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.

Omega-3 fatty acid supplements are ineffective for the prevention of cardiovascular disease

Omega-3 fatty acid supplements are ineffective for the prevention of cardiovascular disease

OVERVIEW

  • The VITAL study in participants who did not have cardiovascular disease and the ASCEND study in diabetic patients did not show a beneficial effect of omega-3 fatty acid supplements on cardiovascular health.
  • The REDUCE-IT study reported a beneficial effect of an omega-3 fatty acid supplement (Vascepa®), while the STRENGTH study reported no effect of another supplement (Epanova®).
  • The divergent results of the REDUCE-IT and STRENGTH studies have raised scientific controversy, mainly about the questionable use of mineral oil as a neutral placebo in the REDUCE-IT study.
  • Overall, the results of the studies lead to the conclusion that omega-3 fatty acid supplements are ineffective in preventing cardiovascular disease, in primary prevention and most likely also in secondary prevention.

Consuming fish on a regular basis (1–2 times per week) is associated with a reduced risk of death from coronary heart disease (see these meta-analyses here and here). In addition, favourable associations between fish consumption and the risks of type 2 diabetes, stroke, dementia, Alzheimer’s disease and cognitive decline have also been identified.

A large number of studies have suggested that it is mainly omega-3 (O-3) fatty acids, a type of very long-chain polyunsaturated fatty acid found in high amounts in several fish species, that are the cause of the positive health effects of eating fish and other seafood. For example, a meta-analysis of 17 prospective studies published in 2021 indicates that the risk of dying prematurely was significantly lower (15–18%) in participants who had the most circulating O-3s, compared to those who had the least. In addition, favourable associations of the same magnitude were observed for cardiovascular and cancer-related mortality.

Since eating fish is associated with better cardiovascular health, why not isolate the “active ingredient”, i.e. the omega-3 fatty acids it contains and make supplements with them? This seemed like a great idea; the same pharmacological approach has been applied successfully to a host of plants, fungi and microorganisms, which has made it possible to create drugs. One such example is aspirin, a derivative of salicylic acid found in the bark of certain tree species, quinine extracted from the cinchona shrub (antimalarial), digitoxin extracted from purple digitalis (treatment of heart problems), paclitaxel from yew (anticancer), etc.

Are marine O-3 supplements just as or even more effective than the whole food from which they are extracted? Several randomized controlled studies (RCTs) have been carried out in recent years to try to prove the effectiveness of O-3s. Meta-analyses of RCTs (see here and here) indicate that O-3 supplements (EPA and DHA) have little or no effect in primary prevention, i.e. on the risk of developing cardiovascular disease or dying prematurely from cardiovascular disease or any other cause. In contrast, data from some studies indicated that O-3 supplements may have beneficial effects in secondary prevention, i.e. in people with cardiovascular disease.

In order to obtain a higher level of evidence, several large, well-planned and controlled studies have been carried out recently: ASCEND, VITAL, STRENGTH and REDUCE-IT. The VITAL study (VITamin D and omegA-3 TriaL) in 25,871 participants who did not have cardiovascular disease and the ASCEND study (A Study of Cardiovascular Events in Diabetes) in 15,480 diabetic patients did not demonstrate any beneficial effects of O-3 supplements on cardiovascular health.

The results of the REDUCE-IT (REDUction of Cardiovascular Events with Icosapent ethyl-Intervention Trial) and STRENGTH (Outcomes Study to Assess STatin Residual Risk Reduction With EpaNova in HiGh CV Risk PatienTs With Hypertriglyceridemia) studies were then published. The results of these studies were eagerly anticipated since they tested the effect of O-3 supplements on major strokes at high doses (3000–4000 mg O-3/day) in patients at risk treated with a statin to lower blood cholesterol, but who had high triglyceride levels.

The results of these two studies are divergent, which has raised scientific controversy. The REDUCE-IT study reported a significant reduction of 25% in the number of cardiovascular events in the group of patients who took daily O-3 supplementation (Vascepa®; ethyl-EPA), compared to the group of patients who took a placebo (mineral oil). The STRENGTH study reported an absence of effect of O-3 supplements (Epanova®; a mixture of EPA and DHA in the form of carboxylic acids) on major cardiovascular events in patients treated with a statin, compared to the group of patients who took a corn oil placebo.

