A pro-inflammatory diet increases the risk of dementia

A pro-inflammatory diet increases the risk of dementia

OVERVIEW

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

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

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

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

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

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

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

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

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

Childhood obesity, a ticking time bomb for cardiometabolic diseases

Childhood obesity, a ticking time bomb for cardiometabolic diseases

OVERVIEW

  • Obesity rates among Canadian children and teens have more than tripled over the past 40 years.
  • Childhood obesity is associated with a marked increase in the risk of type 2 diabetes and cardiovascular disease in adulthood, which can significantly reduce healthy life expectancy.
  • Policies to improve the diet of young people are key to reversing this trend and preventing an epidemic ofcardiometabolic diseases affecting young adults in the coming years.

One of the most dramatic changes to have occurred in recent years is undoubtedly the marked increase in the number of overweight children. For example, obesity rates among Canadian children and adolescents have more than tripled over the past 40 years. Whereas in 1975, obesity was a fairly rare problem affecting less than 3% of children aged 5–19, the prevalence of obesity has made a gigantic leap since that time, affecting nearly 14% of boys and 10% of girls in 2016 (Figure 1). If data on overweight is added to these figures, then approximately 25% of young Canadians are overweight (a similar trend is observed in Quebec). This prevalence of obesity appears to have plateaued in recent years, but recent US surveys suggest that the COVID-19 pandemic may have caused an upsurge in the number of overweight young people, particularly among 5-11-year-olds.

Figure 1. Increase in the prevalence of obesity among Canadian children over the past 40 years. From NCD Risk Factor Collaboration (2017).

Measuring childhood obesity
Although not perfect, the most common measure used to determine the presence of overweight in young people under the age of 19 is the body mass index (BMI), calculated by dividing the weight by the square of height (kg/m²). However, the values obtained must be adjusted according to age and sex to take into account changes in body composition during growth, as shown in Figure 2.

Figure 2. WHO growth standards for boys aged 5–19 living in Canada. Data comes from WHO (2007).

Note that a wide range of BMI on either side of the median (50th percentile) is considered normal. Overweight children have a BMI higher than that of 85–95% of the population of the same age (85th-95th percentile), while the BMI of obese children is higher than that of 97% of the population of the same age (97th percentile and above). Using z-scores is another way to visualize childhood overweight and obesity. This measurement expresses the deviation of the BMI from the mean value, in standard deviation. For example, a z-score of 1 means that the BMI is one standard deviation above normal (corresponding to overweight), while z-scores of 2 and 3 indicate, respectively, the presence of obesity and severe obesity.

This marked increase in the proportion of overweight children, and particularly obese children, is a worrying trend that bodes very badly for the health of future generations of adults. On the one hand, it is well established that obesity during childhood (and especially during adolescence) represents a very high risk factor for obesity in adulthood, with more than 80% of obese adults who were already obese during their childhood. This obesity in adulthood is associated with an increased risk of a host of health problems, both from a cardiovascular point of view (hypertension, dyslipidemia, ischemic diseases) and the development of metabolic abnormalities (hyperglycemia, resistance to insulin, type 2 diabetes) and certain types of cancer. Obesity can also cause discrimination and social stigma and therefore have devastating consequences on the quality of life, both physically and mentally.

Another very damaging aspect of childhood obesity, which is rarely mentioned, is the dramatic acceleration of the development of all the diseases associated with overweight. In other words, obese children are not only at higher risk of suffering from the various pathologies caused by obesity in adulthood, but these diseases can also affect them at an early age, sometimes even before reaching adulthood, and thus considerably reduce their healthy life expectancy. These early impacts of childhood obesity on the development of diseases associated with overweight are well illustrated by the results of several recent studies on type 2 diabetes and cardiovascular disease.

Early diabetes
Traditionally, type 2 diabetes was an extremely rare disease among young people (it was even called “adult diabetes” at one time), but its incidence has increased dramatically with the rise in the proportion of obese young people. For example, recent US statistics show that the prevalence of type 2 diabetes in children aged 10–19 has increased from 0.34 per 1000 children in 2001 to 0.67 in 2017, an increase of almost 100% since the beginning of the millennium.

The main risk factors for early diabetes are obesity, especially severe obesity (BMI greater than 35) or when the excess fat is mainly located in the abdomen, a family history of the disease, and belonging to certain ethnic groups. However, obesity remains the main risk factor for type 2 diabetes: in obese children (4–10 years) and adolescents (11–18 years), glucose intolerance is frequently observed during induced hyperglycemia tests, a phenomenon caused by the early development of insulin resistance. A characteristic of type 2 diabetes in young people is its rapid development. Whereas in adults, the transition from a prediabetic state to clearly defined diabetes is generally a gradual process, occurring over a period of 5–10 years, this transition can occur very quickly in young people, in less than 2 years. This means that the disease is much more aggressive in young people than in older people and can cause the early onset of various complications, particularly at the cardiovascular level.

A recent study, published in the prestigious New England Journal of Medicine, clearly illustrates the dangers that arise from early-onset type 2 diabetes, appearing during childhood or adolescence. In this study, the researchers recruited extremely obese children (BMI ≥ 35) who had been diagnosed with type 2 diabetes in adolescence and subsequently examined for ten years the evolution of different risk factors and pathologies associated with this disease.

The results are very worrying, because the vast majority of patients in the study developed one or more complications during follow-up that significantly increased their risk of developing serious health problems (Figure 3). Of particular note is the high incidence of hypertension, dyslipidemia (LDL-cholesterol and triglyceride levels too high), and kidney (nephropathies) and nerve damage (neuropathies) in this population, which, it should be remembered, is only 26 years on average. Worse still, almost a third of these young adults had 2 or more complications, which obviously increases the risk of deterioration of their health even more. Moreover, it should be noted that 17 serious cardiovascular accidents (infarction, heart failure, stroke) occurred during the follow-up period, which is abnormally high given the young age of the patients and the relatively small number of people who participated in the study (500 patients).

Figure 3. Incidence of different complications associated with type 2 diabetes in adolescents. From TODAY Study Group (2021).

It should also be noted that these complications occurred despite the fact that the majority of these patients were treated with antidiabetic drugs such as metformin or insulin. This is consistent with several studies showing that type 2 diabetes is much harder to control in young people than in middle-aged people. The mechanisms responsible for this difference are still poorly understood, but it seems that the development of insulin resistance and the deterioration of the pancreatic cells that produce this hormone progress much faster in young people than in older people, which complicates blood sugar control and increases the risk of complications.

This difficulty in effectively treating early type 2 diabetes means that young diabetics are much more at risk of dying prematurely than non-diabetics (Figure 4). For example, young people who develop early diabetes, before the age of 30, have a mortality rate 3 times higher than the population of the same age who is not diabetic. This increase remains significant, although less pronounced, until about age 50, while cases of diabetes that appear at older ages (60 years and over) do not have a major impact on mortality compared to the general population. It should be noted that this increase in mortality affecting the youngest diabetics is particularly pronounced at a young age, around 40 years of age.

These results therefore show how early type 2 diabetes can lead to a rapid deterioration in health and take decades off life, including years that are often considered the most productive of life (forties and fifties). For all these reasons, type 2 diabetes must be considered one of the main collateral damages of childhood obesity.

Figure 4. Age-standardized mortality rates for diagnosis of type 2 diabetes. Standardized mortality rates represent the ratio of mortality observed in individuals with diabetes to anticipated mortality for each age group. From Al-Saeed et al. (2016).

