It is well established that regular physical exercise improves lipid levels, glucose tolerance, and insulin sensitivity, all of which are cardiovascular risk factors. One question researchers have been asking in recent years is whether a single exercise session can, after a period of prolonged physical inactivity, have a positive impact on the risk factors associated with a sedentary lifestyle. This is an important issue as more and more workers are sitting for long hours at the office or in their car, and many of them do not have time to exercise more than once a week.
In a randomized controlled trial published in 2019 in the Journal of Applied Physiology, participants (n = 10) first spent four days without exercise, sitting for much of the day (≈13.5 hours/day). At the end of the fourth day, half of the participants did one hour of intense treadmill exercise (60–65% VO2max) and the other half remained inactive. On the morning of the fifth day, after fasting for 12 hours, all participants consumed a meal high in fat and glucose. Blood samples were taken before and every hour (up to 6 h) after the meal, and triglycerides, glucose and insulin were measured. After a rest period of several days, the experiment was repeated by swapping the groups (crossover study design).
No significant differences in plasma levels of triglycerides, glucose or insulin were found between the two groups. The authors conclude that prolonged physical inactivity (e.g., sitting about 13.5 hours/day and walking fewer than 4,000 steps/day) creates conditions where people become “resistant” to the metabolic improvements that are normally achieved after an aerobic exercise session. It is therefore important to develop good habits at work and at home (take active breaks, work standing, etc.), in order to fully benefit from the positive effects of exercise during leisure time.
A similar study published in 2016 came to comparable conclusions. The researchers randomized the participants into three groups: 1) sitting >14 h/day and a high-calorie diet; 2) sitting >14 h/day and a balanced diet; 3) active: standing, walking, sitting 8.4 h/day and a balanced diet. In addition to being randomized, the study had a crossover design, i.e., subjects participated in three five-day interventions (one week of rest between each intervention), changing groups each time. On the evening of the fourth day, the participants did treadmill running for 1 hour (67% VO2max). On the third and fifth day, participants consumed a high-fat meal (high-fat tolerance test) and blood tests were taken before and every hour (up to 6 hours) after the meal. Triglycerides, free fatty acids, glucose, and insulin were subsequently assayed in the plasma of the various samples collected.
After two days of sitting for long hours, participants had 27% higher triglyceride levels after consuming a high-fat meal, compared to participants who were more active. In participants who spent four days sitting for more than 14 hours, the 1-hour aerobic exercise did not decrease triglyceride levels in the blood or increase fat oxidation. On the other hand, in participants who were active during the previous four days, aerobic exercise decreased triglycerides by 14% (a non-significant decrease, p = 0.079) and significantly increased fat oxidation (p <0.05). The authors concluded that sitting for a good part of the day for 2 to 4 days was sufficient to increase postprandial triglyceride levels (after a meal) and that this increase cannot be reduced by sustained exercise.
A meta-analysis of 13 population studies assessed the ability of physical activity to eliminate or reduce the association between sitting time and all-cause mortality. These studies were conducted with more than 1 million people who were followed from 2 to 18.1 years. The results (Figure 1) show a very clear dose-effect relationship between the amount of exercise and the reduction in the relative risk of mortality associated with sitting or watching television. High levels of moderate physical activity (i.e., approximately 60–75 min/day) appear to eliminate the increased risk of mortality associated with long periods of sitting (Figure 1A). However, high levels of physical activity significantly alleviate, but do not eliminate the risk of mortality associated with long periods (> 5 h) spent watching television (Figure 1B).
Figure 1. Meta-analyses of joint associations of sitting time and amount of physical activity with all-cause mortality (A) and television-viewing time and amount of physical activity with all-cause mortality (B). 2.5 MET-h/week is equivalent to about 5 minutes of moderate activity per day; 16 MET-h/week is equivalent to 25–35 minutes of moderate activity per day; 30 MET-h/week is equivalent to 50–65 minutes of moderate activity per day, and 35.5 MET-h/week is equivalent to 60–75 minutes of moderate activity per day. From Ekelund et al., 2016.
The amount of physical activity in the highest quartile (> 35.5 MET-h/week) is equivalent to approximately 60–75 minutes of moderate-intensity exercise per day. This is much more than the minimum recommended by public health organizations (150 min/week). However, among those who do 16 MET-h/week, which is equivalent to 25–35 minutes of moderate-intensity physical activity, the increased risk of mortality associated with long periods of sitting (> 8 h/day) is less marked than for people in the least active group (<2.5 MET-h/week, equivalent to about 5 min of exercise per day). The increased risk of mortality (58%) for those who are less active and who sit more than 8 hours a day is similar to that associated with other risk factors such as smoking and obesity.
