events. For example, in patients with periodontitis, removal of subgingival plaque by root planing (under local anesthesia) resulted in improved endothelial function (dilation of vessels by blood flow) within 6 months of treatment. Several other studies have confirmed this positive impact of periodontal treatment on vessel function as well as on other important parameters of cardiovascular health, such as levels of inflammatory molecules and cholesterol levels (total, LDL and HDL). This improvement is particularly noticeable in patients with comorbidities such as metabolic syndrome, diabetes or cardiovascular disease, suggesting that periodontal treatment may be useful for patients at high risk of cardiovascular events. In this sense, it is interesting to note that a recent study reported that periodontal treatment of patients with a recent stroke was associated with a decrease in the overall risk of cardiovascular events in the following year, as measured by a combination of the incidence of stroke, infarction and sudden death.

Overall, these studies raise the possibility that the development of cardiovascular disease may indeed be directly influenced by the presence of periodontal lesions. This close link illustrates how an imbalance affecting one part of the body, in this case the tissues surrounding the teeth, can negatively influence the entire human body. Good health is a global state: even if our organs each have a well-defined role, their proper functioning remains strongly influenced by the general conditions prevailing throughout the body. This is particularly true with regard to inflammation, a condition that favours the development of all chronic diseases and which is responsible for the majority of deaths affecting the population. In this context, the increased risk of several diseases associated with periodontitis, especially cardiovascular disease, is not so surprising, since it essentially represents another example of the damage that can be caused by the presence of these chronic inflammatory conditions.

The close association between oral and cardiovascular health therefore suggests that the prevention and treatment of periodontitis may play important roles in the prevention of cardiovascular disease, particularly in those at higher risk due to being overweight, diabetes or a history of cardiovascular disease. This important link between the teeth and the rest of the body unfortunately remains under-exploited because medicine and dentistry are distinct disciplines, which have evolved in parallel, without much interaction between them. While one can be treated for free for all diseases that affect the body (in Canada), dental care does not benefit from this coverage and is therefore out of reach for those less well off. There is no doubt that this situation contributes to the high prevalence of periodontitis in our society and to the negative repercussions associated with these infections on health in general. Extending health insurance to cover dental care would therefore be an important step forward for cardiovascular prevention and the prevention of several other chronic diseases.

Smart wearable devices: Useful tools to monitor our health

Smart wearable devices: Useful tools to monitor our health

OVERVIEW

  • Smartwatches and other wearable devices are equipped with sophisticated sensors that can record several useful parameters to monitor our health: heart rate, electrocardiogram, amount of physical activity (quantity and intensity), oxygen saturation in the blood, detection of falls and cardiac arrhythmias, etc.
  • Wearing an activity monitor encourages physical activity in general and more specifically moderate to vigorous intensity physical activity, according to all of the studies that have been published on the subject.
  • Smartwatches are not yet sensitive and specific enough for reliable detection of atrial fibrillation, the most common type of cardiac arrhythmia.
  • Smart wearable devices are constantly being improved and have a bright future ahead of them. However, it will be necessary to ensure that these devices are accessible to all and that they do not negatively impact the health system by generating too much biometric data and unnecessary clinical tests.

Exercise monitoring devices, or physical activity monitors, have been used for decades in the physical activity research community. Early versions of these devices simply recorded the duration and intensity of physical activity. Modern versions of physical activity monitors can additionally give direct feedback to the user and thus have the potential to promote behavioural changes, i.e., to encourage physical activity and possibly detect health problems. Review articles on the applications of these wearable devices for cardiovascular disease care have been published here and here.

Smartwatches
There are several types of devices for sale on the market. So-called smartwatches, such as Apple Watch, Fitbit, Garmin, Omron, and TomTom watches, contain sensors that measure physical activity (the number of steps, the energy spent) using the accelerometer and gyroscope, distance travelled (GPS), heart rate, as well as detect falls, monitor sleep, detect cardiac arrhythmias (electrocardiogram), and estimate blood oxygen saturation and cardiorespiratory capacity (VO2max). These devices are increasingly popular for tracking our health and fitness, especially during physical activity sessions, including walking, running, cycling and many other sports.

Other smart wearable devices
There are also devices that are worn around the thorax (e.g., BioHarness, Polar straps), around the wrist (bracelets), or that are inserted into “patches” that are attached to the chest (e.g., Zio Patch, Nuvant MCT, S-Patch cardio), clothing (e.g., AIO Smart Sleeve), or shoes. These smart wearable devices mostly measure heart rate and record electrocardiograms. These devices are less popular because they are bulkier and their functions are more limited.

An encouragement to exercise more?
A systematic review and meta-analysis of studies on the effect of interventions based on physical activity monitors was carried out by Danish researchers in 2022. As a first step, the researchers did a systematic review where they analyzed 876 articles published on the subject, of which 755 articles were excluded because they did not meet the established quality criteria (poor study design, protocol, intervention, comparison, population, etc.). They then contacted the authors of 105 studies to obtain detailed protocols and relevant data that would not have been included in their studies. This illustrates how difficult it is to carry out this type of synthesis study and that the studies published are of variable quality.

The systematic review retained 121 randomized controlled studies with 16,743 participants, where the average duration of the interventions was 12 weeks. At the very beginning of the intervention, the number of steps taken daily was 6994 on average, and the average body mass index was 27.8 (overweight). The three main aims of the study were to assess the impact of the intervention (wearing a monitor) on: 1) physical activity in general; 2) moderate to high intensity physical activity; 3) sedentary lifestyle.