Cardiovascular disease
In recent years, there has been an upsurge in the incidence of cardiovascular disease in young adults. This new trend is surprising given that mortality from cardiovascular diseases has been in constant decline for several years in the general population (thanks in particular to a reduction in the number of smokers and improved treatments), and one might have expected that young people would also benefit from these positive developments.

The data collected so far strongly suggests that the increase in the prevalence of obesity among young people contributes to this upsurge of premature cardiovascular diseases, before the age of 55. On the one hand, it has been shown that a genetic predisposition to develop overweight during childhood is associated with an increased risk of coronary heart disease (and type 2 diabetes) in adulthood. On the other hand, this increased risk has also been observed in long-term studies examining the association between the weight of individuals during childhood and the incidence of cardiovascular events once they have reached adulthood. For example, a large Danish study of over 275,000 school-aged children (7–13 years old) showed that each one-unit increase in BMI z-score at these ages (see legend to Figure 2 for the definition of the z-score) was associated with an increased risk of cardiovascular disease in adulthood, after 25 years (Figure 5).

This increased risk is directly proportional to the age at which children are overweight, i.e., the more a high BMI is present at older ages, the greater the risk of suffering a cardiovascular event later in adulthood. For example, an increase of 1 in the z -score of 13-year-old children is associated with twice as much of an increase in risk in adulthood as a similar increase in a 7-year-old child (Figure 5). Similar results are observed for girls, but the increased risk of cardiovascular disease is lower than for boys.


Figure 5. Relationship between body mass index in childhood and the risk of cardiovascular disease in adulthood. The values represent the risks associated with a 1-unit increase in BMI z-score at each age. From Baker et al. (2007).

Early atherosclerosis
Several studies suggest that the increased risk of cardiovascular disease in adulthood observed in overweight children is a consequence of the early development of several risk factors that accelerate the process of atherosclerosis. Autopsy studies of obese adolescents who died of non-cardiovascular causes (e.g., accidents) revealed that fibrous atherosclerotic plaques were already present in the aorta and coronary arteries, indicating an abnormally rapid progression of atherosclerosis.

As mentioned earlier, type 2 diabetes is certainly the worst risk factor that can generate this premature progression, because the vast majority of diabetic children and adolescents very quickly develop several abnormalities that considerably increase the risk of serious damage to blood vessels (Figure 3). But even without the presence of early diabetes, studies show that several risk factors for cardiovascular disease are already present in overweight children, such as hypertension, dyslipidemia, chronic inflammation, glucose intolerance or even vascular abnormalities (thickening of the internal wall of the carotid artery, for example). Exposure to these factors that begins in childhood therefore creates favourable conditions for the premature development of atherosclerosis, thereby increasing the risk of cardiovascular events in adulthood.

It should be noted, however, that the negative impact of childhood obesity on health in adulthood is not irreversible. Indeed, studies show that people who were overweight or obese during childhood, but who had a normal weight in adulthood, have a risk of cardiovascular disease similar to that of people who have been thin all their lives. However, obesity is extremely difficult to treat, both in childhood and in adulthood, and the best way to avoid prolonged chronic exposure to excess fat and damage to cardiovascular health (and health in general) which results from it is obviously to prevent the problem at the source by modifying lifestyle factors, which are closely associated with an increased risk of developing overweight, in particular the nature of the diet and physical activity (psychosocial stress may also play a role). Given the catastrophic effects of childhood obesity on health, cardiovascular health in particular, the potential for this early preventive approach (called “primordial prevention”) is immense and could help halt the current rise in diabetes and premature mortality affecting young adults.

Ideal cardiovascular health
A recent study shows how this primordial prevention approach can have an extraordinary impact on cardiovascular health. In this study, researchers determined the ideal cardiovascular health score, as defined by the American Heart Association (Table 1), of more than 3 million South Koreans with an average age of 20–39 years. Excess weight is a very important element of this score because of its influence on other risk factors also used in the score such as hypertension, fasting hyperglycemia and cholesterol.

Participants were followed for a period of approximately 16 years, and the incidence of premature cardiovascular disease (before age 55) was assessed using as the primary endpoint a combination of hospitalization for infarction, stroke, cardiac insufficiency, or sudden cardiac death.

Table 1. Parameters used to define the ideal cardiovascular health score. Since there is 1 point for each target reached, a score of 6 reflects optimal cardiovascular health. Adapted from Lloyd-Jones et al. (2010), excluding dietary factors that were not assessed in the Korean study.

As shown in Figure 6, cardiovascular health in early adulthood has a decisive influence on the risk of cardiovascular events that occur prematurely, before the age of 55. Compared to participants in very poor cardiovascular health at the start (score of 0), each additional target reached reduces the risk of cardiovascular events, with maximum protection of approximately 85% in people whose lifestyle allows achieving 5 or more ideal heart health targets (scores of 5 and 6). Similar results were obtained in the United States and show how early health, from childhood through young adulthood, plays a key role in preventing the development of cardiovascular disease during aging.

Figure 6. Influence of cardiovascular health in young adults on the risk of premature cardiovascular events. From Lee et al. (2021).

Yet our society remains strangely passive in the face of the rise in childhood obesity, as if the increase in body weight of children and adolescents has become the norm and that nothing can be done to reverse this trend. This lack of interest is really difficult to understand, because the current situation is a ticking time bomb that risks causing a tsunami of premature chronic diseases in the near future, affecting young adults. This is an extremely worrying scenario if we consider that our healthcare system, in addition to having to contend with diseases that affect an aging population (1 out of 4 Quebecers will be over 65 in 2030), will also have to deal with younger patients suffering from cardiometabolic diseases caused by overweight. Needless to say, this will be a significant burden on healthcare systems.

This situation is not inevitable, however, as governments have concrete legislative means that can be used to try to reverse this trend. Several policies aimed at improving diet quality to prevent disease can be quickly implemented:

  • Taxing sugary drinks. A simple and straightforward approach that has been adopted by several countries is to introduce a tax on industrial food products, especially soft drinks. The principle is the same as for all taxes affecting other products harmful to health such as alcohol and tobacco, i.e., an increase in prices is generally associated with a reduction in consumption. Studies that have examined the impact of this approach for soft drinks indicate that this is indeed the case, with reductions in consumption observed (among others) in Mexico, Berkeley (California) and Barbados. This approach therefore represents a promising tool, especially if the amounts collected are reinvested in order to improve the diet of the population (subsidies for the purchase of fruit and vegetables, for example).
  • Requiring clear nutrition labels on packaging. We can help consumers make informed choices by clearly indicating on the front of the product whether it is high in sugar, fat or salt, as is the case in Chile (see our article on this subject).
  • Eliminating the marketing of unhealthy foods for children. The example of Chile also shows that severe restrictions can be imposed on the marketing of junk food products by prohibiting the advertising of these products in programs or websites aimed at young people as well as by prohibiting their sale in schools. The United Kingdom plans to take such an approach very soon by eliminating all advertising online and on television of products high in sugar, salt and fat before 9 p.m., while Mexico has gone even further by banning all sales of junk food products to children.

There is no reason Canada should not adopt such approaches to protect the health of young people.

Lignans: Compounds of plant origin that promote good cardiovascular health

Lignans: Compounds of plant origin that promote good cardiovascular health

OVERVIEW

  • Dietary lignans are phenolic compounds that come mainly from plant-based foods, especially seeds, whole grains, fruits, vegetables, wine, tea and coffee.
  • Consumption of lignans is associated with a reduced risk of developing cardiovascular disease, according to several well-conducted studies.