Why are the results for sitting time and television-viewing time different? This may be due in part to differences in the accuracy with which these behaviours are reported, but the authors of the study propose other plausible explanations: 1) people usually watch television in the evening, normally after dinner, and a prolonged sedentary episode after a meal could be particularly harmful to the metabolism of lipids and glucose; 2) people likely take more active breaks during work than during the viewing of TV programs, and it appears that these breaks are beneficial in reducing several cardiometabolic risk factors; 3) It is also plausible that people who watch television consume more “snacks” or obesogenic food.
Spending long periods of time in a sitting position is very common in our modern societies and this will only increase with future technological and social innovations. In addition to promoting regular physical exercise, public health organizations will likely also need to include a reduction in sedentary time in their guidelines and emphasize the importance of taking “active” breaks. Taking short active breaks may mean walking for a minute, drinking water, and getting up when talking on the phone. We must develop strategies to avoid sitting for long periods of time. In addition, we need to find the time to do at least 150 minutes of moderate exercise a week, up to 300 minutes a week to get maximum health benefits.
The role of dietary fat in the development of obesity, cardiovascular disease and type 2 diabetes has been the subject of vigorous scientific debate for several years. In an article recently published in the prestigious Science, four experts on dietary fat and carbohydrate with very different perspectives on the issue (David Ludwig, Jeff Volek, Walter Willett, and Marian Neuhouser) identified 5 basic principles widely accepted in the scientific community and that can be of great help for non-specialists trying to navigate this issue.
This summary is important as the public is constantly bombarded with contradictory claims about the benefits and harmful effects of dietary fat. Two great, but diametrically opposed currents have emerged over the last few decades:
- The classic low-fat position, i.e., reducing fat intake, adopted since the 1980s by most governments and medical organizations. This approach is based on the fact that fats are twice as caloric as carbohydrates (and therefore more obesigenic) and that saturated fats increase LDL cholesterol levels, a major risk factor for cardiovascular disease. As a result, the main goal of healthy eating should be to reduce the total fat intake (especially saturated fat) and replace it with carbohydrate sources (vegetables, bread, cereals, rice and pasta). An argument in favour of this type of diet is that many cultures that have a low-fat diet (Okinawa’s inhabitants, for example) have exceptional longevity.
- The low-carb position, currently very popular as evidenced by the ketogenic diet, advocates exactly the opposite, i.e., reducing carbohydrate intake and increasing fat intake. This approach is based on several observations showing that increased carbohydrate consumption in recent years coincides with a phenomenal increase in the incidence of obesity in North America, suggesting that it is sugars and not fats that are responsible for excess weight and the resulting chronic diseases (cardiovascular disease, type 2 diabetes, some cancers). One argument in favour of this position is that an increase in insulin in response to carbohydrate consumption can actually promote fat accumulation and that low-carb diets are generally more effective at promoting weight loss, at least in the short term.
Reaching a consensus from two such extreme positions is not easy! Nevertheless, when we look at different forms of carbohydrates and fat in our diet, the reality is much more nuanced, and it becomes possible to see that a number of points are common to both approaches. By critically analyzing the data currently available, the authors have managed to identify at least five major principles they all agree on:
1) Eating unprocessed foods of good nutritional quality helps to stay healthy without having to worry about the amount of fat or carbohydrate consumed.
A common point of the low-fat and low-carb approaches is that each one is convinced it represents the optimal diet for health. In fact, a simple observation of food traditions around the world shows that there are several food combinations that allow you to live longer and be healthy. For example, Japan, France and Israel are the industrialized countries with the two lowest mortality rates from cardiovascular disease (110, 126 and 132 deaths per 100,000, respectively) despite considerable differences in the proportion of carbohydrates and fat from their diet.
It is the massive influx of ultra-processed industrial foods high in fat, sugar and salt that is the major cause of the obesity epidemic currently affecting the world’s population. All countries, without exception, that have shifted their traditional consumption of natural foods to processed foods have seen the incidence of obesity, type 2 diabetes, and cardiovascular disease affecting their population increase dramatically. The first step in combating diet-related chronic diseases is therefore not so much to count the amount of carbohydrate or fat consumed, but rather to eat “real” unprocessed foods. The best way to do this is simply to focus on plant-based foods such as fruits, vegetables, legumes and whole-grain cereals, while reducing those of animal origin and minimizing processed industrial foods such as deli meats, sugary drinks, and other junk food products.
2) Replace saturated fat with unsaturated fat.
The Seven Countries Study showed that the incidence of cardiovascular disease was closely correlated with saturated fat intake (mainly found in foods of animal origin such as meats and dairy products). A large number of studies have shown that replacing these saturated fats with unsaturated fats (e.g., vegetable oils) is associated with a significant reduction in the risk of cardiovascular events and premature mortality. A reduction in saturated fat intake, combined with an increased intake of high quality unsaturated fat (particularly monounsaturated and omega-3 polyunsaturated), is the optimal combination to prevent cardiovascular disease and reduce the risk of premature mortality.
