Category Archives: Nutrition

Nutrition is a key factor in maintaining good health throughout life.
Eating a balance diet, from birth with breastfeeding, and later during childhood, adolescence and adult life, is helpful in achieving and maintaining a good state of health and contributes, when associated with a healthy lifestyle, to the prevention of many chronic diseases such as cardiovascular diseases, osteoporosis, type II diabetes, and many types of cancers, conditions which are increasingly common nowadays.
And it is important to point out the relationship between nutrition and the intestinal microbiota, the community of microorganisms that colonize the gut: diet seems to be main factor in determining its composition, starting from breast milk.
Proper nutrition is essential even in the presence of allergic reactions to food components, as in the case of celiac disease, condition in which all food containing gluten must be avoided for life.
Proper nutrition is essential for athletes, and when combined with adequate training improves the performance in any sports.
And among the different types of diets, the Mediterranean diet is one of the healthiest. This dietary pattern was brought to the attention of the international scientific community in the 1950s by the work of Ancel Keys, an American physiologist. The Mediterranean diet, rich in plant products, such as extra virgin olive oil, vegetables, legumes, and whole grains, and low in red meats and derived products and high fat dairy products, ensures an good supply of fiber, compounds with anti-inflammatory and antioxidant actions, as well as a low intake of saturated fats.

Human gut microbiota: definition, composition, and diet

The human gastrointestinal tract is one of the most fierce and competitive ecological niches. It harbors viruses, eukaryotes, bacteria, and one member of Archaebacteria, Methanobrevibacter smithii.
Bacteria vary in proportion and amount all along the gastrointestinal tract; the greatest amount is found in the colon, which contains over 400 different species belonging to 9 phyla or divisions (of the 30 recognized phyla), and hereafter you refer to them as gut microbiota.
These are the phyla and some of their most represented genera.

  • Actinobacteria (Gram-positive bacteria); Bifidobacterium, Collinsella, Eggerthella, and Propionibacterium.
  • Bacteroidetes (Gram-negative bacteria); more than 20 genera including Bacteroides, Prevotella and Corynebacterium.
  • Cyanobacteria (Gram-negative bacteria).
  • Firmicutes (Gram-positive bacteria); at least 250 genera, including Mycoplasma, Bacillus, Clostridium, Dorea, Faecalibacterium, Ruminococcus, Eubacterium, Staphylococcus, Streptococcus, Lactobacillus, Lactococcus, Enterococcus, Sporobacter, and Roseburia.
  • Fusobacteria (Gram-negative bacteria);
  • Lentisphaerae (Gram-negative bacteria).
  • Proteobacteria (Gram-negative bacteria); Escherichia, Klebsiella, Shigella, Salmonella, Citrobacter, Helicobacter, and Serratia.
  • Spirochaeates (Gram-negative bacteria).
  • Verrucomicrobia (Gram-negative bacteria).

The presence of a small subset of the bacterial world in the colon is the result of a strong selective pressure which acted, during evolution, on both the microbial colonizers, selecting organisms very well adapted to this environment, and the intestinal niche. And nevertheless, each individual harbors an unique bacterial community in his gut.
Despite the high variability existing both with regard to taxa and between individuals, it has been proposed, but not accepted by all researchers, that in most adults the bacterial gut microbiota can be classified into variants or “enterotypes”, on the basis of the ratio of the abundance of the genera Bacteroides and Prevotella. This seems to indicate that there is a limited number of well balanced symbiotic states, which could respond differently to factors such as diet, age, genetics, and drug intake (see below).

Adult’s gut harbors a large and diverse community of DNA and RNA viruses made up of about 2,000 different genotypes, none of which is dominant. Indeed, the most abundant virus accounts for only about 6% of the community, whereas in infants the most abundant virus accounts over 40% of the community. The majority of DNA viruses are bacteriophages or phages, that is, viruses that infect bacteria (they are the most abundant biological entity on earth, with an estimated population of about 1031 units), whereas the majority of RNA viruses are plant viruses.


Factors affecting gut microbiota composition and development

The intestinal bacterial community is regulated by several factors, most of which are listed below.

  • The diet of the host.
    It seems to be the most important factor.
    Traditionally considered sterile, mother’s milk harbors a rich microbiota consisting of more than 700 species, dominated by staphylococci, streptococci, bifidobacteria and lactic acid bacteria. Therefore, it is a major source for the colonization of the breastfed infant gut, and it was suggested that this mode of colonization is closely correlated with infant’s health status, because, among other functions, it could protect against infections and contribute to the maturation of the immune system. Breast milk affects intestinal microbiota also indirectly, through the presence of oligosaccharides with prebiotic activity that stimulate the growth of specific bacterial groups including staphylococci and bifidobacteria.
    A recent study has compared the intestinal microbiota of European and African children (respectively from Florence and a rural village in Burkina Faso) between the ages of 1 and 6 years old. It has highlighted the dominant role of diet over variables such as climate, geography, hygiene and health services (it was also observed the absence of significant differences in the expression of key genes regulating the immune function, which suggests a functional similarity between the two groups). Indeed infants, as long as they are breastfed, have a very similar gut microbiota, rich in Actinobacteria, mainly Bifidobacterium (see below). The subsequent introduction of solid foods in the two groups, a Western diet rich in animal fats and proteins in European children, and low in animal protein but rich in complex carbohydrates in African children, leads to a differentiation in the Firmicutes/Bacteroidetes ratio between the two groups. Gram-positive bacteria, mainly Firmicutes, were more abundant than Gram-negative bacteria in European children, whereas Gram-negative bacteria, mainly Bacteroidetes, prevailed over Gram-positive bacteria in African children.
    And the long-term diets are strongly associated to the enterotype partitioning. Indeed, it has been observed that:

a diet high in animal fats and proteins, i.e. a Western-type diet, leads to a gut microbiota dominated by the Bacteroides enterotype;
a diet high in complex carbohydrates, typical of agrarian societies, leads to the prevalence of the Prevotella enterotype.

Similar results emerged from the aforementioned study on children. In the Europeans, gut microbiota was dominated by taxa typical of Bacteroides enterotype, whereas in the Burkina Faso children, Prevotella enterotype dominates.
With short-term changes in the diet (10 days), such as the switch from a low-fat and high-fiber diet to a high-fat and low-fiber diet and vice versa, changes were observed in the composition of the microbiome (within 24 hours), but no stable change in the enterotype partitioning. And this underlines as a long-term diet is needed for a change in the enterotypes of the gut microbiota.
Dietary interventions can also result in changes in the gut virome, which moves to a new state, that is, changes occur in the proportions of the pre-existing viral populations, towards which subjects on the same diet converge.

  • pH, bile salts and digestive enzymes.
    The stomach, due to its low pH, is a hostile environment for bacteria, which are not present in high numbers, about 102-103 bacterial cells/gram of tissue. In addition to Helicobacter pylori, able to cause gastritis and gastric ulcers, microorganisms of the genus Lactobacillus are also present.
    Reached the duodenum, an increase in bacterial cell number occurs, 104-105 bacterial cells/gram of tissue; and similar bacterial concentrations are present in the jejunum and proximal ileum. The low number of microorganisms present in the small intestine is due to the inhospitable environment, consequent to the fact that there is the opening of the ampulla of Vater in the descending part of the duodenum, which pours pancreatic juice and bile into the duodenum, that is, pancreatic enzymes and bile salts, which damage microorganisms.
    In the terminal portion of the ileum, where the activities of pancreatic enzymes and bile salts are lower, there are about 107 bacterial cells/gram of tissue, and up to 1012-1014 bacterial cells/gram of tissue in the colon, so that bacteria represent a large proportion, about 40%, of the fecal mass.
    The distribution of bacteria along the intestine is strategic. In the duodenum and jejunum, the amount of available nutrients is much higher than that found in the terminal portion of the ileum, where just water, fiber, and electrolytes remain. Therefore, the presence of large number of bacteria in the terminal portion of the ileum, and even more in the colon, is not a problem. The problem would be to find a high bacterial concentration in the duodenum, jejunum, and proximal parts of the ileum; and there is a disease condition, called small intestinal bacterial overgrowth or SIBO, in which the number of bacteria in the small intestine increases by about 10-15 times. This puts them in a position to compete with the host for nutrients and give rise to gastrointestinal disturbances such as diarrhea.
  • The geographical position and the resulting differences in lifestyle, diet, religion etc.
    For example, a kind of geographical gradient occurs in the microbiota of European infants, with a higher number of Bifidobacterium species and some of Clostridium in Northern infants, whereas Southern infants have higher levels of Bacteroides, Lactobacillus and Eubacterium.
  • The mode of delivery (see below).
  • The genetics of the host.
  • The health status of the infant and mother.
    For example, in mothers with inflammatory bowel disease or IBD, Faecalibacterium prausnitzii, a bacterium that produces butyrate (an important source of energy for intestinal cells), and with anti-inflammatory activity is depleted, whereas there is an increase in the number of adherent Escherichia coli.
  • The treatment with antibiotics.
  • Bacterial infections and predators.
    Bacteriocins, i.e. proteins with antibacterial activity, and bacteriophages.
    Phages play an important role in controlling the abundance and composition of the gut microbiota. In particular, they could play a major role in the colonization of the newborn, infecting the dominant bacteria thus allowing to another bacterial strain to become abundant.
    This model of predator-prey dynamics, called “kill the winner”, suggests that the blooms of a specific bacterial species would lead to blooms of their corresponding bacteriophages, followed by a decline in their abundance. Therefore, the most abundant bacteriophage genotype will not be the same at different times. And although some the gene sequences present in the infant gut virome are stable over the first three months of life, dramatic changes occur in the overall composition of the viral community between the first and second week of life. During this time period also the bacterial community is extremely dynamic (see below).
  • The competition for space and nutrients.