There are over 8,000 phenolic and polyphenolic compounds found in plants. These compounds are not nutrients, but they have various beneficial biological activities in the human body. They are generally grouped into 4 classes: phenolic acids, flavonoids, stilbenes (e.g., resveratrol), and lignans. Lignans are dimers of monolignols, which can also be used in the synthesis of a long branched polymer, lignin, found in the walls of the conductive vessels of plants. From a nutritional standpoint, lignins are considered to be a component of insoluble dietary fibre.

Figure 1. Structures of the main dietary lignans

Dietary lignans, the most important of which are matairesinol, secoisolariciresinol, pinoresinol and lariciresinol, come mainly from plant-based foods, particularly seeds, whole grains, fruits, vegetables, wine, tea and coffee (see Table 1). Other lignans are found only in certain types of food, such as medioresinol (sesame seeds, rye, lemon), syringaresinol (grains), sesamin (sesame seeds). Lignans are converted into enterolignans by the gut microbiota, which are then absorbed into the bloodstream and distributed throughout the body.

Table 1. Lignan content of commonly consumed foods.
Adapted from Peterson et al., 2010 and Rodriguez-Garcia et al., 2019.

Several studies indicate that lignans can prevent cardiovascular disease and other chronic diseases, including cancer, and improve cardiovascular health, through its anti-inflammatory and estrogenic properties (the ability to bind to estrogen receptors).

A recently published US study indicates that there is a significant association between dietary intake of lignans and the incidence of coronary heart disease. Among the 214,108 people from 3 cohorts of healthcare professionals, those who consumed the most lignans (total) had a 15% lower risk of developing coronary heart disease than those who consumed little. Considering each lignan separately, the association was particularly favourable for matairesinol (-24%), compared to secoisolariciresinol (-13%), pinoresinol (-11%), and lariciresinol (-11%). There is a nonlinear dose-response relationship for total lignans, matairesinol, and secoisolariciresinol with a plateau (maximum effect) at approximately 300 µg/day, 10 µg/day, and 100 µg/day, respectively. Canadians consume an average of 857 µg of lignans per day, enough to benefit from the positive effects on cardiovascular health, but residents of some Western countries such as the United Kingdom, the United States and Germany do not have an optimal intake of lignans (Table 2).

The favourable association for lignans was especially apparent among participants who had a high dietary fibre intake. The authors of the study suggest that fibre, by supporting a healthy microbiota, may promote the production of enterolignans in the gut.

Table 2. Daily intake of lignans in Western countries.
Adapted from Peterson et al., 2010.

PREDIMED (Prevención con Dieta Mediterránea), a recognized study conducted among over 7,000 Spaniards (55–80 years old) at high risk of developing cardiovascular disease, compared the Mediterranean diet (supplemented with nuts and extra virgin olive) to a low-fat diet advocated by the American Heart Association for the prevention of cardiovascular disease (CVD). In this study, the Mediterranean diet was clearly superior to the low-fat diet in preventing CVD, so the study was stopped after 4.8 years for ethical reasons. Further analysis of the PREDIMED data showed that there is a very favourable association between a high dietary intake of polyphenols and the risk of CVD. Participants who consumed the most total polyphenols had a 46% lower risk of CVD than those who consumed the least. The polyphenols that were most strongly associated with reduced risk of CVD were flavanols (-60%), hydroxybenzoic acids (-53%), and lignans (-49%). It should be noted that the nuts and extra virgin olive oil that were consumed daily by participants in the PREDIMED study contain appreciable amounts of lignans.

Another analysis  of data from the PREDIMED study showed a favourable association between total polyphenol intake and the risk of death from any cause. A high intake of total polyphenols, compared to a low intake, was associated with a 37% reduction in the risk of premature mortality. Stilbenes and lignans were the most favourable polyphenols for reducing the risk of mortality, by 52% and 40%, respectively. In this case, flavonoids and phenolic acids were not associated with a significant reduction in mortality risk.

No randomized controlled studies on phenolic compounds and the risk of CVD have been performed to date. There is therefore no direct evidence that lignans protect the cardiovascular system, but all the data from population studies suggests that it is beneficial for health to increase the dietary intake of lignans and therefore to eat more fruits, vegetables, whole grains, legumes, nuts and extra virgin olive oil, which are excellent sources of these still too little known plant-based compounds.

Will cultured meat soon be on our plates?

Will cultured meat soon be on our plates?

OVERVIEW

  • To preserve the planet’s environment and produce enough food to meet growing global demand, experts believe that in the future there will be a need to reduce livestock farming and conventional meat consumption.
  • Cultured meat is presented as a sustainable alternative to farmed meat for those who want to protect the environment but do not want to become vegetarians.
  • For cultured meat to be consumed on a large scale, production techniques and social acceptability will have to make significant progress.

Today there are 7.3 billion human beings on our planet, and it is expected that there will be 9 billion by 2050. The Food and Agriculture Organization (FAO) estimates that in 2050, 70% more food will be required to meet the demand of the growing population. This poses a great challenge because of limited resources and arable land. Meat production (especially beef and pork) is the most resource-intensive, and experts believe it would not be responsible, or even possible, to continue to produce more and more of these foods. Even though meat consumption is declining in developed countries, it is increasing globally because consumers in developing countries are getting richer and meat is seen by the new middle class in these countries as a desirable luxury food.

Among the solutions proposed to get out of this impasse is cultured meat (or lab-grown meat), which is presented as a sustainable alternative to farmed meat for those who want to protect the environment, but who do not wish to become vegetarians. It should be noted that some experts consider that cultured meat poses certain problems and that it would not be a viable alternative to conventional meat (see here and here). We will come back to this a little later in the text.

How is meat grown?
To grow meat, you must first obtain a muscle sample from a live adult animal (by biopsy, under anesthesia) and isolate a subpopulation of cells called “stem” or “satellite” cells. These stem cells participate in muscle regeneration and have the ability to differentiate into muscle cells themselves. The muscle stem cells are then cultured in bioreactors in the presence of a nutrient medium containing growth factors that induce rapid proliferation. The cells are then transformed into muscle cells that form structures called “myotubes” no larger than 0.3 mm in length and mechanically assembled into muscle tissue and ultimately into ground meat or artificial “steak”.

Problematic use of fetal calf serum and growth promoters
The best culture medium for growing cells contains fetal calf serum, obtained from fetal blood after slaughtering a pregnant cow. The procedure usually used (cardiac puncture of the still alive calf fetus) is considered cruel and inhumane by many. This is a problem since large numbers of calves would have to be produced to meet the demand for large-scale meat cultivation, and this use is unacceptable to vegetarians and those who follow a vegan diet or lifestyle. Fortunately, it is now possible, on a laboratory scale, to grow muscle cells without the use of fetal calf serum. However, the serum-free culture will need to be adopted on an industrial scale. To replace fetal calf serum, the industry will need to use growth factors and hormones that will need to be produced on an industrial scale. The use of growth promoters is prohibited in the European Union for conventional meat production; however, you cannot grow meat without using these growth factors and hormones. Overexposure to certain growth promoters can have harmful effects on human health, but this is a subject of debate and several countries approve the supervised use of stimulators in animal production.

From cell to steak
Real muscle (meat) is made up of muscle fibres organized into bundles, blood vessels, nerves, connective tissues, and adipocytes (fat cells). Simply producing animal muscle cells is therefore not enough to recreate meat. This is why in 2013 the first dish prepared from cultivated meat was a simple burger-type patty. Industries that develop cultured meat must now attempt to recreate a 3D structure that will resemble real meat as much as possible, a task that is proving difficult. It’s about recreating the taste experience associated with eating a steak, chicken thigh or shrimp.