  • Physical activity in general. For this meta-analysis, the results of 103 studies with 12,840 participants were included. Participants who wore a physical activity tracker did on average more physical activity than those who did not wear it. The increase was significant, albeit modest: 1235 steps more on average daily by wearers of a physical activity monitor.
  • Moderate to vigorous intensity physical activity. The meta-analysis on the effect of a monitor intervention on moderate-to-vigorous intensity physical activity, which included 63 studies with 8250 participants, also showed that wearing a physical activity monitor had a positive impact on the amount of moderate-to-vigorous intensity physical activity, about 48.5 minutes more per week.
  • Sedentary lifestyle. Interventions with a monitor indicated a slight favourable effect on sedentary time, a reduction of 9.9 minutes on average per day.

The authors conclude that the level of evidence for the effects of interventions based on the wearing of physical activity monitors is low for physical activity in general and moderate for moderate-to-vigorous intensity physical activity and for sedentary lifestyle. The effects on physical activity and moderate-to-vigorous physical activity of monitor-based interventions are well established, but may be overestimated due to publication bias, i.e., that researchers sometimes tend to publish their results only if their study is positive.

Detection of atrial fibrillation with a smartwatch
Atrial fibrillation is the most commonly diagnosed type of cardiac arrhythmia and affects more than 37 million people worldwide. This type of cardiac arrhythmia is associated with an increased risk of cardiovascular disease (5 times higher for stroke) and premature mortality.

Smartwatches, such as the Apple Watch for example, contain optical sensors that measure users’ heart rate by emitting green light through the skin of the wrist. An Apple Watch app uses algorithms that help identify abnormalities that suggest atrial fibrillation.

In a study funded by Apple, researchers wanted to test whether the Apple Watch could really be useful for detecting episodes of atrial fibrillation (AF). During the 8 months of the study with 419,297 participants, 2161 (0.52%) of them received irregular pulse notifications. Of these, those whose symptoms were not urgent were mailed an electrocardiogram (ECG) recorder (ePatch), which they wore for 7 days. Of the 450 participants who returned the ECG recorder for data analysis, 34% had confirmed episodes of atrial fibrillation, while 66% of them could not be confirmed. The main criticisms (see here and here) of this study are that the detection of AF by the Apple Watch is not very specific and not very sensitive, and that this type of use could do more harm than good by creating concern, promoting overdiagnosis and overtreatment and therefore causing a waste of health system resources. In addition, the high cost of this type of smartwatch means that it could not be deployed on a large scale, if the technology were to improve one day.

Smartwatches are continually being improved, so the performance gap with medical-grade devices keeps getting smaller. Physicians should be open to reviewing the data generated by smartwatches as it could yield personalized information useful for patient treatment. However, there is a lack of a regulatory framework to standardize these data and incorporate them into regular clinical practice. These devices have the potential to generate huge amounts of biometric data that could lead to unnecessary and costly testing, with consequences for patients and the healthcare system.

Other uses

Blood pressure measurement
Hypertension is a very common cause of several cardiovascular diseases and premature death. The presence of blood pressure sensors in consumer wearable devices could potentially improve the detection of hypertension, particularly nocturnal hypertension which is associated with the worst consequences. There are devices with a cuff, but devices without a cuff have recently been developed, making it possible to consider their use for the measurement of ambulatory blood pressure. The results of comparisons of these new devices with existing medical devices are encouraging, but this new technology is still in its infancy and will need to be further refined and studied.

Other sensors
There are minimally invasive biochemical sensors that measure molecules of interest in physiological fluids. For example, continuous glucose monitors measure glucose in the interstitial fluid (under the skin, not in the blood). These monitors have been clinically validated, but it remains difficult to integrate them into consumer portable devices. Sensors using sweat or saliva could be more easily integrated into wearable devices, but this remains to be developed.

Biomechanical sensors incorporated into clothing or shoes, such as the ballistocardiogram and seismocardiogram or dielectric sensors, have been developed with the aim of passively and continuously measuring cardiac output, as well as the volume and weight of liquids in the lungs. These devices could be useful for monitoring the condition of people with heart failure.

Smart wearables are constantly being perfected and they have a bright future ahead of them. However, it will be necessary to ensure that these devices are accessible to all and that they do not negatively impact the health system by generating too many biometric data and unnecessary clinical tests. In addition, smart wearables will need to be evaluated and subjected to strict standards to ensure their quality and effectiveness. The medical profession will probably have to open up more to the use of these devices, which allow remote monitoring, especially in these times of the COVID-19 pandemic when there has been a significant decrease in patient visits to their doctor’s office.

Sudden cardiac death in senior high-performance athletes

Sudden cardiac death in senior high-performance athletes

OVERVIEW

  • Sudden cardiac death that affects senior athletes during exercise is a very rare phenomenon, with an incidence about 100 times lower than sudden death affecting the general population.
  • On the contrary, regular exercise is associated with a strong reduction in the risk of sudden death and premature mortality in general.
  • The large volumes of exercise performed by senior athletes are associated with an increased risk of certain cardiac anomalies (calcification of the coronary arteries, myocardial fibrosis), but the contribution of these anomalies to the phenomenon of sudden death remains uncertain.
  • In the majority of cases, it is rather the presence of an underlying coronary artery disease that is responsible for sudden death affecting athletes, and they must therefore remain attentive to the appearance of unusual symptoms and ensure that they control well-established risk factors for atherosclerosis, such as cholesterol levels, blood pressure and type 2 diabetes.