Composition throughout life

The development of the intestinal microbial ecosystem is a complex and crucial event in human life, highly variable from individual to individual, and influenced by the factors outlined above.

Development and modifications of gut microbiota throughout life

In utero, the gut is considered sterile, but is rapidly colonized by microbes at birth, as the infant is born with an immunological tolerance instructed by the mother.
However, recent studies show the presence of bacteria in the placental tissue, umbilical cord blood, fetal membranes and amniotic fluid from healthy newborns without signs of infection or inflammation. And for example, the meconium of premature infants, born to healthy mothers, contains a specific microbiota, with Firmicutes as the main phylum, and predominance of staphylococci, whereas Proteobacteria, in particular species such as Escherichia coli, Klebsiella pneumoniae, Serratia marcescens, but also enterococci are more abundant in the faeces.
Note: The meconium is free of detectable viruses.
It seems that both vaginal and gut bacteria may gain access to the fetus, although via different route of entry: by ascending entry the vaginal ones, by dendritic cells of the immune system the gut ones. Therefore, there could exist a fetal microbiota.

Colonization occurs during delivery by a maternal inoculum, generally composed of aerobic and facultative bacteria (the newborn’s gut initially contains oxygen), then replaced by obligate anaerobes,  bacteria typically present in adulthood, to which they have created a hospitable environment.
Furthermore, there is a small number of different taxa, with a relative dominance of the phyla Actinobacteria and Proteobacteria, that remains unchanged during the first month of life, but not in the subsequent ones as there is a large increase in variability and new genetic variants. Many studies underline that the initial exposure is important in defining the “trajectories” which will lead to the adult ecosystems. Additionally, these initial communities may act as a source of protective or pathogenic microorganisms.

Mother’s vaginal and fecal microbiotas are the main sources of inoculum in vaginally delivered infants. Indeed, infants harbor microbial communities dominated by species of the genera Lactobacillus (the most abundant genus in the vaginal microbiota and early gut microbiota) Bifidobacterium, Prevotella, or Sneathia. And it seems likely that anaerobes, such as members of the phyla Firmicutes and Bacteroidetes, not growing outside of their host, rely on the close contact between mother and offspring for transmission. Finally, due to the presence of oxygen in infant gut, the transmission of strict anaerobes could occur not directly at birth but at a later stage by means of spores.
The first bacteria encountered by infants born by caesarean section are those of the skin and hospital environment, and gut microbiota is dominated by species of the genera Corynebacterium, Staphylococcus and Propionibacterium, with a lower bacterial count and diversity in first weeks of life than infants born vaginally.
Further evidence supporting the hypothesis of vertical transmission is the similarity between the microbiota of meconium and samples obtained from possible sites of contamination.
These “maternal bacteria” do not persist indefinitely, and are replaced by other populations within the first year of life.
Objects, animals, mouths and skin of relatives, and breast milk are secondary sources of inoculum; and breast milk (see below) seems to have a primary role in determining the microbial succession in the gut.
The variation and diversity among children reflect instead the individuality of these microbial exposures.
Note: The delivery mode seems also to influence the immune system during the first year of life, perhaps via the influence on the development of gut microbiota. Infants born by cesarean section have:

  • a lower bacterial count in stool samples at one month of age, mainly due to the higher number of bifidobacteria in infants born vaginally;
  • a higher number of antibody secreting cells, which could reflect an excessive antigen exposure (the intestinal barrier would be more vulnerable to the passage of antigens).

Within a days after birth, a thriving community is established. This community is less stable over time and more variable in composition than that of adults. Very soon, it will be more numerous than that of the child’s cells, evolving according to a temporal pattern highly variable from individual to individual.
Viruses, absent at birth, reach about 108 units/gram wet weight of faeces by the end of the first week of life, therefore representing a dynamic and abundant component of the developing gut microbiota. However, viral community has an extremely low diversity, like bacteria, and is dominated by phages, which probably influence the abundance and diversity of co-occurring bacteria, as seen above. The initial source of the viruses is unknown; of course, maternal and/or environmental inocula are among the possibilities. Notably, the earliest viruses could be the result of induction of prophages from the “newborn” gut bacterial flora, hypothesis supported by the observation that more than 25% of the phage sequences seem to be very similar to those of phages infecting bacteria such as Lactococcus, Lactobacillus, Enterococcus, and Streptococcus, which are abundant in breast milk.

By the end of the first month of life it is thought that the initial phase of rapid acquisition of microorganism is over.
In 1-month-old-infants, the most abundant bacteria belong to the genera Bacteroides and Escherichia, whereas Bifidobacterium, along with Ruminococcus, appear and grow to become dominant in the gastrointestinal tract of the breastfed infants between 1 and 11 months. Bifidobacteria such as Bifidobacterium longum subspecies infantis:

  • are known to be closely related to breastfeeding;
  • are among the best characterized commensal bacteria;
  • are considered probiotics, that is, microorganisms which can confer health benefits to the host.

Their abundance confers also benefits through competitive exclusion, that is, they are an obstacle to colonization by pathogens. And indeed, Escherichia and Bacteroides can become preponderant if Bifidobacterium is not adequately present in the gut.
In contrast, bacteria of the genera Escherichia (e.g. E. coli), Clostridium (e.g. C. difficile), Bacteroides (e.g. B. fragilis) and Lactobacillus are present in higher levels in formula-fed infants than in breastfed infants.
Although breast-fed infants receive only breast milk until weaning, their microbiota can show a large variability in the abundances of bacterial taxa, with differences between individuals also with regard to the temporal patterns of variation. These variations may be due to diseases, treatments with antibiotics, changes in host lifestyle, random colonization events, as well as differences in immune responses to the gut colonizing microbes. However, it is not yet clear how these factors contribute to shape infant gut microbiota.
It seems that also the virome changes rapidly after birth, as the majority of the viral sequences present in the first week of life are not found after the second week. Moreover, the repertoire expands rapidly in number and diversity during the first three months. This is in contrast with the stability observed in the adult virome, where 95% of the sequences are conserved over time.

In normal condition, towards the end of the first year of life, babies have consumed an adult-like diet for a significant time period and should have developed a microbial community with characteristics similar to those found in the adult gut, such as:

  • a more stable composition, phylogenetically more complex, and progressively more similar among different subjects;
  • a preponderance of Firmicutes and Bacteroidetes, followed by Verrucomicrobia and a very low abundance of Proteobacteria;
  • an increase in short-chain fatty acid (SCFA) levels and bacterial load in the feces;
  • an increase of genes associated with xenobiotic degradation, vitamin biosynthesis, and carbohydrate utilization.

Interestingly, the significant turnover of taxa occurring from birth to the end of the first year is accompanied by a remarkable constancy in the overall functional capabilities.
Towards the end of the first year of life also the early viral colonizers were replaced by a community specific to the child.

The gut microbiota reaches maturity at about 2.5 years of age, fully resembling the adult gut microbiota.
The selection of the most adapted bacteria is the result of various factors.

  • The transition to an adult diet.
  • An increased fitness to the intestinal environment of the taxa that typically dominate the adult gut microbiota than the early colonizers.
  • The significant changes in the intestinal environment, result of the developmental changes in the intestinal mucosa.
  • The effects of the microbiota itself.

Therefore, the first 2-3 years of life are the most critical period in which you can intervene to shape the microbiota as best as possible, and so optimize child growth and development.

From a chaotic beginning, all this leads to the establishment of the gut ecosystem typical of the young adult, which is relatively stable over time until old age (viral, archaeal and eukaryotic components included), and dominated, at least in the western population, by members of the phyla Firmicutes, about 60% of the bacterial communities, Bacteroidetes and Actinobacteria (mainly belonging to the Bifidobacterium genus), each comprising about 10% of the bacterial community, followed by Proteobacteria and Verrucomicrobia. The genera Bacteroides, Clostridium, Faecalibacterium, Ruminococcus and Eubacterium make up, together with Methanobrevibacter smithii, the large majority of the adult gut microbial community.
It should be noted that different data were obtained from analysis of populations of African rural areas, as seen above.
And the gut microbiota is sufficiently similar among subjects to allow the identification of a shared core microbiome.
Stability and resilience, however, are subject to numerous variables among which, as previously said, diet seems to be one of the most important. Therefore, in order to maintain the stability of the gut microbiota, the variables have to be kept constant, or in the case of diseases prevented (also through vaccinations). However, the stability and resilience could be harmful if the dominant community is pathogenic.