These benefits can be explained by the many negative effects of an excess of saturated fat on health. In addition to increasing LDL cholesterol levels, an important risk factor for cardiovascular disease, a high intake of saturated fat causes an increase in the production of inflammatory molecules, an alteration of the function of the mitochondria (the power plants of the cell), and a disturbance of the normal composition of the intestinal microbiome. Not to mention that the organoleptic properties of a diet rich in saturated fats reduce the feeling of satiety and encourage overconsumption of food and accumulation of excess fat, a major risk factor for cardiovascular disease, type 2 diabetes and some cancers.
3) Replace refined carbohydrates with complex carbohydrates.
The big mistake of the “anti-fat crusade” of the ’80s and ’90s was to believe that any carbohydrate source, even the sugars found in processed industrial foods (refined flours, added sugars), was preferable to saturated fats. This belief was unjustified, as subsequent studies have demonstrated beyond a doubt that these refined sugars promote atherosclerosis and can even triple the risk of cardiovascular mortality when consumed in large quantities. In other words, any benefit that can come from reducing saturated fat intake is immediately countered by the negative effect of refined sugars on the cardiovascular system. On the other hand, when saturated fats are replaced by complex carbohydrates (whole grains, for example), there is actually a significant decrease in the risk of cardiovascular events.
Another reason to avoid foods containing refined or added sugars is that they have low nutritional value and cause significant variations in blood glucose and insulin secretion. These metabolic disturbances promote excess weight and the development of insulin resistance and dyslipidemia, conditions that significantly increase the risk of cardiovascular events. Conversely, increased intake of complex carbohydrates in whole-grain cereals, legumes, and other vegetables helps keep blood glucose and insulin levels stable. In addition, unrefined plant foods represent an exceptional source of vitamins, minerals and antioxidant phytochemicals essential for maintaining health. Their high fibre content also allows the establishment of a diverse intestinal microbiome, whose fermentation activity generates short-chain fatty acids with anti-inflammatory and anticancer properties.
4) A high-fat low-carb diet may be beneficial for people who have disorders of carbohydrate metabolism.
In recent years, research has shown that people who have normal sugar metabolism may tolerate a higher proportion of carbohydrates, while those with glucose intolerance or insulin resistance may benefit from adopting a low-carb diet richer in fat. This seems particularly true for people with diabetes and prediabetes. For example, an Italian study of people with type 2 diabetes showed that a diet high in monounsaturated fat (42% of total calories) was more effective in reducing the accumulation of fat in the liver (a major contributor to the development of type 2 diabetes) than a diet low in fat (28% of total calories).
These benefits seem even more pronounced for the ketogenic diet, in which the consumption of carbohydrates is reduced to a minimum (<50 g per day). Studies show that in people with a metabolic syndrome, this type of diet can generate a fat loss (total and abdominal) greater than a hypocaloric diet low in fat, as well as a higher reduction of blood triglycerides and several markers of inflammation. In people with type 2 diabetes, a recent study shows that in the majority of patients, the ketogenic diet is able to reduce the levels of glycated haemoglobin (a marker of chronic hyperglycaemia) to a normal level, and this without drugs other than metformin. Even people with type 1 diabetes can benefit considerably from a ketogenic diet: a study of 316 children and adults with this disease shows that the adoption of a ketogenic diet allows an exceptional control of glycemia and the maintenance of excellent metabolic health over a 2-year period.
5) A low-carb or ketogenic diet does not require a high intake of proteins and fats of animal origin.
Several forms of low carbohydrate or ketogenic diets recommend a high intake of animal foods (butter, meat, charcuteries, etc.) high in saturated fats. As mentioned above, these saturated fats have several negative effects (increase of LDL, inflammation, etc.), and one can therefore question the long-term impact of this type of low-carb diet on the risk of cardiovascular disease. Moreover, a study recently published in The Lancet indicates that people who consume little carbohydrates (<40% of calories), but a lot of fat and protein of animal origin, have a significantly increased risk of premature death. For those wishing to adopt a ketogenic diet, it is therefore important to realize that it is quite possible to reduce the proportion of carbohydrates in the diet by substituting cereals and other carbohydrate sources with foods rich in unsaturated fats like vegetable oils, vegetables rich in fat (nuts, seeds, avocado, olives) as well as fatty fish.