Several hypotheses have been proposed to explain the different results between the two large studies. One of them is that the mineral oil used as a placebo in the REDUCE-IT study may have caused adverse effects that would have led to a false positive effect of the O-3 supplement. Indeed, mineral oil is not a neutral placebo since it caused an average increase of 37% of C-reactive protein (CRP), a marker of systemic inflammation in the control group, as well as a 7.4% increase in LDL cholesterol and 6.7% in apolipoprotein B compared to the group that took Vascepa. These three biomarkers are associated with an increased risk of cardiovascular events.

Two other hypotheses could explain the difference between the two studies. It is possible that the moderately higher plasma levels of EPA obtained in the REDUCE-IT study could be the cause of the beneficial effects seen in this study, or that the DHA used in combination with EPA in the STRENGTH study may have counteracted the beneficial effects of EPA.

To test these two hypotheses, the researchers responsible for the STRENGTH study performed post-hoc analyses of the data collected during their clinical trial. Patients were classified according to their plasma EPA level after 12 months of daily supplementation with O-3. Thus, in the first tertile, patients had an average plasma EPA concentration of 30 µg/mL, those in the second tertile: 90 µg/mL, and those in the third tertile: 151 µg/mL. The mean plasma concentration of EPA in the third tertile (151 µg/mL) is comparable to that reported in the REDUCE-IT study (144 µg/mL). Analyses show that there was no association between the plasma concentration of EPA or DHA and the number of major cardiovascular events. The authors conclude that there is no benefit to taking O-3 supplements for secondary prevention, but they suggest that more studies should be done in the future to compare mineral oil and corn oil as placebos and also to compare different formulations of omega-3 fatty acids.

Overall, the results of recent studies lead to the conclusion that O-3 supplements are ineffective in preventing cardiovascular disease, in primary prevention and most likely also in secondary prevention. It should be noted that, taken in large amounts, O-3 supplements can have unwanted effects. In fact, in both the STRENGTH and REDUCE-IT studies, the incidence of atrial fibrillation was significantly higher with the use of O-3 supplements. In addition, bleeding was more common in patients who took ethyl-EPA (Vascepa®) in the REDUCE-IT study than in patients who took the placebo. It therefore seems safer to eat fish once or twice a week to maintain good health than to take ineffective and expensive supplements.

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

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

OVERVIEW

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The importance of properly controlling your blood pressure

The importance of properly controlling your blood pressure

OVERVIEW

  • Hypertension is the main risk factor for cardiovascular disease and is responsible for 20% of deaths worldwide.
  • Early hypertension, before the age of 45, is associated with an increased risk of cardiovascular disease, cognitive decline and premature mortality.
  • Adopting an overall healthy lifestyle (normal weight, not smoking, regular physical activity, moderate alcohol consumption, and a good diet including sodium reduction) remains the best way to maintain adequate blood pressure.

According to the latest data from the Global Burden of Disease Study 2019, excessively high blood pressure was responsible for 10.8 million deaths worldwide in 2019, or 19.2% of all deaths recorded. This devastating impact is a direct consequence of the enormous damage caused by hypertension on the cardiovascular system. Indeed, a very large number of studies have clearly shown that excessive blood pressure, above 130/80 mm Hg (see box for a better understanding of blood pressure values), is closely linked to a significant increased risk of coronary heart disease and stroke.

 

Systolic and diastolic

It is important to remember that blood pressure is always expressed in the form of two values, namely systolic pressure and diastolic pressure. Systolic pressure is the pressure of the blood ejected by the left ventricle during the contraction of the heart (systole), while diastolic pressure is that measured between two beats, during the filling of the heart (diastole). To measure both pressures, the arterial circulation in the arm is completely blocked using an inflatable cuff, then the cuff pressure is allowed to gradually decrease until blood begins to flow back into the artery. This is the systolic pressure. By continuing to decrease the swelling of the cuff, we then arrive at a pressure from which there is no longer any obstacle to the passage of blood in the artery, even when the heart is filling. This is the diastolic pressure. A blood pressure value of 120/80 mm Hg, for example, therefore represents the ratio of systolic (120 mm Hg) and diastolic (80 mm Hg) pressures.