The gut microbiota undergoes substantial changes in the elderly. In a study conducted in Ireland on 161 healthy people aged 65 years and over, the gut microbiota is distinct from that of younger adults in the majority of subjects, with a composition that seems to be dominated by the phyla Bacteroidetes, the main ones, and Firmicutes, with almost inverted percentages than those found in younger adults (although large variations across subjects were observed). And there are Faecalibacterium, about 6% of the main genera, followed by species of the genera Ruminococcus, Roseburia and Bifidobacterium (the latter about 0.4%) among the most abundant genera.
Also the variability in the composition of the community is greater than in younger adults; this could be due to the increase in morbidities associated with aging and the subsequent increased intake of medications, as well as to changes in the diet.


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Human microbiota: definition, composition, function, and effect of antibiotics

It has been known for almost a century that humans harbor a microbial ecosystem, known as human microbiota, remarkably dense and diverse, made up of a  number of viruses and cells much higher than those of the human body, and that accounts for one to three percent of body weight. All the genes encoded by the human body’s microbial ecosystem, which are about 1,000 times more numerous than those of our genome, make up the human microbiome. Microorganisms colonize all the surfaces of the body that are exposed to the environment. Indeed, distinct microbial communities are found on the skin, in the vagina, in the respiratory tract, and along the whole intestinal tract, from the mouth up to rectum, the last part of the intestine.


Composition of the human microbiota

It is composed of organisms from all taxa.

  • Bacteria, at least 100 trillion (1014) cells, a number ten times greater than that of the human body. They are found in very high concentration in the intestinal tract, up to 1012-1014/gram of tissue, where they form one of the most densely populated microbial habitats on Earth. In the gut, bacteria mainly belong to the Firmicutes, Bacteroidetes and Actinobacteria phyla. Fusobacteria (oropharynx), Tenericutes, Proteobacteria, and Verrucomicrobia are other phyla present in our body.
    Note: Bacterial communities in a given body region resemble themselves much more across individuals than those from different body regions of the same individual; for example, bacterial communities of the upper respiratory tract are much more similar across individuals than those of the skin or intestine of the same individual.
  • Viruses, by far the most numerous organisms, about quadrillion units. The genomes of all the viruses harbored in the human body make up the human virome. In the past, viruses and eukaryotes (see below) have been studied focusing on pathogenic microorganisms, but in recent years the attention has also shifted on many non-pathogenic members of these groups. And many of the viral gene sequences found are new, which suggests that there is still much to learn about the human virome. Finally, just like for bacteria, there is considerable interpersonal variability.
  • Archaebacteria, primarily those belonging to the order Methanobacteriales, with Methanobrevibacter smithii predominant in the human gut (up to 10% of all anaerobes).
  • Eukaryotes, and the parasites of the genera Giardia and Entamoeba have probably been among the first to be identified. But there is also a great abundance and diversity of fungal species, belonging to genera such as Candida, Penicillium, Aspergillus, Hemispora, Fusarium, Geotrichum, Hormodendrum, Cryptococcus, Saccharomyces, and Blastocystis.

Candida albicans, a component of Human Microbiota

Based on the relationships with the human host, microorganisms may be classified as commensals or pathogens.

  • Commensals cause no harm to the host, with which they establish a symbiotic relationship that generally brings benefits to both.
  • On the contrary, pathogens are able to cause diseases, but fortunately represent a small percentage of the human microbiota. These microorganisms establish a symbiosis with the human host and benefit from it at the expense of the host. They can cause disease:

if they move from their niche, such as the intestine, into another one where they do not usually reside, such as the vagina or bladder (as in the case of Candida albicans, normally present in the intestine, but in very small quantities);
in patients with impaired immunological defenses, such as after an immunosuppressive therapy.

Functions of the human microbiota

Sometimes referred to as “the forgotten organ“, human microbiota, mainly with its intestinal bacterial members, plays many important functions that can lead to nutritional, immunological, and developmental benefits, but can also cause diseases. Here are some examples.

  • It is involved in the development of the gastrointestinal system of the newborn, as shown by experiments carried out on germ-free animals in which, for example, the thickness of the intestinal mucosa is thinner than that of colonized animals, therefore more easily subject to rupture.
  • It contributes to energy harvest from nutrients, due to its ability to ferment indigestible carbohydrates, promote the absorption of monosaccharides and the storage of the derived energy. This has probably been a very strong evolutionary force that has played a major role in favor of the fact that these bacteria became our symbionts.
  • It contributes to the maintenance of the acidic pH of the skin and in the colon.
  • It is involved in the metabolism of xenobiotics and several polyphenols.
  • It improves water and mineral absorption in the colon.
  • It increases the speed of intestinal transit, slower in germ-free animals.
  • It has an important role in resistance to colonization by pathogens, primarily in the vagina and gut.
  • It is involved in the biosynthesis of isoprenoids and vitamins through the methylerythritol phosphate pathway.
  • It stimulates angiogenesis.
  • In the intestinal tract, it interacts with the immune system, providing signals for promoting the maturation of immune cells and the normal development of immune functions. And this is perhaps the most important effect of the symbiosis between the human host and microorganisms. Experiments carried out on germ-free animals have shown, for example, that:

macrophages, the cells that engulf pathogens and then present their antigens to the immune system, are found in much smaller amounts than those present in the colonized intestine, and if placed in the presence of bacteria they fail to find and therefore engulf them, unlike macrophages extracted from a colonized intestine;
there is not the chronic non-specific inflammation, present in the normal intestine as a result of the presence of bacteria (and of what we eat).

  • Changes in its composition can contribute to the development of obesity and metabolic syndrome.
  • It protects against the development of type I diabetes.
  • Many diseases, both in children and adults, such as stomach cancer, lymphoma of mucosa-associated lymphoid tissue, necrotizing enterocolitis (an important cause of morbidity and mortality in premature babies) or chronic intestinal diseases, are, and others seem to be, related to the gut microbiota.

In conclusion, it seems very likely that the human body represents a superorganism, result of years of evolution and made up of human cells, and the resulting metabolic and physiological capacities, as well as an additional organ, the microbiota.

Human Microbiome Project

The bacterial component of the human microbiota is the subject of most studies including a large-scale project started in 2008 called “Human Microbiome Project“, whose aim is to characterize the microbiome associated with multiple body sites, such as the skin, mouth, nose, vagina and intestine, in 242 healthy adults. These studies have shown a great variability in the composition of the human microbiota; for example, twins share less than 50% of their bacterial taxa at the species level, and an even smaller percentage of viruses. The factors that shape the composition of bacterial communities begin to be understood: for example, the genetic characteristics of the host play an important, although this is not true for the viral community. And metagenomic studies have shown that, despite the great interpersonal variability in microbial community composition, there is a core of shared genes encoding signaling and metabolic pathways. It appears namely that the assembly and the structure of the microbial community does not occur according to the species but the more functional set of genes. Therefore, disease states of these communities might be better identified by atypical distribution of functional classes of genes.

Effect of antibiotics

The microbiota in healthy adult humans is generally stable over time. However, its composition can be altered by factors such as dietary changes, urbanization, travel, and especially the use of broad-spectrum antibiotics. Here are some examples of the effect of antibiotic treatments.

  • There is a long-term reduction in microbial diversity.
  • The taxa affected vary from individual to individual (even up to a third of the taxa).
  • Several taxa do not recover even after 6 months from treatment.
  • Once the bacterial communities have reshaped, a reduced resistance to colonization occurs. This allows foreign and/or pathogen bacteria, able to grow more than the commensals, to cause permanent changes in human microbiota structure, as well as acute diseases, such as the dangerous pseudomembranous colitis, and chronic diseases, as it is suspected for asthma following the use and abuse of antibiotics in childhood. Moreover, their repeated use has been suggested to increase the pool of antibiotic-resistance genes in our microbiome. In support of this hypothesis, a decrease in the number of antibiotic-resistant pathogens has been observed in some European countries following the reduction in the number of antibiotics prescribed.

Finally, you must not underestimate the fact that the intestinal microflora is involved in many chemical transformations, and its alteration could be implicated in the development of cancer and obesity. However, regarding use of antibiotics, you should be underlined that if western population has a life expectancy higher than in the past is also because you do not die of infectious diseases!