In short, the current debate about the merits of low-fat and low-carb diets is not really relevant: for the vast majority of the population, several combinations of fat and carbohydrate make it possible to remain in good health and at low risk of chronic diseases, provided that these fats and carbohydrates come from foods of good nutritional quality. It is the overconsumption of ultra-processed foods, high in fat and refined sugars, which is responsible for the dramatic rise in food-related diseases, particularly obesity and type 2 diabetes. Restricting the consumption of these industrial foods and replacing them with “natural” foods, especially those of plant origin, remains the best way to reduce the risk of developing these diseases. On the other hand, for overweight individuals with metabolic syndrome or type 2 diabetes, currently available scientific evidence suggests that a reduction in carbohydrate intake by adopting low-carb and ketogenic diets could be beneficial.
Heat waves are sporadic events of high temperatures, which can have serious consequences on human life. More than 70,000 people died during the heat wave that hit Europe in 2003, and another 10,860 died during a heat wave in Russia in 2010. The criteria for defining a heat wave vary from country to country. In Canada, a heat wave occurs when it is 30°C or higher for at least three consecutive days. It has been estimated that the average temperature of our planet will increase by 1°C by 2100 if we reduce greenhouse gas (GHG) emissions or 3.7°C if we do not. In 2000, about 30% of the world’s population was exposed to heat waves for at least 20 days a year. By 2100, it is expected that this proportion will increase to about 48% if we drastically reduce GHG emissions and 74% if we continue to increase GHG emissions.
When it is very hot, humid or both, the excess heat absorbed by the body must be dissipated by the skin and the respiratory system in order to maintain body temperature at 37°C: this is the thermoregulation process. The hypothalamus initiates a cardiovascular response by dilating blood vessels to redistribute blood to the body surface (the skin) where heat can be dissipated into the environment. Sweating is activated, allowing heat to dissipate by evaporation (600 kcal/hour). When it is very hot and humid, the evaporation of sweat is greatly reduced and the body struggles to maintain an adequate temperature. Heat stroke is a serious and life-threatening condition, which is defined as a body temperature above 40°C, accompanied by neurological signs such as confusion, seizures or loss of consciousness. The main risk factors for heat stroke are shown in Table 1.
Table 1. Risk factors for heat stroke. From Yeo, 2004.
|Extremes of age (younger than 15, older than 65)
|Skin-altering conditions (psoriasis, eczema, burns)
|Lack of air conditioning in home
|Living in a multi-storey building
|Low socioeconomic status
|Occupations with prolonged exertion and environmental exposure to temperature extremes (e.g., athletes, military workers, miners, steel workers, firefighters, factory workers, rescue workers)
· Impaired thermoregulation (diuretics, beta blockers, anticholinergics, phenothiazines, alcohol, butyrophenones)
· Increased metabolic heat production (benzotropin, trifluoperazine, ephedra containing dietary supplements, diet pills, amphetamines, cocaine, ecstasy)
|Previous history of heat-related illness
|Prolonged sun exposure
|Wearing heavy or excessive clothing
In a review of the literature on the causes of death during heat waves, 5 physiological mechanisms disrupting 7 vital organs have been identified (brain, heart, intestines, kidneys, liver, lungs, pancreas). The authors have identified 27 different ways in which heat-activated physiological mechanisms can lead to organ failure and ultimately death.
1- Ischemia. When the human body is exposed to heat, the hypothalamus initiates a cardiovascular response by dilating the blood vessels to redistribute blood to the body surface (the skin) where heat can be dissipated into the environment. This compensatory process can lead to an insufficient supply of blood to the internal organs (ischemia) and consequently to a lack of oxygen (hypoxia).
2- Toxicity due to thermal shock. High body temperature causes stress the body reacts to by producing stress proteins and free radicals that damage cells. This damage, combined with that caused by ischemia, affects the functioning of several organs.
3- Inflammatory response. Erosion of the intestinal mucosa allows bacteria and endotoxins to enter the bloodstream, leading to sepsis and activation of a systemic inflammatory response. If hyperthermia persists, the exaggerated inflammatory response causes damage to various organs.
4- Disseminated intravascular coagulation. Systemic inflammation and damage to the vascular endothelium caused by ischemia and heat shock can initiate this harmful mechanism. The proteins responsible for the control of coagulation become overactive and this can lead to the formation of clots that block the blood supply to vital organs. Depletion of blood clotting proteins can lead to subsequent bleeding (even in the absence of injury), which can be fatal.
5- Rhabdomyolysis. This is the rapid degradation of skeletal muscle cells caused by heat shock and ischemia. Muscle proteins such as myoglobin are released into the bloodstream and are toxic to the kidneys and can lead to kidney failure.