As the name suggests, sudden cardiac death is defined as death caused by the sudden and unexpected stopping of the heartbeat, usually an hour or less after the onset of the first symptoms. Sudden death is responsible for approximately 50% of deaths from cardiovascular disease and is often the first (and last) symptom of an underlying cardiovascular disease. In Western countries, the incidence of sudden cardiac death ranges from 50–100 events per 100,000 people per year and is caused in approximately 75% of cases by the presence of coronary artery disease (known or unknown), the remainder being mainly of congenital origin (cardiomyopathies, channelopathies). In Canada, for example, it is estimated that sudden cardiac death affects 97 people per 100,000, which corresponds to about 35,000 deaths annually (about 9,000 per year in Quebec), or about 10% of overall mortality (there were 307,132 deaths in Canada in 2020-21).

Sudden death of athletes: A rare phenomenon
Although sudden cardiac death is very common, we mainly hear about this phenomenon when it affects athletes, for example, during a marathon. This is paradoxical, because while it is understandable that the deaths of people in excellent physical shape and in the prime of life might strike the imagination, the heavy media coverage surrounding these deaths can give the impression that the practice of sports activities represents an important risk factor for sudden death, which is absolutely not the case. In fact, it is well established that sudden deaths associated with sports are very rare phenomena, accounting for only about 5% of all sudden deaths that occur each year in the general population.

Despite this low incidence, it is important to understand the factors responsible for these sudden deaths in athletes. A very large number of studies have looked into this question in recent years to better understand the mechanisms involved, of course, but also to determine whether the risk of these premature deaths could be related, at least in part, to the very large volumes of exercise that are required to achieve athletic performance. In other words, can you exercise too much? Is there a limit beyond which the amount of exercise becomes excessive for the heart and can cause damage that will increase the risk of sudden death?

Senior athletes
Sudden cardiac death in sports is defined as death that occurs during or within one hour of the completion of a sports activity. A French study, which has since become a classic, has shown that the vast majority of these deaths affect people aged 35 and over and occur mainly (90%) in the context of leisure sports activities (Figure 1). These senior athletes (master athletes) represent the sub-population most at risk of sudden sports death, especially since this group of people is constantly increasing, with more and more middle-aged people participating in endurance sports. In the United States, for example, the number of people who have completed a marathon has quadrupled over the past 25 years, increasing from 5 to 20 million runners per year, more than half of whom are over the age of 35.

Figure 1. Distribution of sports-related sudden cardiac death by age. The values represent the total number of athletes who died in France during a 5-year period in the general population (blue rectangles) and among young people participating in individual or team organized competitive sports (red rectangles). Note that the vast majority (95%) of deaths occurred among people aged 35 and over. Taken from Marijon et al. (2011).


Men at risk
As mentioned earlier, sudden death caused by intense physical exertion remains a rare phenomenon, with an incidence of about 0.5-1.0 deaths per 100,000 participants, which is about 100 times less than the sudden death that occurs in the general population, outside of a sports context (50–100 per 100,000 people) (Table 1).

Male athletes represent the vast majority of these deaths, with a risk of sudden death 10 to 20 times higher than that observed in women. This difference is observed for all sports activities, including the marathon, and is probably related to the protective effect of estrogen against the development of coronary heart disease, one of the main causes of sudden death (see below).

Table 1. Incidence of sports-related sudden cardiac death, by age and sex.
Note the increased risk of sudden death in older men, especially for triathlon.
*For comparison, the incidence of sudden death observed for the Montreal metropolitan area in 2001 is shown.

 Incidence of sudden cardiac death
(per 100,000 participants)
Sport in generalTotalMenWomen
All ages0.551.010.05
35-54 years0.661.250.05
55-75 years0.751.420.07
Marathon
All ages
(22-65 years)
0.540.900.16
Triathlon1.742.40.74
40-49 years3.966.080.96
50-59 years6.679.612.12
≥ 60 years12.918.610
Sudden death in general
(not related to sport)*
5366.739.7

The risk of sudden death for male athletes also seems to increase with age (20% increase among those aged 55-75 compared to 35-55-year-olds for sports in general), while women do not seem to be so affected by aging. This impact of age is particularly striking for triathlon, where the risk of sudden death begins to climb as early as age 40 and increases each decade thereafter to become several times higher at age 60 (18.6 per 100,000) than the risk observed for all triathletes (1.74 per 100,000). It should be noted that two thirds of sudden deaths that occur during triathlons occur in the initial swimming stage, which could explain the much higher risk of death during these events than that observed for the marathon. It has been proposed that this higher incidence of sudden death during the swimming event may be due to a combination of several factors, including 1) a sudden rise in catecholamine (adrenaline, noradrenaline) levels caused by the stress of the beginning of the competition; 2) the chaotic start caused by the simultaneous entry of several participants into the water, which causes contact between the competitors and exposure to difficult conditions (big waves, cold water). These factors could play a role in triggering arrhythmias leading to cardiac arrest, especially in people with underlying coronary artery disease.

Overall, sudden sports-related deaths are therefore relatively infrequent and most senior athletes are not at major risk of death during periods devoted to exercise. On the other hand, older men (40 years and over) should be aware that certain very demanding sports, such as triathlon, carry a higher risk of sudden cardiac death.

The exercise paradox
As mentioned earlier, sudden death caused by exertion is most of the time the clinical manifestation of an underlying and asymptomatic coronary artery disease, but which manifests itself suddenly following the significant increase in the workload of the heart during intense exercise. In most cases, the stress imposed on the heart causes the atherosclerotic plaques present inside the coronary arteries to rupture, leading to the formation of thrombi (clots) that block the flow of blood to the heart muscle.