Burke C., Steinberg P., Rusch D., Kjelleberg S., and Thomas T. Bacterial community assembly based on functional genes rather than species. Proc Natl Acad Sci USA 2011;108:14288-14293. doi:10.1073/pnas.1101591108

Clemente J.C., Ursell L.K., Wegener Parfrey L., and Knight R. The impact of the gut microbiota on human health: an integrative view. Cell 2012;148:1258-1270. doi:10.1016/j.cell.2012.01.035

Gill S.R., Pop M., Deboy R.T., Eckburg P.B., Turnbaugh P.J., Samuel B.S., Gordon J.I., Relman D.A., Fraser-Liggett C.M., and Nelson K.E. Metagenomic analysis of the human distal gut microbiome. Science 2006;312:1355-1359. doi:10.1126/science.1124234

Palmer C., Bik E.M., DiGiulio D.B., Relman D.A., and Brown P.O. Development of the human infant intestinal microbiota. PLoS Biol 2007;5(7):e177. doi:10.1371/journal.pbio.0050177

Turnbaugh P.J., Gordon J.I. The core gut microbiome, energy balance and obesity. J Physiol 2009;587:4153-4158. doi:10.1113/jphysiol.2009.174136

Zhang, T., Breitbart, M., Lee, W., Run, J.-Q., Wei, C., Soh, S., Hibberd, M., Liu, E., Rohwer, F., Ruan, Y. Prevalence of plant viruses in the RNA viral community of human feces. PLoS Biol 2006;4(1):e3. doi:10.1371/journal.pbio.0040003

Chemical composition of olive oil

From a chemical point of view, we can identify in the olive oil two fractions, depending on the behavior in the presence of heating and strong alkaline solutions (concentrated solutions of KOH or NaOH):

  • the saponifiable fraction, which represents 98-99% of the total weight, is composed of substances that form soaps in the above conditions;
  • the unsaponifiable fraction, which represents the remaining 1-2% of the total weight, is composed of substances that fail to form soaps in the above conditions.


Saponifiable fraction

It is composed of saturated fatty acids and unsaturated fatty acids, esterified almost entirely to glycerol to form triglycerides (or triacylglycerols). To a much lesser extent, diglycerides (or diacylglycerols), monoglycerides (monoacylglycerols), and free fatty acids are also found.
Unsaturated fatty acids make up 75 to 85% of the total fatty acids. Oleic (O) and linoleic (L) acids are the most abundant ones; palmitoleic, eptadecenoic, gadoleic and alpha-linolenic (Ln) acids are present in lower/trace amounts.

International Olive Oil Council (IOOC) requirements for fatty acids in olive oil
IOOC Requirements for Olive Oil

Oleic acid is the major fatty acid in olive oils. According to the rules laid down by the International Olive Oil Council (IOOC), its concentration must range from 55% to 83% of total fatty acids.
Linoleic acid is the most abundant polyunsaturated fatty acid in olive oil; its concentration must vary between 2.5% and 21% (IOOC). Because of its high degree of unsaturation, it is subject to oxidation; this means that an oil high in linoleic acid becomes rancid easily, and thus it may be stored for a shorter time.
In a Mediterranean-type diet, olive oil is the main source of fat: therefore, oleic acid, among monounsaturated fatty acids, and linoleic acid, among polyunsaturated fatty acids, are the most abundant fatty acids.
alpha-Linolenic acid must be present in very low amount, according to the IOOC standards ≤1%. It is an omega-3 polyunsaturated fatty acid, which may have health benefits. However, because of to its high degree of unsaturation (higher than that of linoleic acid), it is very susceptible to oxidation, and therefore it promotes rancidity of the olive oil that contains it.
Saturated fatty acids make up 15 to 25% of the total fatty acids.
Palmitic (P) (7.5-20%) and stearic (S) acids (0.5-5%) are the most abundant saturated fatty acids; myristic, heptadecanoic, arachidic, behenic and lignoceric acids may be present in trace amounts.

The presence of fatty acids that should be absent or present in amounts different than those found is a marker of adulteration with other vegetable oils. On this regard, particular attention is paid to myristic, arachidic, behenic, lignoceric, gadoleic and alpha-linolenic acids, whose limits are set by IOOC.

Fatty acid composition is influenced by several factors.

  • The climate.
  • The latitude.
  • The zone of production.
    Italian, Spanish and Greek olive oils are high in oleic acid and low in palmitic and linoleic acids, while Tunisian olive oils are high in palmitic and linoleic acids but lower in oleic acid. Therefore, oils can be divided into two groups:

one rich in oleic acid and low in palmitic and linoleic acids;
the other high in palmitic and linoleic acids and low in oleic acid.

  • The cultivar.
  • The degree of olive ripeness at the time of oil extraction.
    It should be noted that oleic acid is formed first in the fruit, and data seem to indicate a competitive relationship between oleic acid and palmitic, palmitoleic, and linoleic acids.


As previously said, fatty acids in olive oil are almost entirely present as triglycerides.
In small percentage, they are also present as diglycerides, monoglycerides, and in free form.

Sterospecific numbering of triglycerides

During triglyceride biosynthesis, thanks to the presence of specific enzymes, only about 2% of glycerol binds palmitic acid in the sn-2 position (also the percentage of stearic acid in the sn-2 position is very low); for the most part, the sn-2 position is occupied by oleic acid.
On the contrary, if we consider oils that have undergone a nonenzymatic esterification, the percentage of palmitic acid in the sn-2 position increases significantly.
Note: sn = Stereospecific numbering

Among triglycerides present in significant proportions in olive oil, there are:

  • OOO: 40-59%;
  • POO: 12-20%;
  • OOL: 12.5-20%;
  • POL:  5.5-7%;
  • SOO: 3- 7%.

POP, POS, OLnL, OLnO, PLL, PLnO are present in smaller amounts.
Trilinolein (LLL) is a triglyceride that contains three molecules of linoleic acid. Its low content is an indicator of an oil of good quality.
Triglycerides containing three saturated fatty acids or three molecules of alpha-linolenic acid have not been reported.

Diglycerides and monoglycerides

Their presence is due to an incomplete synthesis and/or a partial hydrolysis of triglycerides.
The content of diglycerides in virgin olive oil ranges from 1% to 2.8%. 1,2-Diglycerides prevail in fresh olive oil, representing over 80% of the diglycerides. During oil storage, isomerization occurs with a progressive increase of the more stable 1-3 isomers, which after about 10 months become the major isomers.
Therefore, the ratio 1,2/1,3-diglycerides may be used as an indicator of the age of the oil.
Monoglycerides are present in amounts lower than diglycerides, <0.25%, with 1-monoglycerides far more abundant than 2-monoglycerides.

Unsaponifiable fractions

It is composed of a large number of different molecules, very important from a nutritional point of view, as they contribute significantly to the health effects of olive oil.
Furthermore, they are responsible for the stability and the taste of olive oil, and are also used to detect adulteration with other vegetable oils.
This fraction includes tocopherols, sterols, polyphenols, pigments, hydrocarbons, aromatic and aliphatic alcohol, triterpene acids, waxes, and minor constituents.
Their content is influenced by factors similar to those seen for fatty acid composition, such as:

  • the cultivar;
  • the degree of ripeness of the olive;
  • the zone of production;
  • the crop year and olive harvesting practices;
  • the storage time of olives;
  • the oil extraction process;
  • the storage conditions of the oil.

It should be noted that many of these compounds are not present in refined olive oils, as they are removed during the refining processes.


They make up 18 to 37% of the unsaponifiable fraction.
They are a very heterogeneous group of molecules with nutritional and organoleptic properties  (for example, oleuropein and hydroxytyrosol give oil its bitter and pungent taste).
For a more extensive discussion, see: ” Polyphenols in olive oil: variability and composition.”


They make up 30 to 50% of the unsaponifiable fraction.
Squalene and beta-carotene are the main molecules.
Squalene, isolated for the first time from shark liver, is the major constituent of the unsaponifiable fraction, and constitutes more than 90% of the hydrocarbons. Its concentration ranges from 200 to 7500 mg/kg of olive oil.

Skeletal formula of squalene, an hydrocarbon of the unsaponifiable fraction of olive oil

It is an intermediate in the biosynthesis of the four-ring structure of steroids, and it seems to be responsible of several health effects of olive oil.
In the hydrocarbon fraction of virgin olive oil, n-paraffins, diterpene and triterpene hydrocarbons, isoprenoidal polyolefins are also found.
Beta-carotene acts both as antioxidant, protecting oil during storage, and as dye (see below).


They are important lipids of olive oil, and are:

  • linked to many health benefits for consumers;
  • important to the quality of the oil;
  • widely used for checking its genuineness.
    On this regard, it is to underline that sterols are species-specific molecules; for example, the presence of high concentrations of brassicasterol, a sterol typically found in Brassicaceae (Cruciferae) family, such as rapeseed, indicates adulteration of olive oil with canola oil.