Researchers have recently made progress and successfully created small samples of cultured meat that mimic real meat. Using a new approach, a Japanese research group succeeded in growing beef muscle cells in long filaments aligned in a single direction, a structure that closely resembles muscle fibres. When these cultured cells were stimulated by an electric current, the filaments contracted, similar to muscle fibres. Researchers at the University of Tokyo have so far managed to produce pieces of cultured meat weighing a few grams at most. The next challenge will be to successfully produce larger pieces of cultured meat, up to 100 g, and introduce other tissues (blood vessels, fat cells) to mimic meat more convincingly. It should be noted that the culture medium used in this study contained fetal calf serum, an ingredient that cannot be used industrially for ethical and economic reasons, as mentioned above.

Cultured chicken meat
Singapore’s food regulatory agency approved the sale of meat grown by the US company Eat Just in 2020. It was the first time that the sale of cultured meat had been permitted by a state. Eat Just grows chicken meat using a process that does not require antibiotics. This cultured meat is safe because it contains very low levels of bacteria, much less than conventional chicken meat. Cultured chicken meat contains a little more protein, has a more varied amino acid composition, and contains more monounsaturated fat than conventional meat. The muscle cells are grown in 1200-litre bioreactors and then combined with plant ingredients to make chicken nuggets. The Singapore-approved process uses fetal calf serum, but Eat Just plans to use a serum-free culture medium in their future productions.

Estimation of the environmental cost of cultured meat
Cultivated meat production offers many environmental advantages compared to conventional meat, according to a study published in 2011. It would reduce greenhouse gas (GHG) emissions by 78 to 96%, use 7 to 45% less energy and 82 to 96% less water, depending on the type of product. In contrast, a more recent and rigorous study suggests that in the long term, the impact of cultured meat on the environment may be greater than that associated with livestock farming. Cultivated meat production will certainly reduce global warming in the short term since less GHGs will be emitted compared to cattle farming. In the very long term however (i.e., several hundred years), models predict that this would not necessarily be the case, because the main GHG generated by livestock, methane (CH4), does not accumulate in the atmosphere, unlike CO2 which is practically the only GHG generated by cultivated meat. Another study based on data from 15 companies involved in the production of cultured meat concludes that it is less harmful to the environment than the production of beef, but that it has a greater impact on the environment than the production of chicken, pork and plant-based “meat”. In order for the environmental score of cultivated meat to be better than that of conventional products, the industry would have to use only sustainable energy.

Cost of cultured meat
The first cultivated beef burger was produced in 2013 by a Dutch laboratory at an estimated cost of US $416,000. In 2015, the cost of production (on an industrial scale) was reduced to around $12, and it is expected that the price could be the same as conventional meat within ten years. The cultured chicken nuggets produced by Just Eat each cost $63 to produce in 2019, so industries still have some way to go for cultured meat to become affordable enough for consumers to consume on a regular basis.

Cultured meat: an alternative for Canadians?
According to a 2018 Dalhousie University survey of 1,027 Canadians, 32.2% of respondents planned to reduce their meat consumption in the next 6 months. However, cultured meat is not very popular with Canadians as only 18.3% of those consulted said that this new type of “meat” represented an alternative to real meat for them. There is hope, however, as younger consumers (40 and under) seem more likely (34%) to view cultured meat as an alternative.

Will cultured meat one day replace conventional meat on our plates? Although there is still progress to be made before this is possible, both in terms of production and social acceptability, we can hope that the important efforts made will lead to results within a decade. Ideally, for our health and that of the planet, we should reduce our consumption of meat (of all kinds) and eat mainly plants, as is the case with the Mediterranean diet and other traditional diets.

Environmental impacts associated with food production

Environmental impacts associated with food production

OVERVIEW

  • Food production is responsible for about 25% of the greenhouse gases emitted annually, with half of these GHGs coming from animal farming, mainly in the form of methane.
  • The agricultural sector is also an important source of fine particles responsible for air pollution, with the majority of these pollutants coming from ammonia generated by livestock farming.
  • Overall, a reduction in the consumption of animal products, particularly those from cattle farming, is therefore absolutely essential to limit global warming and improve air quality.

The latest report from the Intergovernmental Panel on Climate Change (IPCC) confirms that, if nothing is done, the constant build-up of greenhouse gases (GHG) in the atmosphere will cause temperatures to increase by more than 1.5ºC above pre-industrial levels over the next century, namely the target set by the Paris Agreement to minimize the negative effects of global warming. There is therefore an urgent need to drastically reduce the emission of these gases if we want to prevent the consequences of this warming, already visible today, from becoming out of control and causing an increase in the incidence of extreme climatic events (droughts, heat waves, hurricanes, forest fires), disrupting life on Earth (extinction of species, fall in agricultural yields, increase in infectious diseases, armed conflicts) and increasing the incidence of several diseases linked to excessive heat.

Carbon dioxide and other greenhouse gases
The main greenhouse gas is carbon dioxide (CO2), which now has a concentration of 417 ppm, about twice as much as in pre-industrial times. However, it should be noted that other gases, even if they are present in smaller quantities, also contribute to global warming. These gases, such as methane or certain molecules used for industrial purposes, capture heat in a much greater way than CO2 and therefore have a higher global warming potential (GWP) than CO2. For example, a tonne of methane has a GWP 28 times greater than a tonne of CO2 over a 100-year period, while the GWP of some industrial gases such as sulfur hexafluoride can reach almost 25,000 times that of CO2 (Table 1). In other words, even if many of these gases are present in minute quantities, on the order of a few parts per billion (10-9) or even per trillion (10–12), their emission is several times that of CO2 and therefore significantly contributes to warming.

Table 1. Global warming potential of various greenhouse gases.1 Values are for the year 2018, except for CO2 which is for 2020. Derived from the United States Environmental Protection Agency (EPA).2 Calculated for a 100-year period. From Greenhouse Gas Protocol. *ppm (part per million or 10-6); **ppb (part per billion or 10-9); ***ppt (part per trillion or 10–12).

To calculate this contribution to global greenhouse gas emissions, the method generally used is to convert these emissions into CO2 equivalents (CO2eq) by multiplying their quantity in the atmosphere by their respective GWP. For example, 1 kg of SF6 is equivalent to 23,500 kg (23.5 tonnes) of CO2 (1 kg × 23,500 = 23,500 CO2eq), while it takes 1000 kg of methane to reach an equivalent amount of CO2 (1000 kg × 28 = 28,000 CO2eq). When this method is applied to all gases, it is estimated that 75% of greenhouse gas emissions are in the form of CO2, the remainder coming from methane (17%), nitrous oxide (6%), and various fluorinated gases (2%) (Figure 1).

Figure 1. Distribution of greenhouse gas emissions. Adapted from Ritchie and Roser (2020).


Emissions sources
The use of fossil fuels to support human activities (transport, electricity production, heating, various industrial processes) is the main source of greenhouse gases, accounting for around three quarters of total emissions (Figure 2). This enormous “carbon footprint” implies that the fight against global warming necessarily requires a transition to “cleaner” sources of energy, in particular with regard to transport and electricity production. This is especially true in a country like Canada, where we emit an average of 20 tonnes of CO2eq per person per year, which ranks us, along with the United States and Australia, among the worst producers of GHGs in the world (Quebec, for its part, does better, with about 10 tonnes of CO2eq per person per year).