First of all, it should be mentioned that athletes are much less at risk of sudden cardiac death caused by intense exertion than people who are sedentary and therefore less physically fit. Several studies (herehere and here, for example) have indeed reported dramatic increases (17 to 56 times) in the risk of sudden death related to effort in these sedentary people, with in particular an increase in the risk of infarction of up to almost 100 times.

In all cases, however, these large increases in the risk of sudden death are greatly mitigated in people who regularly exercise. This protection is particularly dramatic with regard to the risk of infarction caused by exertion, with a reduction in risk of approximately 50 times observed in people who train regularly, at least 5 times per week (Figure 2). There thus seems to be a certain “exercise paradox”: on the one hand, vigorous exercise can considerably increase the risk of sudden cardiac death in the short term, while, on the other hand, regular exercise confers a strong protection against this risk of sudden death. For example, several studies have shown that just 30 minutes of moderate activity such as walking, 5 times a week, reduces the risk of cardiovascular disease by 20%, a reduction that reaches 30–40% for an equivalent amount of vigorous exercise. The benefits associated with regular physical activity therefore far outweigh the low risk of mortality that can occur during sporting activities.

Figure 2. Effect of regular physical exercise on the risk of myocardial infarction caused by vigorous exercise. Taken from Mittelman et al. (1993).

Cap on the health benefits
It is usually recommended to do a minimum of 150 minutes of moderate exercise (e.g., walking) or 75 minutes of vigorous exercise (e.g., running) per week to reap the health benefits of physical activity. It should be mentioned, however, that these recommendations are a little “timid”, as several studies indicate that higher volumes of exercise maximize the reduction in the risk of premature mortality associated with physical activity (Figure 3).

Figure 3. Reduction in the risk of mortality according to the volume of exercise carried out per week. Note the cap of benefits (40% reduction in mortality) observed from a volume of exercise corresponding to 2–3 times the amount recommended by the WHO. Adapted from Arem et al. (2015).

Someone who follows the WHO recommendations to the letter, for example by doing 150 minutes of moderate activity, which corresponds to approximately 7.5 MET-h per week (see the box for the calculation), sees their risk of dying prematurely decrease by 20%. An interesting protection, but which nevertheless remains well below that obtained if the volume of exercise is increased to reach 2 to 3 times the recommended quantities (40% reduction in mortality). On the other hand, it is important to note that there is a limit to the benefits of exercise, since higher volumes of physical activity do not bring additional reductions in mortality, even at amounts 10 times greater than those recommended (Figure 3). As a result, the considerable volumes of exercise that are carried out by senior athletes must above all be considered as sporting feats, often remarkable and beyond the reach of ordinary people, but not as a way to improve health.

Exercise intensity and volume
Exercise intensity is usually expressed as a metabolic equivalent (MET), using resting basal energy expenditure as a benchmark. For example, brisk walking, which is considered moderate-intensity physical activity, causes 3 to 4 times more energy expenditure than sitting still (3 to 4 METs). The energy expenditure of running, which is considered vigorous physical activity, is 6 to 8 times greater than at rest (6 to 8 METs). The volume of exercise performed by a person can be easily calculated by multiplying the duration of the exercise by its intensity. Thus, 150 minutes of moderate activity (4 METs) or 75 minutes of vigorous activity (8 METs) correspond in both cases to a volume of 600 MET-min or 10 MET-h per week.

In the study presented in Figure 3, the greatest reduction in the risk of premature death is observed in people who do 2 to 3 times the recommended amounts of exercise, i.e., 300–450 minutes of moderate activity or 150–225 minutes of vigorous activity (15–22.5 MET-h per week). In concrete terms, these volumes of exercise correspond to approximately one hour of walking or half an hour of running per day.

While the cap on the benefits of regular physical activity on reducing mortality is well established, there is still a gray area with regard to the extremely high volumes of exercise carried out over many years by some senior athletes. In several studies (hereherehereherehere and here, for example), it is indeed observed that athletes who do enormous amounts of exercise (10 times or more of the recommended amounts) have a risk of mortality slightly higher than those who do it optimally (3 times the recommended amounts) (see for example Figure 3). This diminished benefit is not statistically significant due to the small number of extremely active athletes (typically less than 3% of study participants), but it nevertheless raises the possibility that very large amounts of exercise, repeatedly performed for many years, can exceed the physiological capacities of the body and cause certain damages that reduce the benefits normally associated with an optimal amount of exercise. Sudden deaths affecting athletes despite their great physical condition could therefore be a manifestation of this damage.

Athlete’s heart
It has been observed that very high levels of exercise promote the appearance of three main cardiac abnormalities, namely atrial fibrillation, calcification of the coronary arteries, and myocardial fibrosis. The increased risk of atrial fibrillation in senior athletes is a very well-documented phenomenon, but this electrical disorder does not seem to play a major role in the phenomenon of sudden death in healthy people and so will not be discussed in more detail here.

However, coronary artery calcification and myocardial fibrosis deserve special attention because of the potential contribution of these abnormalities to the two main causes of sudden cardiac death, i.e., cardiac ischemia (blockage of blood supply) and ventricular arrhythmia (dysregulation of electrical signals allowing the orderly contraction of the heart).

Calcification of the coronary arteries. Coronary artery atherosclerosis is the leading cause of sports-related sudden cardiac death, both in the general population and in athletes, including high-level athletes such as marathon runners. A frequently used method to visualize these plaques is to measure the presence of calcium in the coronary wall by cardiac computed tomography (CT scan) and multiply the area by the signal density to obtain what is called a calcium score (CAC score). These scores have some prognostic value: a score between 1 and 100 is associated with a probability of 13% of cardiovascular events over the next 3 years, a risk that reaches 16% for scores 101–400 and 34% for scores >400.