The heart is hit hard
In the heart, the combination of ischemia, heat shock cytotoxicity, and hypokalemia (potassium deficiency caused by excessive sweating) can lead to cardiac muscle breakdown. This myocardial injury increases the risk of cardiac arrest due to loss of myofibrils and reduced efficiency of the body in controlling heart rate and blood pressure. Stress on the heart can be exacerbated by dehydration, which thickens the blood and causes vasoconstriction, increasing the risk of coronary thrombosis and stroke. In the pancreas, erosion of the endothelial lining allows leukocytes to infiltrate the tissue, exacerbating inflammation. In the brain, the permeability of the blood-brain barrier allows toxins and pathogens to enter, increasing the risk of neuronal damage. All these physiological responses are interconnected in such a way that the failure of one organ can lead to negative effects on others, initiating a vicious cycle of deterioration that often leads to permanent damage, long-term recovery, or death.
To prevent heat stroke (according to Peiris et al., JAMA, 2014):
- Schedule outdoor activities during cool times of the day.
- Drink plenty of fluids. Avoid drinks with too much sugar or alcohol, which can cause dehydration.
- Wear loose-fitting, light-coloured clothing.
- Acclimate to new hot environments, over many days if possible.
- Be aware of medication side effects. If taking medications, be aware of those that may cause fluid losses, decrease sweating, or slow the heart rate. Common medications include those used for depression, blood pressure and heart disease, and coughs and colds.
- Never leave an impaired adult or a child in a car unattended.
What to do if you suspect a heat stroke
Call 911 if you notice these signs of heat stroke: body temperature over 40°C; accelerated heart rate; accelerated breathing; hot and red skin; nausea or vomiting; change of mental state (confusion, headache, difficulty in articulating words, convulsions or coma).
What to do while you wait for help:
- Move the individual out of the heat.
- Remove clothing to promote cooling.
- Position the person on his or her side to minimize aspiration.
- Immerse the individual in cold water or apply cold, wet cloths or ice packs to the skin (neck, armpits, and groin areas, where large blood vessels are located) to lower the body temperature.
- Continue cooling the individual until the body temperature reaches 38.4°C to 39°C (101°F to 102°F).
- Do not give any fluids to the person because it is not safe to drink during an altered level of consciousness. If the person is alert and requests water, give small sips.
- Avoid aspirin and acetaminophen; they do not help with cooling.
Berries are becoming increasingly popular in our diet, whether consumed fresh, frozen, dried or canned, and in related products such as jams, jellies, yogurts, juices and wines. Berries provide significant health benefits because of their high content of phenolic compounds, antioxidants, vitamins, minerals and fibres. Recognizing these health benefits has recently led to a 21% increase in world berry production.
The generic term “berries” is sometimes used to refer to small fruits, but from a botanical point of view, if some berries are genuineberries (blueberries, bilberries, cranberries, currants, lingonberries, elderberries), others are polydrupes (raspberries, blackberries), and the strawberry is a “false fruit” since the achenes (the small seeds on the outer surface of the strawberry) are the actual fruits of the strawberry. Berry fruits are rich in phenolic compounds such as phenolic acids, stilbenes, flavonoids, lignans and tannins (see the classification and structure of these compounds in Figure 1). Berries are particularly rich in anthocyanidins, pigments that give the skin and flesh of these fruits their distinctive red, blue or purple colour (Table 1).
Figure 1. Classification and chemical structure of phenolic compounds contained in berries. Adapted from Parades-López et al., 2010 and Nile & Park, 2014.
Like most flavonoids, anthocyanidins are found in nature as glycosides (compounds made of a sugar and another molecule) called anthocyanins. These anthocyanins can be absorbed in their whole form (linked to different sugars) both in the stomach and in the intestine. Anthocyanins that reach the large intestine can be metabolized by the microbiota (intestinal flora). The maximum concentration of anthocyanins in the bloodstream is reached from 30 minutes to 2 hours after eating berries. However, the maximum plasma concentration (1–100 nmol/L) of anthocyanins is much lower than what is measured in intestinal tissues, indicating that these compounds are metabolized extensively before entering the systemic circulation as metabolites. After administering a radiolabelled anthocyanin to humans, 35 metabolites were identified, 17 in blood, 31 in urine and 28 in feces. Thus, it is likely that these metabolites, rather than the intact molecule, are responsible for the health benefits associated with anthocyanins.
Table 1. Content of phenolic compounds, flavonoids, and anthocyanins of different berries. Adapted from Parades-López et al., 2010 and Nile & Park, 2014.