As shown in Figure 1, this risk of dying prematurely from coronary heart disease is moderate up to a systolic pressure of 130 mm Hg or a diastolic pressure of 90 mm Hg, but increases rapidly thereafter to almost 4 times for pressures equal to or greater than 150/98 mm Hg. This impact of hypertension is even more pronounced for stroke, with an 8 times higher risk of mortality for people with systolic pressure above 150 mm Hg and 4 times higher for a diastolic pressure greater than 98 mm Hg (Figure 1, bottom graph). Consequently, high blood pressure is by far the main risk factor for stroke, being responsible for about half of the mortality associated with this disease.


Figure 1. Association between blood pressure levels and the risk of death from coronary heart disease or stroke. From Stamler et al. (1993).

Early hypertension
Blood pressure tends to increase with aging as blood vessels become thicker and less elastic over time (blood circulates less easily and creates greater mechanical stress on the vessel wall). On the other hand, age is not the only risk factor for high blood pressure: sedentary lifestyle, poor diet (too much sodium intake, in particular), and excess body weight are all lifestyle factors that promote the development of hypertension, including in younger people.

In industrialized countries, these poor lifestyle habits are very common and contribute to a fairly high prevalence of hypertensive people, even among young adults. In Canada, for example, as many as 15% of adults aged 20–39 and 39% of those aged 40–59 have blood pressure above 130/80 mm Hg (Figure 2).


Figure 2. Prevalence of hypertension in the Canadian population. Hypertension is defined as systolic pressure ≥ 130 mm Hg or diastolic pressure ≥ 80 mm Hg, according to the 2017 criteria of the American College of Cardiology and the American Heart Association. The data are from Statistics Canada.

This proportion of young adults with hypertension is lower than that observed in older people (three in four people aged 70 and over have hypertension), but it can nevertheless have major repercussions on the health of these people in the longer term. Several recent studies indicate that it is not only hypertension per se that represents a risk factor for cardiovascular disease, but also the length of time a person is exposed to these high blood pressures. For example, a recent study reported that onset of hypertension before the age of 45 doubles the risk of cardiovascular disease and premature death, while onset of hypertension later in life (55 years and older) has a much less pronounced impact (Figure 3). These findings are consistent with studies showing that early hypertension is associated with an increased risk of cardiovascular mortality and damage to target organs (heart, kidneys, brain). In the case of the brain, high blood pressure in young adults has been reported to be associated with an increased risk of cognitive decline at older ages. Conversely, a recent meta-analysis suggests that a reduction in blood pressure with the help of antihypertensive drugs is associated with a lower risk of dementia or reduced cognitive function.

Figure 3. Change in risk of cardiovascular disease (red) or death from all causes (blue) depending on the age at which hypertension begins. Adapted from Wang et al. (2020).

Early hypertension should therefore be considered an important risk factor, and young adults can benefit from managingtheir blood pressure as early as possible, before this excessively high blood pressure causes irreparable damage.

The study of barbershops
In African-American culture, barbershops are gathering places that play a very important role in community cohesion. For health professionals, frequent attendance at these barbershops also represents a golden opportunity to regularly meet Black men to raise their awareness of certain health problems that disproportionately affect them. This is particularly the case with hypertension: African American men 20 years and older have one of the highest prevalence of high blood pressure in the world, with as many as 59% of them being hypertensive. Also, compared to whites, Black men develop high blood pressure earlier in their lives and this pressure is on average much higher.

A recent study indicates that barbershops may raise awareness among African Americans about the importance of controlling their blood pressure and promoting the treatment of hypertension. In this study, researchers recruited 319 African Americans aged 35 to 79 who were hypertensive (average blood pressure approximately 153 mm Hg) and who were regular barbershop customers. Participants were randomly assigned to two groups: 1) an intervention group, in which clients were encouraged to see, in the barbershops, pharmacists specially trained to diagnose and treat hypertension and 2) a control group, in which barbers suggested that clients make lifestyle changes and seek medical attention. In the intervention group, pharmacists met regularly with clients during their barbershop visits, prescribed antihypertensive drugs, and monitored their blood pressure.