This approach was used to compare the degree of coronary artery calcification of 284 men with an average age of 55 years based on the usual amount of exercise carried out each week since the age of 12 years. The results show that 68% of the most active participants throughout their life (>2000 MET-min per week, which is equivalent to approximately one hour of running each day) had a calcium score greater than zero, compared to only 43% in those who were moderately active (<1000 MET-min per week) (Figure 4).

Figure 4. Comparison of the prevalence of coronary artery calcification according to the amount of exercise performed each week over several years. Note the increase in the percentage of athletes with a calcium score greater than zero (red rectangles) for higher volumes of exercise (>2000 MET-min per week for more than 30 years). Taken from Aengevaeren et al. (2017).

In the same vein, a study carried out among senior athletes (over 40 years old) who had practised a very intensive training program for at least 10 years (more than 16 km of running or 50 km of cycling per day, with participation in at least 10 endurance competitions such as marathons and half-marathons) showed that these athletes had a higher prevalence of atherosclerotic plaques in the coronary arteries than men in the control group who exercised much less (44% compared to 22%). In this study, high CAC scores (>300) were observed only in athletes, as well as a significant narrowing (≥50%) of the diameter of the arteries (stenosis) and the presence of this narrowing in more than one vessel. Similar results have also been observed in marathon runners over the age of 50, and so it seems increasingly clear that high amounts of exercise are closely correlated with a higher prevalence of atherosclerotic plaques in the coronary arteries. A very athletic lifestyle therefore does not prevent the development of atherosclerosis, both in the coronary and peripheral arteries.

However, the very low prevalence of sudden cardiac death (and cardiovascular events as a whole) observed in senior athletes suggests that this acceleration of atherosclerosis is not as risky as in the general population. On the one hand, studies indicate that the majority of calcified plaques found in athletes are present in a stable form, unlikely to crack and form a thrombus (clot) blocking the coronaries. In other words, a higher calcium score in an athlete would not have the same prognostic value as a score of the same value in a sedentary individual. On the other hand, the physiological adaptations associated with regular exercise (increased diameter and elasticity of vessels, among others) improve coronary blood flow, which would allow athletes to be less affected by the presence of stenoses and thus avoid coronary events that would affect most people with a similar degree of atherosclerosis.

That being said, atherosclerosis still remains an important cardiovascular risk factor and it would be premature to conclude that the increased presence of plaques in the coronaries of athletes has no impact on their health. In this sense, it should be noted that a follow-up of marathon runners after 6 years showed that an increase in the calcium score is nevertheless associated with an increased risk of cardiovascular accidents in these athletes, going from 1% for scores <100, to 12% for scores of 100–400, and to 21% for scores >400. This is consistent with a study showing that the cardiac arrests suffered by marathon runners during an event were largely caused by an underlying coronary disease that caused an insufficient supply of blood to the heart (ischemia) to sustain the effort. On the other hand, and contrary to what is observed in the general population, none of these ischemia had been caused by a rupture of the atherosclerotic plaques. Overall, it therefore seems that atherosclerotic plaques are indeed more stable in athletes and that their rupture does not represent a major risk of ischemia and sudden death. However, in some athletes, the presence of these plaques can still reduce blood flow to the heart and cause cardiac arrest during sustained and intense effort.

The contribution of coronary artery calcification to the phenomenon of sudden death associated with sports should therefore not be overlooked, even in athletes who display exemplary physical fitness. This is especially true for those who have “converted” to sports later in life, after being exposed for several years to factors that accelerate the development of atherosclerotic plaques, in particular smoking and poor diet. Since atherosclerosis is a generally irreversible process, the burden of plaques that have accumulated during the period preceding the adoption of a more athletic lifestyle remains present and can be expressed in the event of intense and sustained effort. It is thus important to remain attentive to certain signals that could suggest the presence of an underlying coronary disease (unusual shortness of breath, palpitations, pain in the chest, arms or throat). Moreover, it should be noted that about half of senior athletes who suffered a sports cardiac arrest had experienced symptoms in the month preceding the cardiac event.

Myocardial fibrosis. Intense and prolonged exercise (marathon) was observed to be associated with a significant increase in the blood levels of certain markers of damage to cardiac cells (troponin, natriuretic peptide type B) and with dysfunction (reduction in ejection fraction) of the right ventricle (RV) of the heart immediately after the test. This reduction in RV function in response to very intense exercise has been observed in several other studies (see this meta-analysis), suggesting that this area of the heart is particularly at risk of being damaged by very high levels of exercise performed repeatedly and over long periods of time.

These myocardial injuries cause cell breakage and the appearance of fibrotic areas that can be visualized by cardiac magnetic resonance using the late gadolinium enhancement (LGE) technique. A contrast product (gadolinium) is injected and rapidly eliminated from the normal myocardium, but persists longer in the fibrotic areas. By acquiring images more than 10 minutes after the injection, the signal obtained late makes it possible to identify areas of fibrosis.

An analysis of 19 studies involving a total of 509 healthy endurance athletes found that approximately 6% of athletes had a positive LGE signal, indicative of myocardial fibrosis. Studies that have compared LGE in endurance athletes with that affecting less active people (physical activity equal to or lower than the recommendations) show that fibrosis is much more frequent in athletes, with a prevalence of 12% compared to only 1.5%. More recently, a meta-analysis of 12 studies (1350 participants) estimated that the risk of fibrosis is increased by about 7 times in endurance athletes compared to sedentary or less active people (Figure 5).