Figure 2. Contribution of the food sector to the annual production of greenhouse gases. Adapted from Ritchie and Roser (2020).

Another industry that contributes significantly to greenhouse gas emissions, but that we hear much less about, is food production. It is estimated that around 25% of all these gases come from the production and distribution of food, a proportion that rises to 33% when food waste is taken into account. The food sector involved in animal protein production alone is responsible for half of these food-related GHG emissions, mainly due to methane produced by livestock and aquaculture (31%) (see box). Livestock farming also requires large spaces, created in some cases by massive deforestation (in the Amazon, for example), which eliminates huge areas of plants that can sequester COs. Livestock farming also requires large quantities of forage plants and therefore the use of nitrogen fertilizers to accelerate the growth of these plants. The CO2 and nitrous oxide released into the atmosphere during the production of these fertilizers therefore contribute to the GHG generated by livestock.

Where does methane come from?
Methane (CH4) is the end product of the decomposition of organic matter. Methanogenesis is made possible by certain anaerobic microorganisms from the archaea domain (methanogens) which reduce carbon, present in the form of CO2 or certain simple organic acids (acetate, for example), to methane, according to the following reactions:

CO+ 4 H2 → CH4 + 2 H2O

CH3COOH → CH4 + CO2

The methane generated by livestock comes mainly from the fermentation of carbonaceous products inside the digestive system of ruminants. In these animals, the digestion of plant matter generates volatile fatty acids (acetate, propionate, butyrate), which are absorbed by the animal and used as a source of energy, and lead in parallel to the production of methane, about 500 L per day per animal, most of it being released through the mouth of the animal. Globally, livestock is estimated to emit about 3.1 Gt of CO2-eq as methane, which represents almost half of all anthropogenic methane emissions.

Aquaculture is another rapidly expanding form of farming, now accounting for over 60% of the global supply of fish and seafood for human consumption. Although GHG emissions from this sector are still much lower than those associated with livestock, recent measurements nonetheless indicate a sharp increase in its global warming potential, mainly due to an increase in methane production. In these systems, the sediments accumulate food residues used for the growth of fish and seafood as well as the droppings generated by these animals. The transformation of this organic material leads to the production of methane, which can then be diffused into the atmosphere.

Finally, it should be noted that the majority of aquaculture systems are located in Asia, where they are often established in regions previously occupied by mangroves, ecosystems located along the coasts and deltas of tropical regions. The destruction of these mangroves (very often for shrimp farming) is very harmful to global warming, because mangrove forests collectively store around 4 billion tonnes of CO2 and their elimination therefore has a concrete impact on the climate.

A good way to visualize the impact of livestock farming on GHG production is to compare the emissions associated with different foods of animal and plant origin based on the amount of protein in these foods (Figure 3). These comparisons clearly show that products derived from livestock products, beef in particular, represent a much greater source of GHGs than plants. The production of 100 g of beef protein, for example, generates on average 100 times more GHGs than the same amount of protein from nuts or legumes. This is true even for beef produced in the traditional way, i.e., from animals that feed exclusively on grass: these animals grow more slowly and therefore emit methane for a longer period, which cancels out the benefits that could be associated with the sequestration of CO2 by the grass that they eat.

Figure 3. Comparison of GHG levels generated during the production of different protein sources. Based on Poore and Nemecek (2018), as modified by Eikenberry (2018).

These huge differences in GHGs associated with the production of everyday food therefore clearly show that our food choices can have a significant influence on global warming. Since the majority of GHG emissions come from livestock, it is evident that a reduction in the consumption of meat, and animal products as a whole, will have the most positive impact. These benefits can be observed even with a fairly modest reduction in meat intake, as in the Mediterranean diet, or simply by replacing products from ruminants (beef and dairy products) by other sources of animal protein (poultry, pork, fish) (Figure 4). Obviously, a more drastic reduction in meat intake is even more beneficial, whether through the adoption of a flexitarian diet (high intake of plants, but little meat and animal products), vegetarian (no animal products, with the exception of eggs, dairy products and sometimes fish), and vegan (no animal products). This remains true even if the plants consumed come from abroad and sometimes travel long distances, because contrary to popular belief, transport only accounts for a small proportion (less than 10%) of the GHGs associated with a given food.

Figure 4. Potential for mitigation of GHG emissions by different types of diets. Adapted from IPCC (2019).

It is impossible to completely decarbonize food production, especially in a world where there are over 9 billion people to feed daily. On the other hand, there is no doubt that the GHG footprint of food can be significantly reduced by reducing the consumption of products derived from ruminants, such as beef and dairy products. This is extremely important, because the status quo is untenable. According to recent models, even if GHG emissions from fossil fuels ceased immediately, we would still not succeed in reaching the target of a maximum warming of 1.5ºC due to emissions produced by the current food production system.

Another aspect that is often overlooked is how fast and significant this positive impact of a reduction in cattle breeding products can be. Even though methane is a GHG almost 30 times more powerful than CO2, its life in the atmosphere is much shorter, around 10–20 years vs. several thousand years for CO2. Concretely, this means that an immediate drop in methane emissions, for example following a drastic reduction in the consumption of beef and dairy products, can have measurable effects on GHG levels in the following years and therefore represents the fastest and most efficient way to slow global warming.

Pollution from food
In addition to contributing to global GHG emissions, another environmental impact of food production is its contribution to air pollution. This negative impact of the food sector should not be overlooked, because while the influence of global warming caused by GHGs will be felt above all in the medium and longer term, atmospheric pollutants have an immediate effect on health: air pollution is currently the 7th leading cause of premature death worldwide, being directly responsible for around 4 million deaths annually (Figure 5). In some countries, such as the United States, it is estimated that agriculture and livestock are responsible for about 20% of this air pollution-related mortality.

Figure 5. Leading causes of premature mortality worldwide. Note that air pollution is the only risk factor of environmental origin, not related to lifestyle. From GBD 2016 Risk Factors Collaborators (2016).

Fine particles of 2.5 µm and less (PM2.5) are mainly responsible for these negative impacts of air pollution on health. Due to their small size, these particles easily penetrate the lungs to the pulmonary alveoli, where they pass directly to the pulmonary blood vessels and then to all arteries in the body. They then produce an inflammatory reaction and oxidative stress that damage the vascular endothelium, the thin layer of cells that covers the inner walls of the arteries and ensures their proper functioning. The arteries therefore dilate less easily and tend to contract more, which interferes with normal blood circulation. For all these reasons, it is cardiovascular diseases (coronary heart disease and stroke) that represent the main consequence of exposure to fine particles, and alone are responsible for about 80% of all deaths caused by ambient air pollution (Figure 6).

Figure 6. Distribution of premature deaths (in millions) caused by fine particles PM2.5.
Note the predominance of cardiovascular disease as a cause of death linked to air pollution. Adapted from Lelieveld et al. (2015).

Primary and secondary particles
Fine particles can be emitted directly from polluting sources (primary PM2.5) or indirectly, following the combination of several distinct particles present in the atmosphere (secondary PM2.5) (Figure 7). Much of the primary PM2.5 is in the form of carbon soot, produced by the incomplete combustion of fossil fuels (diesel and coal, especially) or biomass (forest fires, for example). Carbon soot is also associated with various organic compounds (polycyclic aromatic hydrocarbons), acids, metals, etc., which contribute to its toxicity after inhalation. These particles can be transported aloft over very long distances and, once deposited, be resuspended in the wind. In urban areas, this resuspension also takes place under the action of road traffic. This turbulence associated with automobile traffic is also responsible for the production of another class of primary PM2.5 called fugitive road dust.