|Berries (genus and species)||Phenolic compounds||Flavonoids||Anthocyanins
|(mg/100 g fresh fruit)||(mg/100 g fresh fruit)||(mg/100 g fresh fruit)
|Raspberry (Rubus ideaous)||121||6||99
|Blackberry (Rubus fruticosus)||486||276||82–326
|Strawberry (Fragaria x. ananassa)||313||–||54
|Blueberry (Vaccinium corymbosum)||261–585||50||25–495
|Bilberry (Vaccinium myrtillus )||525||44||300
|Cranberry (Vaccinium macrocarpon)||315||157||67–140
|Redcurrant (Ribes rubrum)||1400||9||22
|Blackcurrant (Ribes nigrum)||29-60||46||44
|Elderberry (Sambucus nigra)||104||42||45-791
|Red cranberry (Vitis vitis-idea)||652||74||77
Biological activities of berries
Data from in vitro and animal experimental models indicate that the phenolic compounds in berries may produce their beneficial effects through their antioxidant, anti-inflammatory, antihypertensive, and lipid-lowering activities, which could prevent or mitigate atherosclerosis. Perhaps the best-known of the biological activities of phenolic compounds is their antioxidant activity, which helps protect the body’s cells from damage caused by free radicals and counteract certain chronic diseases associated with aging. According to several studies using in vitro and animal models, berries also have anti-cancer properties involving several complementary mechanisms such as induction of metabolic enzymes, modulation of the expression of specific genes and their effects on cell proliferation, apoptosis (programmed cell death, an unsettled process in cancer cells), and signalling pathways inside the cell.
In a prospective study conducted in China with 512,891 participants, daily consumption of fruit (all types of fruit) was associated with an average decrease in systolic blood pressure of 4.0 mmHg on average, a decrease of 0.5 mmol/L of blood glucose concentration, a 34% reduction in the risk of major coronary events and a 40% reduction in the risk of cardiovascular mortality. These results were obtained by comparing participants who ate fruits daily to those who did not consume them at all or very rarely. In this study, there was a strong dose-response correlation between the incidence of cardiovascular events or cardiovascular mortality and the amount of fruit consumed. Studies suggest that among the constituents of fruit, it is the flavonoids, and especially the anthocyanins, that are responsible for these protective effects.
A number of prospective and cross-sectional studies have examined the association between the consumption of anthocyanins and cardiovascular risk factors (see this review). In four out of five studies that examined the risks of coronary heart disease or nonfatal myocardial infarction, anthocyanin consumption was associatedwith a reduction in coronary artery disease risk from 12% to 32%. The impact of anthocyanins on the risk of stroke was investigated in 5 studies, but no evidence of a protective effect was found in this case.
With respect to cardiovascular risk factors, studies indicate that higher consumption of anthocyanins is associated with decreased arterial stiffness, arterial pressure, and insulinemia. The decrease in blood pressure associated with the consumption of anthocyanins, -4 mmHg, is similar to that seen in a person after quitting smoking. The effect of anthocyanins on insulin concentration, an average reduction of 0.7 mIU/L, is similar to the effects of a low-fat diet or a one-hour walk per day. A decrease in inflammation has been associated with the consumption of anthocyanins and flavonols, a mechanism that may underlie the reduction of cardiovascular risk and other chronic diseases.
Randomized controlled trials
A systematic review and meta-analysis of 22 randomized controlled trials, representing 1,251 people, report that berry consumption significantly reduces several cardiovascular risk factors, such as blood LDL cholesterol [-0.21 mmol/L on average], systolic blood pressure [-2.72 mmHg on average], fasting glucose concentration [-0.10 mmol/L on average], body mass index [-0.36 kg/m2on average], glycated haemoglobin [HbA1c, -0.20% on average], and tumour necrosis factor alpha [TNF-alpha, 0.99 pg/mL on average], a cytokine involved in systemic inflammation. In contrast, no significant changes were observed for the other markers of cardiovascular disease that were tested: total cholesterol, HDL cholesterol, triglycerides, diastolic blood pressure, ApoAI, ApoB, Ox-LDL, IL-6, CRP, sICAM-1,and sICAM-2.
Another systematic review published in 2018 evaluated randomized controlled trials [RCTs] on the effects of berry consumption on cardiovascular health. Among the 17 high-quality RCTs, 12 reported a beneficial effect of berry consumption on cardiovascular and metabolic health markers. Four out of eleven RCTs reported a reduction in systolic and/or diastolic blood pressure; 3/7 studies reported a favourable effect on endothelial function; 2/3 studies reported an improvement in arterial stiffness; 7/17 studies reported beneficial effects for the lipid balance; and 3/6 studies reported an improvement in the glycemic profile.
Berries and cognitive decline
Greater consumption of blueberries and strawberries was associated with a slowdown in cognitive decline in a prospective study of 16,010 participants in the Nurses’ Health Study aged 70 or older. Consumption of berries was associated with delayed cognitive decline of approximately 2.5 years. In addition, nurses who had consumed more anthocyanidins and total flavonoids had a slower cognitive decline than participants who consumed less.
The exceptional content of phenolic compounds in berries and their positive effects on health remind us that the quality of food is not just about nutrients: proteins, carbohydrates, lipids, vitamins and minerals; a wide variety of other molecules found in plants are absorbed from the intestines and routed through the bloodstream to all cells in the body. While not essential nutrients, phytochemicals such as flavonoids can contribute to better cardiovascular health and healthier aging.