Figure 5. Increased risk of myocardial fibrosis in senior athletes. Athletes who perform large volumes of exercise over several years have a significantly higher LGE signal than controls who exercise 3 hours or less per week. Taken from Zhang et al. (2020).

This higher prevalence of the LGE signal (and therefore of fibrosis) in athletes is strongly correlated with the number of years of intensive training as well as the number of endurance competitions completed, which strongly suggests that large volumes of high-intensity exercise represent a risk factor for myocardial fibrosis. As mentioned before, the right ventricle seems more sensitive to the stress imposed by intense exercise, and the majority of cases of fibrosis detected in athletes are located in this ventricle, especially in the area that is in contact with the septum separating the two ventricles of the heart.

The presence of these fibrotic areas can in principle disturb the electrical signal and create a “short-circuit” that can cause rapid ventricular tachycardia, capable of degenerating into ventricular fibrillation (causing sudden death). It would therefore be possible that myocardial fibrosis, which preferentially affects endurance athletes, could play a role in the sudden death affecting some of them. In this sense, it should be noted that one study observed that marathon runners who presented an LGE signal were more at risk of cardiovascular events in the two years following diagnosis than athletes without an LGE signal, and another study observed ventricular arrhythmia in athletes with areas of fibrosis (at the level of the epicardium).

In sum, the studies carried out so far indicate that senior athletes who have done large volumes of high-intensity exercise for long periods of time are more likely to have fibrotic lesions in the myocardium. However, the consequences of these fibrosis remain uncertain given the low incidence of sudden cardiac death in this population, and because of studies showing that vigorous physical activity does not seem to increase the risk of ventricular arrhythmia and that people in excellent physical shape are at lower risk of premature mortality. For example, elite athletes (Olympic medallists, for example) live 3–6 years longer than the general population.

In conclusion, sudden cardiac death that occurs during a sports activity remains an extremely rare phenomenon, especially among senior athletes who are regularly active. The health benefits provided by physical activity thus far exceed the very slight risks involved in practising a sport. The amounts of exercise required to benefit the most from this protection are equivalent to approximately 1 hour of walking or ½ hour of running per day, which is far from excessive and represents a goal within reach of most people.

Very large volumes of intense exercise, such as those performed by high-level senior athletes, can induce certain cardiac abnormalities (coronary artery calcification, myocardial fibrosis), but the impact of these abnormalities on the risk of sudden death affecting these athletes remains uncertain. Large-scale prospective studies focusing specifically on athletes, for example the Master Athlete’s Heart study recently initiated in Europe, should make it possible to better identify the risk factors for sudden death in athletes.

In the current state of knowledge, the main risk factor for sudden death in athletes seems to be the same as that of the general population, i.e., the presence of an underlying coronary artery disease which blocks the supply of blood to the heart muscle. For example, in the study of sudden deaths during triathlons, researchers found that 30% of deceased athletes had signs of advanced coronary atherosclerosis. Putting on running shoes every morning does not completely prevent the development of coronary plaques and above all does not eliminate the atherosclerosis that has developed over the years. This is particularly true for athletes who have adopted sports later in life, after having had a suboptimal lifestyle (sedentary lifestyle, smoking, poor diet) for several years. Like the general population, senior athletes who regularly engage in large volumes of exercise and/or participate in endurance events therefore have every advantage in controlling well-established risk factors for atherosclerosis, such as cholesterol levels, blood pressure and type 2 diabetes.

We should also not neglect certain factors such as electrolyte imbalances (hyponatremia, in particular), heat stroke or pure and simple exhaustion which can alter cardiac function, regardless of the state of health of the coronaries. These factors cause intense physiological stress that could explain why the vast majority of deaths that occur during marathons occur in the last quarter of the race

A pro-inflammatory diet increases the risk of dementia

A pro-inflammatory diet increases the risk of dementia

OVERVIEW

  • In a study on aging and diet conducted in Greece, 1,059 older people reported in detail what they ate for three years.
  • At the end of the study, people with the most inflammatory diet had a 3-fold higher risk of developing dementia compared to those whose diet had a low-inflammatory index.
  • The main anti-inflammatory foods are vegetables, fruits, whole grains, tea, and coffee. The main pro-inflammatory foods that should be avoided or eaten infrequently and in small amounts are red meat, deli meats, refined flours, added sugars, and ultra-processed foods.

Dietary Inflammatory Index
Several studies suggest that the nature of the foods we eat can greatly influence the degree of chronic inflammation and, in turn, the risk of chronic disease, including cardiovascular disease. For example, a pro-inflammatory diet has been associated with an increased risk of cardiovascular disease, with a 40% increase in risk in people with the highest index (see our article on the subject).

Pro-inflammatory diet and risk of dementia
In order to see if there is an association between a diet that promotes systemic inflammation and the risk of developing dementia, 1,059 elderly people residing in Greece were recruited as part of the study Hellenic Longitudinal Investigation of Aging and Diet (HELIAD). Only people without a diagnosis of dementia at the start of the study were included in the cohort. The inflammatory potential of the participants’ diet was estimated using the Dietary Inflammatory Index (DII) based on the known effect of various foods on the blood levels of inflammatory markers . The main pro-inflammatory foods are red meat, deli meats, refined flour, added sugars, and ultra-processed foods. Some of the main anti-inflammatory foods are vegetables, fruits, whole grains, tea, coffee, and red wine.

After a follow-up of 3 years on average, 62 people were diagnosed with dementia. Participants who had the diet with the highest inflammatory index had a three-fold higher risk of developing dementia at the end of the study, compared to those with the least inflammatory index. In addition, there appears to be a dose-response relationship, with an increased risk of dementia that increases by 21% for each unit of the inflammatory index.