Secondary PM2.5, on the other hand, are formed from precursors such as sulfur dioxide (SO2), nitrogen oxides (NOx), various volatile organic compounds containing carbon (organic carbon) as well as ammonia (NH3). The chemical reactions that govern the interaction between these different volatile substances to form the secondary fine particles are extraordinarily complex, but let us only mention that it is well established that the presence of the ammonium ion (NH4+), derived from ammonia (NH3), neutralizes the negative charge of certain gases and thus promotes their aggregation in the form of fine particles (Figure 7). Consequently, the presence of NH3 in the atmosphere often represents a limiting step in the formation of these secondary fine particles and a reduction in these emissions can therefore have concrete effects on improving air quality.


Figure 7. Schematic representation of the mechanisms of formation of fine particles PM2.5.

It is this important role of ammonia in the formation of secondary fine particles that explains the contribution of the food production sector to air pollution. Agriculture and livestock are in fact responsible for almost all anthropogenic ammonia emissions, a consequence of intensive livestock farming, the spreading of manure and slurry, and the industrial production of nitrogen fertilizers.

An American study clearly illustrates this contribution of agricultural ammonia to the negative impacts of air pollution on health. In this study, the researchers show that of the approximately 18,000 deaths caused annually by pollution derived from the agricultural sector, the vast majority (70%) of these deaths are a consequence of ammonia emissions (and therefore secondary PM2.5), while the emission of primary PM2.5, from plowing, the combustion of agricultural residues, and machinery, is responsible for the rest. Since the vast majority of ammonia emissions come from animal faeces and the use of natural (manure and slurry) or synthetic fertilizers to grow food for these animals, it is not surprising that the production of food from livestock is the main cause of deaths attributable to pollution from agricultural sources (Figure 8).

Figure 8. Distribution of deaths caused annually by PM2.5 from the agricultural sector in the United States. Note that 70% of the mortality is attributable to livestock products, mainly due to the ammonia generated by the animals as well as by the spreading of manure, slurry and synthetic fertilizers for the cultivation of fodder plants (corn, soybeans). From Domingo et al. (2021).

When we compare the impact of different foods for the same quantity of product, we immediately see that the production of red meat is particularly damaging, being responsible for at least 5 times more deaths than that of poultry, 10 times more than that of nuts and seeds, and at least 50 times more than that of other plants such as fruits and vegetables (Figure 9).

Figure 9. Comparison of PM2.5-related mortality by food types. From Domingo et al. (2021).

In short, whether in terms of reducing GHG emissions or health problems associated with atmospheric pollution, all the studies unequivocally show that a reduction in environmental damage caused by food production necessarily involves a reduction in the consumption of products of animal origin, in particular those from cattle farming. A change that is all the more profitable as the reduction in the intake of food of animal origin, combined with an increase in the consumption of plants, is beneficial for health and could prevent about 11 million premature deaths annually, a decrease of 20%.

Choosing the right sources of carbohydrates is essential for preventing cardiovascular disease

Choosing the right sources of carbohydrates is essential for preventing cardiovascular disease

OVERVIEW

  • Recent studies show that people who regularly consume foods containing low-quality carbohydrates (simple sugars, refined flours) have an increased risk of cardiovascular events and premature mortality.
  • Conversely, a high dietary intake of complex carbohydrates, such as resistant starches and dietary fibre, is associated with a lower risk of cardiovascular disease and improved overall health.
  • Favouring the regular consumption of foods rich in complex carbohydrates (whole grains, legumes, nuts, fruits and vegetables) while reducing that of foods containing simple carbohydrates (processed foods, sugary drinks, etc.) is therefore a simple way to improve cardiovascular health.

It is now well established that a good quality diet is essential for the prevention of cardiovascular disease and the maintenance of good health in general. This link is particularly well documented with regard to dietary fat: several epidemiological studies have indeed reported that too high a dietary intake of saturated fat increases LDL cholesterol levels, an important contributor to the development of atherosclerosis, and is associated with an increased risk of cardiovascular disease. As a result, most experts agree that we should limit the intake of foods containing significant amounts of saturated fat, such as red meat, and instead focus on sources of unsaturated fat, such as vegetable oils (especially extra virgin olive oil and those rich in omega-3s such as canola), as well as nuts, certain seeds (flax, chia, hemp) and fish (see our article on this subject). This roughly corresponds to the Mediterranean diet, a diet that has repeatedly been associated with a lower risk of several chronic diseases, especially cardiovascular disease.

On the carbohydrate side, the consensus that has emerged in recent years is to favour sources of complex carbohydrates such as whole grains, legumes and plants in general while reducing the intake of simple carbohydrates from refined flour and added sugars. Following this recommendation, however, can be much more difficult than one might think, as many available food products contain these low-quality carbohydrates, especially the entire range of ultra-processed products, which account for almost half of the calories consumed by the population. It is therefore very important to learn to distinguish between good and bad carbohydrates, especially since these nutrients are the main source of calories consumed daily by the majority of people. To achieve this, we believe it is useful to recall where carbohydrates come from and how industrial processing of foods can affect their properties and impacts on health.

Sugar polymers
All of the carbohydrates in our diet come from, in one way or another, plants. During the photosynthetic reaction, in addition to forming oxygen (O2) from carbon dioxide in the air (CO2), plants also simultaneously transform the energy contained in solar radiation into chemical energy, in the form of sugar:

6 CO2 + 12 H2O + light → C6H12O6 (glucose) + 6 O2 + 6 H2O

In the vast majority of cases, this sugar made by plants does not remain in this simple sugar form, but is rather used to make complex polymers, i.e., chains containing several hundred (and in some cases thousands) sugar molecules chemically bonded to one another. An important consequence of this arrangement is that the sugar contained in these complex carbohydrates is not immediately accessible and must be extracted by digestion before reaching the bloodstream and serving as a source of energy for the body’s cells. This prerequisite helps prevent sugar from entering the blood too rapidly, which would unbalance the control systems responsible for maintaining the concentration of this molecule at levels just sufficient enough to meet the needs of the body. And these levels are much lower than one might think; on average, the blood of a healthy person contains a maximum of 4 to 5 g of sugar in total, or barely the equivalent of a teaspoon. Dietary intake of complex carbohydrates therefore provides enough energy to support our metabolism, while avoiding excessive fluctuations in blood sugar that could lead to health problems.

Figure 1 illustrates the distribution of the two main types of sugar polymers in the plant cell: starches and fibres.

Figure 1. The physicochemical characteristics and physiological impacts of starches and dietary fibres from plant cells. Adapted from Gill et al. (2021).

Starches. Starches are glucose polymers that the plant stores as an energy reserve in granules (amyloplasts) located inside plant cells. This source of dietary carbohydrates has been part of the human diet since the dawn of time, as evidenced by the recent discovery of genes from bacteria specializing in the digestion of starches in the dental plaque of individuals of the genus Homo who lived more than 100,000 years ago. Even today, a very large number of plants commonly eaten are rich in starch, in particular tubers (potatoes, etc.), cereals (wheat, rice, barley, corn, etc.), pseudocereals (quinoa, chia, etc.), legumes, and fruits.