Four classes of sterols are present in olive oil: common sterols, 4-methylsterols, triterpene alcohols, and triterpene dialcohols. Their content ranges from 1000 mg/kg, the minimum value required by the IOOC standard, to 2000 mg/kg. The lowest values are found in refined oils because of the refining processes may cause losses up to 25%.

Common sterols or 4α-desmethylsterols

Common sterols are present mainly in the free and esterified form; however they have been also found as lipoproteins and sterylglucosides.
The main molecules are beta-sitosterol, which makes up 75 to 90% of the total sterol, Δ5-avenasterol, 5 to  20%, and campesterol, 4%. Other components found in lower amounts or traces are, for example, stigmasterol, 2%, cholesterol, brassicasterol, and ergosterol.Skeletal formula of beta-sitosterol, a sterol of the unsaponifiable fraction of olive oil


They are intermediates in the biosynthesis of sterols, and are present both in the free and esterified form. They are present in small amounts, much lower than those of common sterols and triterpene alcohols, varying between 50 and 360 mg/kg. The main molecules are obtusifoliol, cycloeucalenol, citrostadienol, and gramisterol.

Triterpene alcohols or 4,4-dimethylsterols

They are a complex class of sterols, present both in the free and esterified form. They are found in amounts ranging from 350 to 1500 mg/kg.
The main components are beta-amyrin, 24-methylenecycloartanol, cycloartenol, and butyrospermol; other molecules present in lower/trace amounts are, for example, cyclosadol, cyclobranol, germanicol, and dammaradienol.

Triterpene dialcohols

The main triterpene dialcohols found in olive oil are erythrodiol and uvaol.
Erythrodiol is present both in the free and esterified form; in virgin olive oil, its level varies between 19 and 69 mg/kg, and the free form is generally lower than 50 mg/kg.


They make up 2 to 3% of the unsaponifiable fraction, and include vitamin E.
Of the eight E-vitamers, alpha-tocopherol represents about 90% of tocopherols in virgin olive oil. It is present in the free form and in very variable amount, but on average higher than 100 mg/kg of olive oil. Thanks to its in vivo antioxidant properties, its presence is a protective factor for health. Alpha-tocopherol concentration seems to be related to the high levels of chlorophylls and to the concomitant requirement for deactivation of singlet oxygen.
Beta-tocopherol, delta-tocopherol, and gamma-tocopherol are usually present in low amounts.


In this group we find chlorophylls and carotenoids.
In olive oil, chlorophylls are present as phaeophytins, mainly  phaeophytin a (i.e. a chlorophyll from which magnesium has been removed and substituted with two hydrogen ions), and confer the characteristic green color to olive oil. They are photosensitizer molecules that contribute to the photooxidation of olive oil itself.
Beta-carotene and lutein are the main carotenoids in olive oil. Several xanthophylls are also present, such as antheraxanthin, beta-cryptoxanthin, luteoxanthin, mutatoxanthin, neoxanthin, and violaxanthin.
Olive oil’s color is the result of the presence of chlorophylls and carotenoids and of their green and yellow hues. Their presence is closely related.

Triterpene acids

They are important components of the olive, and are present in trace amounts in the oil.
Oleanolic and maslinic acids are the main triterpene acids in virgin olive oil: they are present in the olive husk, from which they are extracted in small amount during processing.

Aliphatic and aromatic alcohols

Fatty alcohols and diterpene alcohols are the most important ones.
Aliphatic alcohols have a number of carbon atoms between 20 and 30, and are located mostly inside the olive stones, from where they are partially extracted by milling.

Fatty alcohols

They are linear saturated alcohols with more than 16 carbon atoms.
They are found in the free and esterified form and are present, in virgin olive oil, in amount not generally higher than 250 mg/kg.
Docosanol (C22), tetracosanol (C24), hexacosanol (C26), and octacosanol (C28) are the main fatty alcohols in olive oil, with tetracosanol and hexacosanol present in larger amounts.
Waxes, which are minor constituents of olive oil, are esters of fatty alcohols with fatty acids, mainly of palmitic acid and oleic acid. They can be used as a criterion to discriminate between different types of oils; for example, they must be present in virgin and extra virgin olive oil at levels <150 mg/kg, according to the IOOC standards.

Diterpene alcohols

Geranylgeraniol and phytol are two acyclic diterpene alcohols, present in the free and esterified form. Among esters present in the wax fraction of extra virgin olive oil, oleate, eicosenoate , eicosanoate, docosanoate, and tetracosanoate have been found, mainly as phytyl derivatives.

Volatile compounds

More than 280 volatile compounds have been identified in olive oil, such as hydrocarbons, the most abundant fraction, alcohols, aldehydes, ketones, esters, acids, ethers and many others. However, only about 70 of them are present at levels higher than the perception threshold beyond which they may contribute to the aroma of virgin olive oil.

Minor components

Phospholipids are found among the minor components of olive oil; the main ones are phosphatidylserine, phosphatidylethanolamine, phosphatidylcholine, phosphatidylinositol.
In the unfiltered oils, trace amounts of proteins may be found.


Gunstone F.D. Vegetable oils in food technology: composition, properties and uses. 2th Edition. Wiley J. & Sons, Inc., Publication, 2011

Caponio F., Bilancia M.T., Pasqualone A., Sikorska E., Gomes T. Influence of the exposure to light on extra virgin olive oil quality during storage. Eur Food Res Technol 2005;221:92-98. doi:10.1007/s00217-004-1126-8

Servili M., Sordini B., Esposto S., Urbani S., Veneziani G., Di Maio I., Selvaggini R. and Taticchi A. Biological activities of phenolic compounds of extra virgin olive oil. Antioxidants 2014;3:1-23. doi:10.3390/antiox3010001

Gluten: definition, gliadins, glutenins, and containing grains

Gluten is not a single protein but a mixture of cereal proteins, about 80% of its dry weight (for example gliadins and glutenins in wheat grains), lipids, 5-7%, starch, 5-10%, water, 5-8%, and mineral substances, <2%.
It forms when components naturally present in the grain of cereals, the caryopsis, and in their flours, are joined together by means of mechanical stress in aqueous environment, i.e. during the formation of the dough.
The term is also related to the family of proteins that cause problems for celiac patients (see below).
Isolated for the first time in 1745 from wheat flour by the Italian chemist Jacopo Bartolomeo Beccari, it can be extracted from the dough by washing it gently under running water: starch, albumins and globulins, that are water-soluble, are washed out, and a sticky and elastic mass remains, precisely the gluten (it means glue in Latin).


Cereals containing gluten

It is present in:

  • wheat, such as:

durum wheat (Triticum durum); groats and semolina for dry pasta making are obtained from it;
common wheat or bread wheat (Triticum aestivum), so called because it is used in bread and fresh pasta making, and in bakery products;

  • rye (Secale cereale);
  • barley (Hordeum vulgare);
  • spelt, in the three species:

einkorn (Triticun monococcum);
emmer (Triticum dicoccum Schrank);
spelta (Triticum spelta);

  • khorasan wheat (Triticum turanicum); a variety of it is Kamut®;
  • triticale (× Triticosecale Wittmack), which is a hybrid of rye and common wheat;
  • bulgur, which is whole durum wheat, sprouted and then processed;
  • seitan, which is not a cereal, but a wheat derivative, also defined by some as “gluten steak”.

Given that most of the dietary intake of gluten comes from wheat flour, of which about 700 million tons per year are harvested, representing about 30% of the global cereal production, the following discussion will focus on wheat gluten, and mainly on its proteins.

Note: The term gluten is also used to indicate the protein fraction that remains after removal of starch and soluble proteins from the dough obtained with corn flour: however, this “corn gluten” is “functionally” different from that obtained from wheat flour.

Cereal grain proteins

The study of cereal grain proteins, as seen, began with the work of Beccari. 150 years later, in 1924, the English chemist Osborne T.B., which can rightly be considered the father of plant protein chemistry, developed a classification based on their solubility in various solvents.
The classification, still in use today, divides plant proteins into 4 families.

  • Albumins, soluble in water.
  • Globulins, soluble in saline solutions; for example avenalin of oat.
  • Prolamins, soluble in 70% alcohol solution, but not in water or absolute alcohol.
    They include:

gliadins of wheat;
zein of corn;
avenin of oats;
hordein of barley;
secalin of rye.

They are the toxic fraction of gluten for celiac patients.

  • Glutelins, insoluble in water and neutral salt solutions, but soluble in acidic and basic solutions.
    They include glutenins of wheat.
Proteins found in cereal grains: albumins, globulins, prolamins, glutelins
Cereal Grain Proteins

Albumins and globulins are cytoplasmic proteins, often enzymes, rich in essential amino acids, such as lysine, tryptophan and methionine. They are found in the aleurone layer and embryo of the caryopsis.
Prolamins and glutelins are the storage proteins of cereal grains. They are rich in glutamine and proline, but very low in lysine, tryptophan and methionine. They are found in the endosperm, and are the vast majority of the proteins in the grains of wheat, corn, barley, oat, and rye.
Although Osborne classification is still widely used, it would be more appropriate to divide cereal grain proteins into three groups: structural and metabolic proteins, storage proteins, and defense proteins.