The recent death of eminent American researcher Gerald Reaven, nicknamed the “father of insulin resistance,” is a good opportunity to recall the leading role this metabolic disorder plays in the development of type 2 diabetes and cardiovascular disease.
What is insulin resistance?
After a meal, insulin is secreted by the pancreas to signal to the body that circulating sugar levels need to be lowered, either by capturing it in the muscles and adipose tissue, or by promoting its storage in the liver. Under normal conditions, this mechanism is highly accurate and helps to keep the blood sugar level at an adequate level.
In people who are overweight, and especially those whose excess fat is located at the abdominal level, this insulin action is often disrupted and organs are no longer able to capture and store sugar effectively; they are said to be “insulin-resistant”. In its early stages, this insulin resistance often goes unnoticed because the pancreas is able to produce larger amounts of the hormone to compensate for this loss of effectiveness and thus allows organs to continue to collect and store enough sugar (see left portion of the figure). This compensatory hyperinsulinemia makes it possible to maintain blood glucose at approximately normal levels, but it unfortunately causes several metabolic abnormalities that can lead to the development of certain serious diseases. For example, excess insulin stimulates the production of triglycerides by the liver, which promotes the accumulation of fat and can result in the development of hepatic steatosis (fatty liver). Increased secretion of these fats into the bloodstream causes dyslipidemia, characterized by high triglycerides, an increase in LDL cholesterol, and a decrease in HDL cholesterol. Meanwhile, hyperinsulinemia increases sodium retention in the kidneys, contributing to the increased incidence of hypertension seen in insulin-resistant individuals.
All of these factors (dyslipidemia, hepatic steatosis, hypertension), combined with increased inflammation and a change in the properties of the endothelial cells lining the blood vessels (inflammation, procoagulant properties), make insulin resistance an important risk factor for cardiovascular disease.
Type 2 diabetes
In the longer term, overproduction of insulin can lead to pancreas depletion, which ultimately leads to the cessation of hormone production and the onset of type 2 diabetes, i.e., a state of chronic hyperglycaemia (see the right portion of the figure). This excess of blood sugar is very harmful to the blood vessels and significantly increases the risk of cardiovascular disease (heart attack and stroke) as well as damage to tissues whose function depends on the small blood vessels such as the retina, kidneys or nerves. Insulin resistance can be considered as a prediabetic state, the harbinger of diabetes developing insidiously.
“Excess abdominal fat should be considered as the first clinical sign of insulin resistance.”
One problem with insulin resistance is that it is often difficult to diagnose at an early stage, not only because it does not cause clinical symptoms but also because blood glucose is normal. As mentioned earlier, in the early stages of resistance, the pancreas offsets the loss of insulin efficiency by secreting larger amounts of the hormone, which is sufficient to maintain blood sugar at normal levels. Patients (just like their doctors) then have the false impression that they are in perfect health, even if in fact they are prediabetic and will become diabetic in the coming years if nothing is done. Overall, the studies suggest that a slight elevation of glycated haemoglobin (Hb1Ac 5.5% and above), a marker of chronic hyperglycaemia, may be a better approach for early detection of insulin resistance than tests that are used to measure blood glucose (fasting glucose, glucose tolerance). For example, it has recently been shown that people with normal fasting glucose but a HbA1c greater than 5.9% were eight times more likely to develop diabetes in the next four years than those whose HbA1c was less than 5.7%.
In short, it is important to remain vigilant and realize that excess fat, although somehow becoming the norm in our society (more than 60% of Canadians are overweight), is far from harmless. In practice, excess abdominal fat (waist circumference greater than 102 cm for men and 88 cm for women) should be considered as the first clinical sign of insulin resistance and an increased risk of developing type 2 diabetes, with disastrous consequences for cardiovascular health.
Fortunately, insulin resistance is not an irreversible phenomenon: several studies show that people with glucose metabolism disorders can reverse the situation by simply changing their lifestyle. For example, a recent study reports that the adoption of a diet consisting primarily of low-fat plant foods is associated with a significant improvement in insulin sensitivity in overweight individuals. Being more active also seems beneficial: a study of 44,828 Chinese adults (20–80 years old) with above-average fasting blood glucose showed that people who were the most physically active were 25% less likely to develop type 2 diabetes.
Physical inactivity and unhealthy eating have become major public health issues since, combined, these two poor lifestyle habits are the second leading cause of death after smoking in the United States. Physical inactivity is also associated with an increased risk of developing or worsening chronic diseases such as heart failure, cardiovascular disease, stroke, type 2 diabetes, hypertension, some cancers, and osteoporosis. In Canada, 76% of adult men and 79% of adult women do not perform the minimum physical activity recommended by the World Health Organization, i.e., 150 minutes/week, and Canadian adults spend an average of 9 hours 48 minutes of their waking hours doing sedentary activities. Recent research on physical activity suggests that it is no longer sufficient to follow the minimal recommendations of public health agencies to minimize the risk of cardiovascular disease. Physical inactivity and sedentary behaviour each have their own health effects that need to be addressed separately to better understand their distinct mechanisms.