Inflammation, interleukin-6, and cognitive decline
The study in Greece is not the first to be conducted on the impact of a pro-inflammatory diet on the incidence of dementia. In a Polish study of 222 postmenopausal women, those with cognitive deficits had significantly higher blood levels of interleukin-6 (IL-6; a marker of inflammation), were less educated, and were less physically active, compared to women with normal cognitive functions. Postmenopausal women who had a pro-inflammatory diet were much more likely to have cognitive impairment compared to those who had an anti-inflammatory diet, even after adjusting for age, height, body mass index, level of education, and levels of physical activity. Each one-point increase in the dietary inflammatory index was associated with a 1.55-fold increase in the risk of cognitive impairment.

In addition to these studies, it is interesting to see that a meta-analysis of 7 prospective studies including 15,828 participants showed that there is an association between the concentration of IL-6 in the blood and the overall cognitive decline in the elderly. Participants who had the most circulating IL-6 had a 42% higher risk of suffering cognitive decline than those with low blood IL-6 levels.

Several studies have suggested that systemic inflammation (i.e., outside the central nervous system) may play a role in neurodegeneration, Alzheimer’s disease, and cognitive decline in older adults. People with Alzheimer’s disease and mild cognitive impairment tend to have high blood levels of markers of inflammation (IL-6, TNF-α, CRP). In addition, a study indicates that people who have elevated levels of markers of inflammation during midlife have an increased risk of cognitive decline in subsequent decades.

Since the studies described above are observational, they do not establish a causal link between inflammatory diet and dementia. They only show that there is an association. Further studies are needed in the future to establish a cause and effect relationship and identify the underlying molecular mechanisms.

Evidence from recent studies should encourage experts to more often recommend diets high in flavonoids that decrease systemic inflammation and are conducive to the maintenance of good cognitive health. Mediterranean-type diets or the hybrid MIND diet (Mediterranean-DASH Intervention for Neurodegenerative Delay) with an abundance of plants are particularly effective in reducing or delaying cognitive decline.

Phthalates: A component of certain plastics and cosmetic products harmful to human health

Phthalates: A component of certain plastics and cosmetic products harmful to human health

OVERVIEW

  • Phthalates are chemicals added to plastics to make them more flexible and to some cosmetics to preserve their fragrance.
  • A certain amount of these products are released into the environment, including in food and beverages sold in some plastic containers.
  • Due to their widespread use, phthalates are ingested or absorbed without our knowledge and metabolites of these products are found in most people.
  • Phthalates are endocrine and metabolic disruptors, which are associated with adverse effects on neurodevelopment, childhood asthma, type 2 diabetes, ADHD, childhood and adult obesity, breast and uterine cancer, endometriosis and infertility.
  • Exposure to high-molecular weight phthalates, such as DEHP, has been associated with increased cardiovascular and all-cause mortality.
  • Voices are being raised in the scientific community for the use of phthalates to be subject to stricter regulations.

Phthalates are part of a class of chemicals that are widely used in industry (see Table 1 and Figure 1). High-molecular weight phthalates, such as di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DiNP), are used as plasticizers to impart flexibility to polyvinyl chloride (PVC) materials used to make food packaging, flooring, and medical equipment (tubing, blood bags). Low-molecular weight phthalates, such as diethyl phthalate (DEP) and dibutyl phthalate (DBP), are added to shampoos, lotions and other personal care products to preserve their fragrance.

Since these phthalates are not chemically bound to plastics, they are released into the environment over time and can enter the human body by ingestion, inhalation and absorption through the skin. Once in the body, phthalates are rapidly metabolized and excreted in urine and faeces, so that half of the phthalates are eliminated within 24 hours of entering the body. Despite this rapid elimination, the population is permanently exposed to phthalates since these products are present in consumer products used almost every day. Metabolites of the phthalates DEHP and DiNP are detected in 98% of the total United States population. Daily exposure to a widely used phthalate, DEHP, has been estimated to range from 3 to 30 µg/kg/day, or 0.21 mg to 2.1 mg per day for a person weighing 70 kg (154 lb.).

Table 1. Main phthalates used in consumer products.   Adapted from Zota et al., 2014.

Phthalate  Abbrev.Restricted use in the United StatesCommon sources
Low-molecular weight
Dimethyl phthalateDMPInsect repellents, plastic bottles, food
Diethyl phthalateDEPPerfumes, deodorants, cosmetics, soaps
Di-n-butyl phthalateDnBP++Cosmetics, medications, food packaging, food, PVC applications
Diisobutyl phthalateDiBPCosmetics, food, food packaging
High-molecular weight
Butylbenzyl phthalateBBzP++PVC flooring, food, food packaging
Dicyclohexyl phthalateDCHPFood, food packaging
Di(2-ethylhexyl) phthalateDEHP++PVC applications, toys, cosmetics, food, food packaging, blood bags, catheters
Di-n-octyl phthalateDnOP+PVC applications, food, food packaging
Diisononyl phthalateDiNP+PVC applications, toys, flooring, wall covering
Diisodecyl phthalateDiDP+PVC applications, toys, wires and cables, flooring

 

Figure 1. Chemical structure of the phthalates most commonly used in industry.