Wheat gluten proteins

Proteins represent 10-14% of the weight of the wheat caryopsis (about 80% of its weight consists of carbohydrates).
According to the Osborne classification, albumins and globulins represent 15-20% of the proteins, while prolamins and glutelins are the remaining 80-85%, composed respectively of gliadins, 30-40%, and glutenins, 40-50%. Therefore, and unlike prolamins and glutelins in the grains of other cereals, gliadins and glutenins are present in similar amounts, about 40% (see Fig. 2).

Gluten and other proteins found in wheat grains
Wheat Grain Proteins

Technologically, gliadins and glutenins are very important. Why?
These proteins are insoluble in water, and in the dough, that contains water, they bind to each other through a combination of intermolecular bonds, such as:

  • covalent bonds, i.e. disulfide bridges;
  • noncovalent bonds, such as hydrophobic interactions, van der Waals forces, hydrogen bonds, and ionic bonds.

Thanks to the formation of these intermolecular bonds, a three-dimensional lattice is formed. This structure entraps starch granules and carbon dioxide bubbles produced during leavening, and gives strength and elasticity to the dough, two properties of gluten widely exploited industrially.
In the usual diet of the European adult population, and in particular in Italian diet that is very rich in derivatives of wheat flour, gliadin and glutenin are the most abundant proteins, about 15 g per day. What does this mean? It means that gluten-free diet engages celiac patients both from a psychological and social point of view.

Note: The lipids of the gluten are strongly associated with the hydrophobic regions of gliadins and glutenins and, unlike what you can do with the flour, they are extracted with more difficulty (the lipid content of the gluten depends on the lipid content of the flour from which it was obtained).

Gliadins: extensibility and viscosity

Gliadins are hydrophobic monomeric prolamins, of globular nature and with low molecular weight. On the basis of electrophoretic mobility in low pH conditions, they are separated into the following types:

  • alpha/beta, and gamma, rich in sulfur, containing cysteines, that are involved in the formation of intramolecular disulfide bonds, and methionines;
  • omega, low in sulfur, given the almost total absence of cysteine and methionine.

They have a low nutritional value and are toxic to celiac patients because of the presence of particular amino acid sequences in the primary structure, such as proline-serine-glutamine-glutamine and glutamine-glutamine-glutamine-proline.
Gliadins are associated with each other and with glutenins through noncovalent interactions; thanks to that, they act as “plasticizers” in dough making. Indeed, they are responsible for viscosity and extensibility of gluten, whose three-dimensional lattice can deform, allowing the increase in volume of the dough as a result of gas production during leavening. This property is important in bread-making.
Their excess leads to the formation of a very extensible dough.

Glutenins: elasticity and toughness

Glutenins are polymeric proteins, that is, formed of multiple subunits, of fibrous nature, linked together by intermolecular disulfide bonds. The reduction of these bonds allows to divide them, by SDS-PAGE, into two groups.

  • High molecular weight (HMW) subunits, low in sulfur, that account for about 12% of total gluten proteins. The noncovalent bonds between them are responsible for the elasticity and tenacity of the gluten protein network, that is, of the viscoelastic properties of gluten, and so of the dough.
  • Low molecular weight (LMW) subunits, rich in sulfur (cysteine residues).
    These proteins form intermolecular disulfide bridges to each other and with HMW subunits, leading to the formation of a glutenin macropolymer.

Glutenins allow dough to hold its shape during mechanical (kneading) and not mechanical stresses (increase in volume due to both the leavening and the heat of cooking that increases the volume occupied by gases present) which is submitted. This property is important in pasta making.
If in excess, glutenins lead to the formation of a strong and rigid dough.

Properties of wheat gluten

From the nutritional point of view, gluten proteins do not have a high biological value, being low in lysine, an essential amino acid. Therefore, a gluten-free diet does not cause any important nutritional deficiencies.
On the other hand, it is of great importance in food industry: the combination, in aqueous solution, of gliadins and glutenins to form a three-dimensional lattice, provides viscoelastic properties, that is, extensibility-viscosity and elasticity-tenacity, to the dough, and then, a good structure to bread, pasta, and in general, to all foods made with wheat flour.
It has a high degree of palatability.
It has a high fermenting power in the small intestine.
It is an exorphin: some peptides produced from intestinal digestion of gluten proteins may have an effect in central nervous system.

Gluten-free cereals

The following is a list of gluten-free cereals, minor cereals, and pseudocereals used as foods.

  • Cereals

corn or maize (Zea mays)
rice (Oryza sativa)

  • Minor cereals
    They are defined “minor” not because they have a low nutritional value, but because they are grown in small areas and in lower quantities than wheat, rice and maize.

Fonio (Digitaria exilis)
Millet (Panicum miliaceum)
Panic (Panicum italicum)
Sorghum (Sorghum vulgare)
Teff (Eragrostis tef)
Teosinte; it is a group of four species of the genus Zea. They are plants that grow in Mexico (Sierra Madre), Guatemala and Venezuela.

  • Pseudocereals.
    They are so called because they combine in their botany and nutritional properties characteristics of cereals and legumes, therefore of another plant family.

Amaranth; the most common species are:

Amaranthus caudatus;
Amaranthus cruentus;
Amarantus hypochondriacus.

Buckwheat (Fagopyrum esculentum)
Quinoa (Chenopodium quinoa), a pseudocereal with excellent nutritional properties, containing fibers, iron, zinc and magnesium. It belongs to Chenopodiaceae family, such as beets.

  • Cassava, also known as tapioca, manioc, or yuca (Manihot useful). It is grown mainly in the south of the Sahara and South America. It is an edible root tuber from which tapioca starch is extracted.

It should be noted that naturally gluten-free foods may not be truly gluten-free after processing. Indeed, the use of derivatives of gliadins in processed foods, or contamination in the production chain may occur, and this is obviously important because even traces of gluten are harmful for celiac patients.

Oats and gluten

Oats (Avena sativa) is among the cereals that celiac patients can eat. Recent studies have shown that it is tolerated by celiac patients, adult and child, even in subjects with dermatitis herpetiformis. Obviously, oats must be certified as gluten-free (from contamination).


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Calories burned, and water and minerals lost during running

Calorie, carbohydrate, fat, and protein expenditure, and water and mineral losses during runningDuring running, athletes burn calorie, and lose water and salts in amounts depending on various factors such as the technique, training level, environmental conditions, and physiological characteristics of each runner. The knowledge of these factors allows to plan an adequate diet both during workout  and recovery, with the aim of optimizing performance.
Below we will analyze the energy expenditure of runners engaged in workouts on various distances, the amounts of carbohydrates, lipids, and proteins oxidized to meet the energy requirements, and which minerals are lost in sweat.


Energy expenditure during running

During running energy expenditure is equal to 0.85-1.05 kcal per kilogram per kilometer.
This range is due to the fact that athletes with a good technique spend less than those with a poor technique.
A 70 kilogram (154 pound) athlete has an energy expenditure per kilometer between:

70 x 0.85 x 1 = 59.5 kcal
70 x 1.05 x 1 = 73.5 kcal

The table shows the calculations to determine the energy expenditure of the athlete to run 10, 20, 30, and 40 kilometers.


Energy expenditure

10 km 0.85 x 70 x 10 = 595 kcal
1.05 x 70 x 10 = 735 kcal
20 km 0.85 x 70 x 20 = 1190 kcal
1.05 x 70 x 20 = 1470 kcal
30 km 0.85 x 70 x 30 = 1785 kcal
1.05 x 70 x 30 = 2205 kcal
40 km 0.85 x 70 x 40 = 2380 kcal
1.05 x 70 x 40 = 2940 kcal

Note: who has started running for a short time ago has an energy expenditure even higher than 1.05 kcal per kilogram per kilometer.

During running, the energy for muscle work derives from the oxidation of carbohydrates, lipids, and proteins. Carbohydrates and lipids are the main energy source, and their oxidation rate depends on the intensity of exercise: as it increases, the percentage of lipid oxidation decreases whereas that of carbohydrates increases, as summarized below.

Intensity Fuel
30% VO2max Mainly fats
40-60% VO2max Equally fats and carbohydrates
75% VO2max Mainly carbohydrates
80% VO2max Almost only carbohydrates

Note: The failure to use the suitable fuel can promote fatigue and lead to overtraining.

Then, when running above the anaerobic threshold, the oxidation of carbohydrates can provide the entire energy requirement. At marathon pace, carbohydrates provide 60-70% of the energy requirement, whereas at lower pace they provide less than 50% of energy requirement.
Below, the amounts of carbohydrates, lipids, and proteins oxidized during workout are analyzed. During workout ,the energy expenditure is covered for about 60% by carbohydrates, for about 40% by lipids, whereas the residual percentage, between 3 and 5%, by proteins.