Digestion of the starches present in these plants releases units of glucose into the bloodstream and thus provides the energy necessary to support cell metabolism. However, several factors can influence the degree and speed of digestion of these starches (and the resulting rise in blood sugar). This is particularly the case with “resistant starches” which are not at all (or very little) digested during gastrointestinal transit and therefore remain intact until they reach the colon. Depending on the factors responsible for their resistance to digestion, three main types of these resistant starches (RS) can be identified:

  • RS-1: These starches are physically inaccessible for digestion because they are trapped inside unbroken plant cells, such as whole grains.
  • RS-2: The sensitivity of starches to digestion can also vary considerably depending on the source and the degree of organization of the glucose chains within the granules. For example, the most common form of starch in the plant kingdom is amylopectin (70–80% of total starch), a polymer made up of several branches of glucose chains. This branched structure increases the contact surface with enzymes specialized in the digestion of starches (amylases) and allows better extraction of the glucose units present in the polymer. The other constituent of starch, amylose, has a much more linear structure which reduces the efficiency of enzymes to extract the glucose present in the polymer. As a result, foods with a higher proportion of amylose are more resistant to breakdown, release less glucose, and therefore cause lower blood sugar levels. This is the case, for example, with legumes, which contain up to 50% of their starch in the form of amylose, which is much more than other commonly consumed sources of starches, such as tubers and grains.
  • RS-3: These resistant starches are formed when starch granules are heated and subsequently cooled. The resulting starch crystallization, a phenomenon called retrogradation, creates a rigid structure that protects the starch from digestive enzymes. Pasta salads, potato salads, and sushi rice are all examples of foods containing resistant starches of this type.

An immediate consequence of this resistance of digestion-resistant starches is that these glucose polymers can be considered dietary fibre from a functional point of view. This is important because, as discussed below, the fermentation of fibre by the hundreds of billions of bacteria (microbiota) present in the colon generates several metabolites that play extremely important roles in the maintenance of good health.

Dietary fibre. Fibres are polymers of glucose present in large quantities in the wall of plant cells where they play an important role in maintaining the structure and rigidity of plants. The structure of these fibres makes them completely resistant to digestion and the sugar they contain does not contribute to energy supply. Traditionally, there are two main types of dietary fibre, soluble and insoluble, each with its own physicochemical properties and physiological effects. Everyone has heard of insoluble fibre (in wheat bran, for example), which increases stool volume and speeds up gastrointestinal transit (the famous “regularity”). This mechanical role of insoluble fibres is important, but from a physiological point of view, it is mainly soluble fibres that deserve special attention because of the many positive effects they have on health.

By capturing water, these soluble fibres increase the viscosity of the digestive contents, which helps to reduce the absorption of sugar and dietary fats and thus to avoid excessive increases in blood sugar and blood lipid levels that can contribute to atherosclerosis (LDL cholesterol, triglycerides). The presence of soluble fibre also slows down gastric emptying and can therefore decrease calorie intake by increasing feelings of satiety. Finally, the bacterial community that resides in the colon (the microbiota) loves soluble fibres (and resistant starches), and this bacterial fermentation generates several bioactive substances, in particular the short chain fatty acids (SCFA) acetate, propionate and butyrate. Several studies carried out in recent years have shown that these molecules exert a myriad of positive effects on the body, whether by reducing chronic inflammation, improving insulin resistance, lowering blood pressure and the risk of cardiovascular disease, or promoting the establishment of a diversified microbiota, optimal for colon health (Table 1).

A compilation of many studies carried out in recent years (185 observational studies and 58 randomized trials, which equates to 135 million person-years) indicates that consuming 25 to 30 g of fibre per day seems optimal to benefit from these protective effects, approximately double the current average consumption.

Table 1. Main physiological effects of dietary fibre. Adapted from Barber (2020).

Physiological effectsBeneficial health impacts
MetabolismImproved insulin sensitivity
Reduced risk of type 2 diabetes
Improved blood sugar and lipid profile
Body weight control
Gut microbiotaPromotes a diversified microbiota
Production of short-chain fatty acids
Cardiovascular systemDecrease in chronic inflammation
Reduced risk of cardiovascular events
Reduction of cardiovascular mortality
Digestive systemDecreased risk of colorectal cancer

Overall, we can therefore see that the consumption of complex carbohydrates is optimal for our metabolism, not only because it ensures an adequate supply of energy in the form of sugar, without causing large fluctuations in blood sugar, but also because it provides the intestinal microbiota with the elements necessary for the production of metabolites essential for the prevention of several chronic diseases and for the maintenance of good health in general.

Modern sugars
The situation is quite different, however, for several sources of carbohydrates in modern diets, especially those found in processed industrial foods. Three main problems are associated with processing:

Simple sugars. Simple sugars (glucose, fructose, galactose, etc.) are the molecules responsible for the sweet taste: the interaction of these sugars with receptors present in the tongue sends a signal to the brain warning it of the presence of an energy source. The brain, which alone consumes no less than 120 g of sugar per day, loves sugar and responds positively to this information, which explains our innate attraction to foods with a sweet taste. On the other hand, since the vast majority of carbohydrates produced by plants are in the form of polymers (starches and fibres), simple sugars are actually quite rare in nature, being mainly found in fruits, vegetables such as beets, or even some grasses (sugar cane). It is therefore only with the industrial production of sugar from sugar cane and beets that consumers’ “sweet tooth” could be satisfied on a large scale and that simple sugars became commonly consumed. For example, data collected in the United States shows that between 1820 and 2016, the intake of simple sugars increased from 6 lb (2.7 kg) to 95 lb (43 kg) per person per year, an increase of about 15 times in just under 200 years (Figure 2).

 

 

Figure 2. Consumption of simple sugars in the United States between 1820 and 2016.  From Guyenet (2018).

Our metabolism is obviously not adapted to this very high intake of simple sugars, far beyond what is normally found in nature. Unlike the sugars found in complex carbohydrates, these simple sugars are absorbed very quickly into the bloodstream and cause very rapid and significant increases in blood sugar. Several studies have shown that people who frequently consume foods containing these simple sugars are more likely to suffer from obesity, type 2 diabetes and cardiovascular disease. For example, studies have found that consuming 2 servings of sugary drinks daily was associated with a 35% increase in the risk of coronary heart disease. When the amount of added sugars consumed represents 25% of daily calories, the risk of heart disease nearly triples. Factors that contribute to this detrimental effect of simple sugars on cardiovascular health include increased blood pressure and triglyceride levels, lowered HDL cholesterol, and increased LDL cholesterol (specifically small, very dense LDLs, which are more harmful to the arteries), as well as an increase in inflammation and oxidative stress.

It is therefore necessary to restrict as much as possible the intake of simple sugars, which should not exceed 10% of the daily energy intake according to the World Health Organization. For the average adult who consumes 2,000 calories per day, that’s just 200 calories, or about 12 teaspoons of sugar or the equivalent of a single can of soft drink.

Refined flour.  Cereals are a major source of carbohydrates (and calories) in most food cultures around the world. When they are in whole form, i.e., they retain the outer shell rich in fibre and the germ containing several vitamins and minerals, cereals are a source of complex carbohydrates (starches) of high quality and beneficial to health. This positive impact of whole grains is well illustrated by the reduced risk of coronary heart disease and mortality observed in a large number of population studies. For example, recent meta-analyses have shown that the consumption of about 50 g of whole grains perday is associated with a 22–30% reduction in cardiovascular disease mortality, a 14–18% reduction in cancer-relatedmortality, and a 19–22% reduction in total mortality.