 

Phthalates and cardiovascular and all-cause mortality
A study of 5,303 adults in the National Health and Nutrition Examination Survey (NHANES) cohort assessed the association between phthalate exposure and mortality. Participants provided a urine sample in which the major metabolites of phthalates were measured. Exposure to high-molecular weight phthalates was associated with a significant increase in cardiovascular and all-cause mortality during the duration of the study (2001 to 2010). No significant association was observed for exposure to low-molecular weight total phthalates. Participants who were more exposed to high-molecular weight phthalates (third tertile) had a 48% higher risk of death from any cause than participants who were less exposed (first tertile). Examination of the risk associated with each of the phthalate metabolites revealed an association between an elevated urinary level and a 64% increased risk of cardiovascular mortality for monoethyl phthalate (MEP, a low-molecular weight phthalate). The presence of elevated concentrations of two DEHP (high-molecular weight phthalate) metabolites, MEHHP and MECPP, was associated with a 27% and 32% increased risk of all-cause mortality, respectively, compared to the presence of lower concentrations of these metabolites. A third metabolite of DEHP, MEOHP, was associated with a 74% higher risk of cardiovascular mortality (3rd tertile vs. 1st tertile). Extrapolating the results of their study to the US population aged 55 to 64, the authors estimate that approximately 100,000 deaths/year could be attributed to phthalate exposure, at a societal cost of approximately $39 billion.

Phthalates and where food comes from
One study assessed the phthalate exposure of participants in the NHANES cohort, depending on whether they had a meal the day before outside the home (restaurant, fast food chain, cafeteria) or at home. People who ate out had an average of 35% more phthalates in their urine the next day than people who ate at home, mostly foods purchased from the grocery store. The association between eating out and high urinary phthalate concentration was strongest in adolescents. Among teens, those who reported being heavy consumers of fast food and other foods bought outside the home had up to 55% higher phthalate levels than teens who ate at home. Consumption of certain foods in particular, most notably cheeseburgers and similar sandwiches, was associated with increased cumulative exposure to phthalates, but only when these foods were consumed in cafeterias, fast food outlets, and other restaurants. The study authors find the situation worrisome because almost 2/3 of the population in the United States eats food outside of the home at least once a day.

Phthalates and other plasticizers in fast food
A 2021 study measured the levels of phthalates and another plasticizer in samples of burgers, fries, chicken nuggets, chicken burritos and cheese pizza, as well as in plastic gloves used in fast food restaurants to handle food. Samples came from restaurants of major U.S. chains McDonald’s, Burger King, Pizza Hut, Domino’s, Taco Bell, and Chipotle in the San Antonio, Texas area. DEHT, a new plasticizer used as a replacement for phthalates, was detected in highest amounts in food (median: 2.5 mg/kg) and in gloves (28–37% by weight). DnBP and DEHP phthalates were detected in 81% and 70% of food samples, respectively. DEHT concentrations were particularly high in burritos (6 mg/kg) and in burgers (2.2 mg/kg), and this plasticizer was not present in French fries. Cheese pizza contained the lowest levels of plasticizing chemicals (phthalates or not) among the fast food items analyzed. It should be noted that, unlike phthalates, little data is currently available on the toxicity and health effects of new plasticizers such as DEHT, even though they are increasingly used in industry. The results of this study have implications for equity since the African American population in the United States consumes more fast food than other ethnic groups and is more exposed to chemicals from other sources in the United States in their environment.

Phthalates: endocrine disruptors
In a review of all studies on the impact of phthalate exposure on human health, the authors found strong evidence of unfavourable associations for neurodevelopment, sperm quality, and asthma risk in children, as well as moderate to strong evidence of an association with an anogenital distance abnormality in boys (a marker of exposure to endocrine disruptors). Associations between phthalate exposure and the incidence of type 2 diabetes, endometriosis, low birth weight, low testosterone, ADHD, breast and uterine cancer have also been identified with a moderate level of evidence. Finally, other associations have been identified, but with a lower level of evidence, including premature birth, obesity, autism and hearing loss.

Implications for the public
Standards have been adopted in several countries to limit and, in some cases, prohibit the use of phthalates. For example, the use of certain phthalates in toys for very young children has been banned, as they chew and suck their toys. In cosmetics, the use of DEHP, the most problematic phthalate for health, is banned in Europe and in Canada. According to the European Chemicals Agency (ECHA), the derived no-effect levels (DNEL, or “safe dose”) are 34 µg/kg for DEHP, 8.3 µg/kg for DiBP, 6.7 µg/kg for DnBP, and 500 µg/kg for BBzP. This European agency recommended that the use of these 4 phthalates in the form of mixtures in products be limited to 0.1% (w/w) and that the exception for the use of DEHP in the packaging of medical products be abolished.

A significant problem with these “safe doses” was highlighted for DEHP phthalate since, according to a review of 38 articles, the maximum exposure to DEHP measured in the population is more than 6 times greater than the derived no-effect level (242 vs. 34 µg/kg). In addition, for three other phthalates (DiBP, DnBP and BBzP), the authors reported that adverse health effects were associated with exposure levels much lower than the derived no-effect level established by the ECHA. Among these adverse health effects are increased eczema in children, behavioural changes in children, increased body mass index and waist circumference in women and men, and impacts on the fertility of women and men.

Here are some suggestions for limiting exposure to phthalates:

  • Eat at home as much as possible and limit meals from fast food restaurants to a minimum.
  • In the kitchen, use utensils and containers made of glass, porcelain, stainless steel or wood rather than plastic.
  • Do not heat your meals in the microwave in plastic containers, since the heat increases the release of phthalates in food.
  • Carefully read the list of ingredients for body care products (toothpaste, shampoos, etc.) as manufacturers must indicate the presence of phthalates in their products.
  • For body care, choose natural products that contain few ingredients.