Carbohydrate oxidation during workout

For a 70 kilogram runner the amount of carbohydrates oxidized per kilometer is between:

(0.6 x 59.5) /4 = 8.9 g/km
(0.6 x 73.5) /4 = 11 g/km

Note: carbohydrates provide, on average, 4 kcal per gram.
The table shows the calculations to determine the amount of carbohydrates oxidized when the athlete runs 10, 20, 30, and 40 kilometers.

Distance Carbohydrate expenditure

10 km

[(0.85 x 70 x 10) x 0.6 ] / 4 = 89 g
[(1.05 x 70 x 10) x 0.6 ] / 4 = 110 g

20 km

[(0.85 x 70 x 20) x 0.6] / 4 = 179 g
[(1.05 x 70 x 20) x 0.6] / 4 = 221 g

30 km

[(0.85 x 70 x 30) x 0.6] / 4 = 268 g
[(1.05 x 70 x 30) x 0.6] / 4 = 331 g

40 km

[(0.85 x 70 x 40) x 0.6] / 4 = 357 g
[(1.05 x 70 x 40) x 0.6] / 4 = 441 g

Lipid oxidation during workout

By calculations similar to those for carbohydrates, we determine the amount of lipids oxidized per kilometer, which is between:

(0.4 x 59.5) / 9 = 2.6 g/km
(0.4 x 73.5) / 9 = 3.3 g/km

Note: lipids provide, on average, 9 kcal per gram.
The table shows the calculations to determine the amount of lipids oxidized when the athlete runs 10, 20, 30, and 40 kilometers.


Lipid expenditure

10 km [(0.85 x 70 x 10) x 0.4] / 9 = 26 g
[(1.05 x 70 x 10) x 0.4] / 9 = 33 g
20 km [(0.85 x 70 x 20) x 0.4] / 9 = 53 g
[(1.05 x 70 x 20) x 0.4] / 9 = 65 g
30 km [(0.85 x 70 x 30) x 0.4] / 9 = 79 g
((1.05 x 70 x 30) x 0.4] / 9 = 98 g
40 km [(0.85 x 70 x 40) x 0.4] / 9 = 106 g
[(1.05 x 70 x 40) x 0.4] / 9 = 131 g

Protein oxidation during workout

Protein requirements of adults are equal to 0.9 grams per kilogram of body weight, and, for a 70 kilogram athlete is:

70 x 0.9 = 63 g

During workout  the energy expenditure is covered for about 3-5% by protein oxidation.

The table shows the calculations to determine the amount of proteins oxidized when the athlete runs 10, 20, 30, and 40 kilometers, and proteins provide 3% of the energy requirement.


Protein expenditure (3%)

10 km [(0.85 x 70 x 10) x 0.03)] / 4 = 4.5 g
[(1.05 x 70 x 10) x 0.03)] / 4 = 5.5 g
20 km [(0.85 x 70 x 20) x 0.03)] / 4 = 8.9 g
[(1.05 x 70 x 20) x 0.03)] / 4 = 11 g
30 km [(0.85 x 70 x 30) x 0.03)] / 4 = 13.4 g
[(1.05 x 70 x 30) x 0.03)] / 4 = 16.5 g
40 km [(0.85 x 70 x 40) x 0.03)] /4 = 17.9 g
[(1.05 x 70 x 40) x 0.03)] /4 = 22.1 g

Note: proteins provide, on average, 4 kcal per gram.

For energy expenditure of 0.85 and 1.05 kcal per kilogram per kilometer, the average additional protein oxidation per kilogram to run 10, 20, 30, and 40 kilometers, rounded to the second decimal place, is:

  • 10 km: [(4.5 + 5.5) / 2] / 70 = 0.07 g
  • 20 km: [(4.5 + 5.5) / 2] / 70 = 0.14 g
  • 30 km: [(4.5 + 5.5) / 2] / 70 = 0.21 g
  • 40 km: [(4.5 + 5.5) / 2] / 70 = 0.29 g

Finally, adding the daily protein requirement of adults, the total protein requirement of a 70 kilogram runner, for the four distances, is:

  • 10 km: 0.07 + 0.9 = 0.97 g
  • 20 km: 0.14 + 0.9 = 1.04 g
  • 30 km: 0.21 + 0.9 = 1.11 g
  • 40 km: 0.29 + 0.9 = 1.19 g

By calculations similar to the previous ones, we determine the overall protein requirement when proteins provide 5% of the energy requirement.

  • 10 km: 0.12 + 0.9 = 1.02 g
  • 20 km: 0.24 + 0.9 = 1.14 g
  • 30 km: 0.36 + 0.9 = 1.26 g
  • 40 km: 0.48 + 0.9 = 1.38 g

Excluding athletes who run 30 kilometers or more every day, the values are slightly higher than 0.9 grams per kilogram of body weight.
In reality, the daily protein requirement is just slightly higher because a certain amount of nitrogen, hence proteins, is lost, as well as in the urine, also through sweating.

Water and minerals loss during running

Water losses depend on the amount of sweat produced, that depends on:

  • air temperature and humidity;
  • solar radiation.

The loss will be greater the higher these values are.
Finally, the amount of sweat produced is different from person to person.

Minerals lost in sweat are mostly:

  • sodium (Na+) and chlorine (Cl), about 1 gram per liter of sweat in heat acclimatized athletes;
  • potassium (K+), in an amount equal to about 15% of the sodium lost;
  • magnesium (Mg2+), in an amount equal to about 1% of the sodium lost.

The amount of minerals lost depends on how much sweat is produced, and it increases in non-heat acclimatized athletes.

The table shows the values, in grams per liter, of the minerals lost in sweat for non-heat and heat-acclimated athletes.

  Non-heat acclimated athletes

heat acclimated athetes
















Therefore, during physical activity, sodium is the mineral we need most of all.
After physical activity, runner, or who sweats heavily, tends to eat saltier food. This effect, known as selective hunger, was discovered, for sodium, in studies conducted on foundry workers. Probably, the selective hunger doesn’t not exist for potassium and magnesium.


Sawka M.N., Burke L.M., Eichner E.R., Maughan, R.J., Montain S.J., Stachenfeld N.S. American College of Sports Medicine position stand: exercise and fluid replacement. Med Sci Sport Exercise 2007;39(2):377-390. doi:10.1249/mss.0b013e31802ca597

Shirreffs S., Sawka M.N. Fluid and electrolyte needs for training, competition and recovery. J Sport Sci 2011;29:sup1, S39-S46. doi:10.1080/02640414.2011.614269

GLA and physiology and pathophysiology of the skin

gamma-Linolenic acid (GLA), an omega-6 PUFA, like its precursor linoleic acid (the most abundant polyunsaturated fatty acid in human skin epidermis, where it’s involved in the maintenance of the epidermal water barrier), plays important roles in the physiology and pathophysiology of the skin.
Studies conducted on humans revealed that gamma-linolenic acid:

  • improves skin moisture, firmness, roughness;
  • decreases transepidermal water loss (one of the abnormalities of the skin in essential fatty acid deficiency animals).
Skelatal formula of Prostaglandin E1, a derivative of gamma-linolenic acid, an omega-6 PUFA
Prostaglandin E1

Using guinea pig skin epidermis as a model of human epidermis (they are functionally similar), it was demonstrated that supplementation of animals with gamma-linolenic acid-rich foods results in a major production of PGE1 and 15-HETrE in the skin (as previously demonstrated in in vitro experiments).
Because these molecules have both anti-inflammatory/anti-proliferative properties supplementation of diet with gamma-linolenic acid acid-rich foods may be an adjuncts to standard therapy for inflammatory/proliferative skin disorders.

Supplemental sources of GLA

The main supplemental sources of gamma-linolenic acid are oils of the seeds of:

  • borage (20%-27% of the total fatty acids);
  • black currant (from 15% to 19% of the total fatty acids);
  • evening primrose (from 7% to 14% of the total fatty acids), and

Role of gamma-linolenic acid in lowering blood pressure

The relationship between dietary fatty acid intake and blood pressure mainly comes from studies conducted on genetically modified rats that spontaneously develops hypertension (a commonly used animal model for human hypertension).
In these studies many membrane abnormalities were seen so hypertension in rat model may be related to change in polyunsaturated fatty acid metabolism at cell membrane level.
About polyunsaturated fatty acids, several research teams have reported that gamma-linolenic acid reduces blood pressure in normal and genetically modified rats (greater effect) and it was purported by interfering with Renin-Angiotensin System (that promote vascular resistance and renal retention) altering the properties of the vascular smooth muscle cell membrane and so interfering with the action of angiotensin II.
Another possible mechanism of action of gamma-linolenic acid to lower blood pressure could be by its metabolite dihomo-gamma-linolenic acid: it may be incorporated in vascular smooth muscle cell membrane phospholipids, then released by the action of phospholipase A2 and transformed by COX-1 in PGE1 that induces vascular smooth muscle relaxation.