According to a systematic review and meta-analysis of 16 prospective studies and 2 cross-sectional studies of 794,577 participants, highly sedentary people are 112% more likely to have diabetes than those who are not sedentary, and they have a 147% higher risk of cardiovascular events, a 90% higher risk of mortality from cardiovascular disease, and a 49% higher risk of all-cause mortality. Another study on sedentary behaviours (driving and watching television) was conducted in the United States from 1989 to 2003 among 7,744 men aged 20 to 89 who had no history of cardiovascular disease. Participants who reported driving more than 10 hours/week or engaging in two sedentary behaviours (driving and watching television) more than 23 hours/week had an 82% and 64% higher risk of dying from cardiovascular disease than those who reported driving less than 4 h/week or driving and watching TV less than 11 h/week, respectively. Participants who were physically active at work and in their leisure time, but were otherwise sedentary, were less at risk of dying from cardiovascular disease than those who were both sedentary and physically inactive. Moreover, having a normal blood pressure, a healthy weight, and being older were associated with a lower risk of cardiovascular death.
“Physical activity” has been defined as any body movement produced by skeletal muscles that requires energy expenditure, and “exercise” as a subcategory of physical activity. Exercise involves structured and repeated behaviour in order to maintain or improve physical fitness. One method to more accurately estimate the intensity of physical activity is to use the Metabolic Equivalent of Task (MET) method. A MET unit is the energy spent at rest. Physical activity can be considered low intensity (<3 METs), moderate intensity (3-6 METs), and high intensity (>6 METs). Defining what is “sedentary behaviour” or “physical inactivity” is more difficult, and not everyone agrees on a definition. The objective measurement of physical activity, using an accelerometer-type physical activity monitor, for example, makes it possible to better assess sedentary behaviours than with the data obtained by questionnaires. Accelerometry allows researchers to record daily the time participants devote to activities at all levels of intensity: sedentary, light, moderate and high. To illustrate the usefulness of this technique, Pate et al. present the cases of two people who have very different activity profiles. Subject A could be considered a sedentary person in several studies since they do not engage in moderate or intense physical activity for at least 30 minutes a day. However, if the analysis of the accelerometer data shows that the subject was sedentary for 25% of the day, they were doing low intensity activities for about 75% of that day. Subject B could be considered as an active person in most studies, as they engage in medium-high intensity physical activity during the day for 1 hour. The accelerometer data, however, show that subject B spends most of the day (70%) in sedentary life (sitting on a chair, for example) or engaging in low-intensity physical activity (23%). In total, subject A, considered “inactive” according to conventional criteria, expended more energy (26.3 METs) than subject B, considered “active” (23.6 METs).
A study of the sedentary behaviours of Americans aged 45 and over showed that a large proportion of total sedentary time is accumulated over long, uninterrupted periods. Participants in this study spent an average of more than 11 hours of their day being sedentary and almost half of this sedentary time was accumulated over periods of 30 minutes or more. Sedentary periods of more than 20, 30, 60 and 90 minutes accounted for 60%, 48%, 26% and 14% of total sedentary time, respectively. Several factors, including older age, male gender, obesity, winter, and low levels of physical activity, were associated with prolonged sedentary behaviours. Laboratory studies have shown that long periods of uninterrupted sedentary behaviours have cardiometabolic effects, suggesting that it is not only the total sedentary time that is important for the risk of cardiovascular disease but also how this time is accumulated.
Data from an epidemiological study seem to confirm this hypothesis since adults whose sedentary behaviour extended over long uninterrupted periods had a less favourable cardiometabolic profile (larger waist circumference, lower HDL cholesterol level, and other markers) compared to that of people who interrupt their periods of inactivity, regardless of the total duration of sedentary time. A recent study of 7,985 people aged 45 or older indicates that the risk of mortality increases not only with the number of hours of sedentary life but also with the duration of each of the uninterrupted sedentary periods. People who were both very sedentary (≥12.5 hours per day) and for long uninterrupted periods (≥10 min/period) had the highest risk of death.
Spending long periods of time sitting is very common in modern societies, and this will only increase with future technological and social innovations. In addition to promoting regular physical exercise, public health organizations will likely also need to include a reduction in sedentary time in their guidelines and emphasize the importance of taking “active” breaks. It is important to note that taking breaks does not necessarily mean exercising, but may include walking for a minute, getting a glass of water, or doing light housework for those working at home. It’s as simple as that!