On the other hand, these positive effects are completely eliminated when the grains are refined with modern industrial metal mills to produce the flour used in the manufacture of a very large number of commonly consumed products (breads, pastries, pasta, desserts, etc.). By removing the outer shell of the grain and its germ, this process improves the texture and shelf life of the flour (the unsaturated fatty acids in the germ are sensitive to rancidity), but at the cost of the almost total elimination of fibres and a marked depletion of several nutrients (minerals, vitamins, unsaturated fatty acids, etc.). Refined flours therefore essentially only contain sugar in the form of starch, this sugar being much easier to assimilate due to the absence of fibres that normally slow down the digestion of starch and the absorption of released sugar (Figure 3).

Figure 3. Schematic representation of a whole and refined grain of wheat.

Fibre deficiency. Fortification processes partially compensate for the losses of certain nutrients (e.g., folic acid) that occur during the refining of cereal grains. On the other hand, the loss of fibre during grain refining is irreversible and is directly responsible for one of the most serious modern dietary deficiencies given the many positive effects of fibre on the prevention of several chronic diseases.

Poor-quality carbohydrates
Low-quality carbohydrate sources with a negative impact on health are therefore foods containing a high amount of simple sugars, having a higher content of refined grains than whole grains, or containing a low amount of fibre (or several of these characteristics simultaneously). A common way to describe these poor-quality carbohydrates is to compare the rise in blood sugar they produce to that of pure glucose, called the glycemic index (GI) (see box). The consumption of food with a high glycemic index causes a rapid and dramatic rise in blood sugar levels, which causes the pancreas to secrete a large amount of insulin to get glucose into the cells. This hyperinsulinemia can cause glucose to drop to too low levels, and the resulting hypoglycemia can ironically stimulate appetite, despite ingesting a large amount of sugar a few hours earlier. Conversely, a food with a low glycemic index produces lower, but sustained, blood sugar levels, which reduces the demand for insulin and helps prevent the fluctuations in blood glucose levels often seen with foods with a high glycemic index. Potatoes, breakfast cereals, white bread, and pastries are all examples of high glycemic index foods, while legumes, vegetables, and nuts are conversely foods with a low glycemic index.

Glycemic index and load
The glycemic index (GI) is calculated by comparing the increase in blood sugar levels produced by the absorption of a given food with that of pure glucose. For example, a food that has a glycemic index of 50 (lentils, for example) produces a blood sugar half as important as glucose (which has a glycemic index of 100). As a general rule, values below 50 are considered to correspond to a low GI, while those above 70 are considered high. The glycemic index, however, does not take into account the amount of carbohydrate in foods, so it is often more appropriate to use the concept of glycemic load (GL). For example, although watermelon and breakfast cereals both have high GIs (75), the low-carbohydrate content of melon (11 g per 100 g) equates to a glycemic load of 8, while 26 g of carbohydrates present in breakfast cereals result in a load of 22, which is three times more. GLs ≥ 20 are considered high, intermediate when between 11 and 19, and low when ≤ 10.

PURE study
Results from the PURE (Prospective Urban and Rural Epidemiology) epidemiological study conducted by Canadian cardiologist Salim Yusuf have confirmed the link between low-quality carbohydrates and the risk of cardiovascular disease. In the first of these studies, published in the prestigious New England Journal of Medicine, researchers examined the association between the glycemic index and the total glycemic load of the diet and the incidence of major cardiovascular events (heart attack, stroke, sudden death, heart failure) in more than 130,000 participants aged 35 to 70, spread across all five continents. The study finds that a diet with a high glycemic index is associated with a significant (25%) increase in the risk of having a major cardiovascular event in people without cardiovascular disease, an increase that reaches 51% in those with pre-existing cardiovascular disease (Figure 4). A similar trend is observed for the glycemic load, but in the latter case, the increased risk seems to affect only those with cardiovascular disease at the start of the study.

Figure 4. Comparison of the risk of cardiovascular events according to the glycemic index or the glycemic load of the diet of healthy people (blue) or with a history of cardiovascular disease (red). The median glycemic index values were 76 for quintile 1 and 91 for quintile 5. For glycemic load, the mean values were 136 g of carbohydrates per day for Q1 and 468 g per day for Q5. Note that the increased risk of cardiovascular events associated with a high glycemic index or load is primarily seen in participants with pre-existing cardiovascular disease. From Jenkins et al. (2021).

The impact of the glycemic index appears to be particularly pronounced in overweight people (Figure 5). Thus, while the increase in the risk of major cardiovascular events is 14% in thin people with a BMI less than 25, it reaches 38% in those who are overweight (BMI over 25).

 

Figure 5. Impact of overweight on the increased risk of cardiovascular events related to the glycemic index of the diet. The values shown represent the increased risk of cardiovascular events observed for each category (quintiles 2 to 5) of the glycemic index compared to the category with the lowest index (quintile 1). The median values of the glycemic indices were 76 for quintile 1; 81 for quintile 2; 86 for quintile 3; 89 for quintile 4; and 91 for quintile 5. Taken from Jenkins et al. (2021).

This result is not so surprising, since it has long been known that excess fat disrupts sugar metabolism, especially by producing insulin resistance. A diet with a high glycemic index therefore exacerbates the rise in postprandial blood sugar already in place due to excess weight, which leads to a greater increase in the risk of cardiovascular disease. The message to be drawn from this study is therefore very clear: a diet containing too many easily assimilated sugars, as measured using the glycemic index, is associated with a significant increase in the risk of suffering a major cardiovascular event. The risk of these events is particularly pronounced for people with less than optimal health, either due to the presence of excess fat or pre-existing cardiovascular disease (or both). Reducing the glycemic index of the diet by consuming more foods containing complex carbohydrates (fruits, vegetables, legumes, nuts) and fewer products containing added sugars or refined flour is therefore an essential prerequisite for preventing the development of cardiovascular disease.

Refined flours
Another part of the PURE study looked more specifically at refined flours as a source of easily assimilated sugars that can abnormally increase blood sugar levels and increase the risk of cardiovascular disease. Researchers observed that a high intake (350 g per day, or 7 servings) of products containing refined flours (white bread, breakfast cereals, cookies, crackers, pastries) was associated with a 33% increase in the risk of coronary heart disease, 47% in the risk of stroke, and 27% in the risk of premature death. These observations therefore confirm the negative impact of refined flours on health and the importance of including as much as possible foods containing whole grains in the diet. The preventive potential of this simple dietary change is enormous since the consumption of whole grains remains extremely low, with the majority of the population of industrialized countries consuming less than 1 serving of whole grains daily, well below the recommended minimum (half of all grain products consumed, or about 5 servings per day).

Wholemeal breads are still a great way to boost the whole-grain intake. However, special attention must be paid to the list of ingredients. In Canada, the law allows up to 5% of the grain to be removed when making whole wheat flour, and the part removed contains most of the germ and a fraction of the bran (fibres). This type of bread is superior to white bread, but it is preferable to choose products made from whole-grain flour which contains all the parts of the grain. Note also that multigrain breads (7-14 grains) always contain 80% wheat flour and a maximum of 20% of a mixture of other grains (otherwise the bread does not rise), so the number of grains does not matter, but what does matter is whether the flour is whole wheat or ideally integral, which is not always the case.

In short, a simple way to reduce the risk of cardiovascular events and improve health in general is to replace as much as possible the intake of foods rich in simple sugars and refined flour with plant-based foods containing complex carbohydrates. In addition to carbohydrates, this simple change alone will influence the nature of the proteins and lipids ingested as well as, at the same time, all the phenomena that promote the appearance and progression of atherosclerotic plaques.