After only 6 months, the results obtained were nothing short of spectacular: the blood pressure of the intervention group fell by 27 mm Hg (to reach 125.8 mm Hg on average), compared to only 9.3 mm Hg (to reach 145 mm Hg on average) for the control group. Normal blood pressure (less than 130/80 mm Hg) was achieved in 64% of participants in the intervention group, while only 12% of those in the control group were successful. A recent update of the study showed that the beneficial effects of the intervention were long-lasting, with continued pressure reductions still observed one year after the start of the study.

These reductions in blood pressure obtained in the intervention group are of great importance, as several studies have clearly shown that pharmacological treatment of hypertension causes a significant reduction in the risk of cardiovascular diseases, including coronary heart disease and stroke, as well as kidney failure. This study therefore shows how important it is to know your blood pressure and, if it is above normal, to normalize it with medication or through lifestyle changes.

The importance of lifestyle
This last point is particularly important for the many people who have blood pressure slightly above normal, but without reaching values ​​as high as those of the participants of the study mentioned above (150/90 mm Hg and above). In these people, an increase in the level of physical activity, a reduction in sodium intake, and body weight loss can lower blood pressure enough to allow it to reach normal levels. For example, obesity is a major risk factor for hypertension and a weight loss of 10 kg is associated with a reduction in systolic pressure from 5 mm to 10 mm Hg. This positive influence of lifestyle is observed even in people who have certain genetic variants that predispose them to high blood pressure. For example, adopting an overall healthy lifestyle (normal weight, not smoking, regular physical activity, moderate alcohol consumption, and a good diet including sodium reduction) has been shown to be associated with blood pressure approximately 3 mm Hg lower and a 30% reduction in the risk of cardiovascular disease, regardless of the genetic risk. Conversely, an unhealthy lifestyle increases blood pressure and the risk of cardiovascular disease, even in those who are genetically less at risk of hypertension.

In short, taking your blood pressure regularly, even at a young age, can literally save your life. The easiest way to regularly check your blood pressure is to purchase one of the many models of blood pressure monitors available in pharmacies or specialty stores. Take the measurement in a seated position, legs uncrossed and with the arm resting on a table so that the middle of the arm is at the level of the heart. Two measurements in the morning before having breakfast and drinking coffee and two more measurements in the evening before bedtime (wait at least 2 hours after the end of the meal) generally give an accurate picture of blood pressure, which should be below 135/85 mm Hg on average according to Hypertension Canada.

Aspirin for primary prevention of cardiovascular events?

Aspirin for primary prevention of cardiovascular events?

Updated on January 24, 2019

It is well established that aspirin is beneficial in secondary prevention, that is, for patients who have already suffered a myocardial infarction or stroke or who have a condition such as angina, acute coronary syndrome, or myocardial ischemia, and for those who have undergone coronary artery bypass grafting or coronary angioplasty. It has been suggested that aspirin may also be beneficial in primary prevention, i.e., to prevent cardiovascular events in those who have never had one, but are at risk. For the last few decades, aspirin has been used at low doses to prevent myocardial infarction and stroke; however, a recent study indicates that this drug does not prevent a first heart attack or stroke in people with moderate cardiovascular risk. In another study, this time of people with type 2 diabetes, taking aspirin modestly reduced the risk of cardiovascular events, but increased the risk of serious bleeding.

Primary prevention in people at moderate risk
Low-dose aspirin (100 mg/day) does not prevent a first heart attack or stroke in people at moderate risk of developing cardiovascular disease according to the ARRIVE study (Aspirin to Reduce Risk of Initial Vascular Events), published in The Lancet in August 2018. Aspirin has been tested in primary prevention over an average of 5 years, with 12,546 people living in the United Kingdom, Poland, Germany, Italy, Ireland, Spain and the USA. During these years, participants who took 100 mg of aspirin daily did not have significantly fewer vascular events than those who took a placebo . There were fewer vascular events than expected in this study, suggesting that participants had low cardiovascular risk rather than moderate risk. Gastrointestinal bleeding, which was mostly mild, was significantly higher in the aspirin group than in the placebo group .

The authors of the ARRIVE study conclude that “The use of aspirin remains a decision that should involve a thoughtful discussion between a clinician and a patient, given the need to weigh cardiovascular and possible cancer prevention benefits against the bleeding risks, patient preferences, cost, and other factors. The ARRIVE data must be interpreted and used in the context of other studies, which have tended to show a reduction primarily in myocardial infarction, with less of an effect on total stroke (including both ischaemic and haemorrhagic stroke).

Primary prevention in people with diabetes
Aspirin has been tested for primary prevention in 15,480 people with type 2 diabetes, who are therefore at increased risk of developing or dying from cardiovascular disease. During the seven years of the randomized study, people who took 100 mg of aspirin daily had significantly fewer serious vascular events than those who took a placebo . In contrast, major bleeding was greater in the aspirin group than in the placebo group . There was no significant difference between the group that took aspirin and the placebo group for gastrointestinal cancer incidence or any type of cancer . The authors of this study conclude that the benefits of aspirin for people with diabetes are largely outweighed by the risk of bleeding.

Aspirin for prevention in the elderly
The effects of daily low-dose aspirin were evaluated specifically in the elderly in the ASPREE study (Aspirin in Reducing Events in the Elderly), the results of which were published as three articles in the New England Journal Of Medicine (see here, here, and here). The study enlisted 19,114 Australians and Americans aged 70 or older who did not have cardiovascular disease, dementia, or physical disability. Participants were randomly assigned to take a 100 mg enteric-coated aspirin or placebo tablet daily for 5 years. The primary endpoint was a composite endpoint including death, dementia, and persistent physical disability. Secondary endpoints included severe bleeding and cardiovascular disease (nonfatal myocardial infarction, fatal coronary heart disease, fatal or nonfatal stroke, hospitalization for heart failure).

Aspirin did not prolong disability-free survival in the elderly and did not decrease the risk of cardiovascular disease, but it increased the rate of serious bleeding compared with placebo. The composite rate of mortality, dementia, and persistent physical disability was 21.5 and 21.2 events per 1,000 person-years in the group who took aspirin and in the placebo group, respectively. The rates of cardiovascular events were 10.7 and 11.3 events per 1,000 person-years in the aspirin group and the placebo group, respectively. The rate of serious bleeding was significantly higher (P <0.001) in the aspirin group (8.6 events per 1,000 person-years) than in the placebo group (6.2 events per 1,000 person-years). Finally, the all-cause mortality rate was higher in the aspirin group than in the placebo group, a result mainly attributable to deaths from cancer. Since an increase in mortality has not been observed in previous studies on aspirin used for prevention, this unexpected result should be interpreted with caution according to the authors.

Systematic review and meta-analysis
A synthesis of 13 randomized controlled trials of aspirin for primary prevention of cardiovascular disease, including the 3 major trials in 2018, was published in January 2019 in JAMA. All studies included 164,225 participants aged 53 to 74 and a follow-up of 1,050,511 person-years. This meta-analysis confirms that aspirin is associated with a decreased risk of cardiovascular events (cardiovascular mortality, nonfatal myocardial infarction, nonfatal stroke) and an increased risk of major bleeding. Aspirin was associated with an 11% reduction in relative risk (absolute risk reduction of 0.38%) of cardiovascular events and a 43% greater relative risk of major bleeding (absolute risk increase of 0.47%). As a result, 265 people will need to be treated with aspirin for 5 years to prevent a cardiovascular event, but one in 210 treated people will experience major bleeding. Because of the unfavourable benefit-to-disadvantage ratio, the European guidelines do not recommend taking aspirin until cardiovascular disease occurs (secondary prevention), i.e., at a time when the benefits outweigh the risks of adverse effects. On the other hand, the US Preventive Services Task Force (USPSTF) recommends improving the benefit-harm ratio for aspirin in primary prevention by estimating the risks of cardiovascular events and bleeding for each patient, considering the potential longer-term benefits of aspirin for the prevention of colorectal cancer, and carefully discussing with patients the balance between the risks of vascular and haemorrhagic events.