Role gamma-linolenic acid in treatment of rheumatoid arthritis

In a study conducted by Leventhal et al. on 1993 it was demonstrated the dietary intake of higher concentration of borage oil (about 1400 mg of gamma-linolenic acid/day) for 24 weeks resulted in clinically significant reductions in signs and symptoms of rheumatoid arthritis activity.
In a subsequent study by Zurier et al. on 1996 the dietary intake of an higher dose (about 2.8 g/day gamma-linolenic acid) for 6 months reduced, in a clinically relevant manner, signs and symptoms of the disease activity; patients who remained for 1 year on the 2.8 g/day dietary gamma-linolenic acid exhibited continued improvement in symptoms (the use of gamma-linolenic acid also at the above higher dose is well tolerated, with minimal deleterious effects). These data underscore that the daily amount and the duration of gamma-linolenic acid dietary intake do correlate with the clinical efficacy.


Akoh C.C. and Min D.B. “Food lipids: chemistry, nutrition, and biotechnology” 3th ed. 2008

Chow Ching K. “Fatty acids in foods and their health implication” 3th ed. 2008

Fan Y.Y. and Chapkin R.S. Importance of dietary γ-linolenic acid in human health and nutrition. J Nutr 1998;128:1411-1414. doi:10.1093/jn/128.9.1411

Leventhal L.J., Boyce E.G. and Zurier R.B. Treatment of rheumatoid arthritis with gammalinolenic acid. Ann Intern Med 1993 119:867-873. doi:10.7326/0003-4819-119-9-199311010-00001

Miller C.C. and Ziboh V.A. Gammalinolenic acid-enriched diet alters cutaneous eicosanoids. Biochem Biophys Res Commun 1988 154:967-974. doi:10.1016/0006-291X(88)90234-3

Zurier R.B., Rossetti R.G., Jacobson E.W., DeMarco D.M., Liu N.Y., Temming J.E., White B.M. and Laposata M. Gamma-linolenic acid treatment of rheumatoid arthritis. A randomized, placebocontrolled trial. Arthritis Rheum 1996 39:1808-1817. doi:10.1002/art.1780391106

Alcohol, blood pressure, and hypertension

Many studies have shown a direct, dose-dependent relationship between alcohol intake and blood pressure, particularly for intake above two drinks per day.
This relationship is independent of:

  • age;
  • salt intake;
  • obesity;
  • finally, it persists regardless of beverage type.

Furthermore, heavy consumption of alcoholic beverages for long periods of time is one of the factors predisposing to hypertension: from 5 to 7% of hypertension cases is due to an excessive alcohol consumption.
A meta-analysis of 15 randomized controlled trials has shown that decreasing alcoholic beverage intake intake has therapeutic benefit to hypertensive and normotensive with similar systolic and diastolic blood pressure reductions (in hypertensive reduction occurs within weeks).


Alcohol intake and prevention of hypertension

Guidelines on the primary prevention of hypertension recommend that alcohol (ethanol) consumption in most men, in absence of other contra, should be less than 28 g/day, the limit in which it may reduce coronary heart disease risk.
Relationship Between Ethanol Intake and HypertensionThe consumption limited to these quantities must be obtained by intake of drinks with low ethanol content, preferably at meals (drinking even lightly to moderately outside of meals increases the probability to have hypertension). This means no more than 680 ml or 24 oz of regular beer or 280 ml or 10 oz of wine (12% ethanol), especially in hypertension; for women and thinner subjects consumption should be halved1.
To avoid intake of drinks with high ethanol content even though the total ethanol content not exceeding 28 g/day.

Relationship between ethanol intake and blood pressure

Anyway, uncertainty remains regarding benefits or risks attributable to light-to-moderate alcoholic beverage intake on the risk of hypertension.
In a study published on April 2008, the authors examined the association between ethanol intake and the risk of developing hypertension in 28848 women from “The Women’s Health Study” and 13455 men from the “Physicians’ Health Study”, (the follow-up lasted respectively for 10.9 and 21.8 years). The study confirms that heavy ethanol intake (exceeding 2 drinks/day) increases hypertension risk in both men and women but, surprisingly, found that the association between light-to-moderate alcohol intake (up to 2 drinks/day) and the risk of developing hypertension is different in women and men. Women have a potential reduced risk of hypertension from a light-to-moderate ethanol consumption with a J-shaped association2; men have no benefits of light-to-moderate ethanol consumption but an increased risk of hypertension.
However, guidelines for the primary prevention of hypertension limit alcohol consumption to less 2 drinks/day in men and less 1 drink/day in thinner subjects and women.

1. A standard drink contains approximately 14 g of ethanol i.e. a 340 ml or 12 oz of regular beer, 140 ml or 5 oz wine (12% alcohol), or 42 ml or 1,5 oz of distilled spirits (inadvisable).

2. Many studies have shown a J-shaped relationship between ethanol intake and blood pressure. Light drinker (no more than 28 g of ethanol/day) have lower blood pressure than teetotalers; instead, who consumes more than 28 g ethanol/day have higher blood pressure than non drinker. So alcohol is a vasodilator at low doses but a vasoconstrictor at higher doses.


Pickering T.G. New guidelines on diet and blood pressure. Hypertension 2006;47:135-136. doi:10.1161/01.HYP.0000202417.57909.26

Sesso H.D., Cook N.R., Buring J.E., Manson J.E. and Gaziano J.M. Alcohol consumption and the risk of hypertension in women and men. Hypertension 2008;51:1080-1087. doi:10.1161/HYPERTENSIONAHA.107.104968

Writing Group of the PREMIER Collaborative Research Group. Effects of comprehensive lifestyle modification on blood pressure control: main results of the PREMIER Clinical Trial. JAMA 2003;289:2083-2093. doi:10.1001/jama.289.16.2083

World Health Organization, International Society of Hypertension Writing Group. 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension. Guidelines and recommendations. J Hyperten 2003;21:1983-1992.

Overweight, physical activity, and blood pressure

Body weight, especially overweight and obesity, is a determinant of blood pressure at all age; in fact:

  • it has been estimated that the risk of developing elevated blood pressure is two to six time higher in overweight than in normal-weight individuals;
  • there is a linear correlation between blood pressure and body weight or body mass index (BMI) (a BMI greater than 27, i.e. overweight or obesity, is correlated with increased blood pressure): even when dietary sodium intake is held constant, the correlation between change in weight and change in blood pressure is linear;
  • 60% of hypertensives are more than 20% overweight;
  • centripetal distribution of body fat (waist circumference greater than 34 inches in women and 39 inches in man), also associated with insulin resistance, is more important determinant of blood pressure elevation than that peripherally located in both man and women;
  • it has been shown that weight loss, both in hypertensive and normotensive individual, can reduce blood pressure and reductions occur before, and without, attainment of a desirable body weight.

In view of the difficulties of sustaining weight loss, efforts to prevent weight gain among those who have normal body weight are critically important.

How to calculate BMI

BMI is total body weight, expressed in kilograms [kg] or pounds [lb], divided by the height squared, expressed in meters or inches (in.).
It can be calculated using the following equations:

BMI = weight [kg]/height2 [m] or
BMI = (weight [lb.]/heigth2 [in.]) x 705

BMI is a good indication of body fat because most of the weight differential among adults is due to body fat; its major flaw is that some muscular individuals may be classified as obese even if they are not.
A healthy BMI is between 18 to 24,9.
Overweight is considered to be between 25 to 29,9.
Obesity is categorized by BMI according to three grades:

  • 30 to 34,9 I grade obesity;
  • 35 to 40 II grade obesity:
  • 40 and above III grade obesity.

Physical activity, overweight and blood pressure

Maintaining a high level of physical activity is a critical factor in sustaining weight loss.
In addition to the effect on body weight, activity and exercise in itself reduce the rise in blood pressure.
Physical activity to help control overweight and high blood pressurePhysical activity produces a fall in systolic blood pressure and diastolic blood pressure; so, increasing physical activity of low to moderate intensity to 30 to 45 minutes 3-4 days/week up to 1 hour nearly every day, as recommended by World Health Organization, is important for the primary prevention of hypertension.
Less active persons are 30% to 50% more likely to develop hypertension than active ones.
Remember: a rolling stone gathers no moss!


Writing Group of the PREMIER Collaborative Research Group. Effects of comprehensive lifestyle modification on blood pressure control: main results of the PREMIER Clinical Trial. JAMA 2003;289:2083-2093. doi:10.1001/jama.289.16.2083

World Health Organization, International Society of Hypertension Writing Group. 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension. Guidelines and recommendations. J Hyperten 2003;21:1983-92.

Trans fatty acids (TFA): structure, sources, health effects, examples

Trans fatty acids (TFA) or trans-unsaturated fatty acids or trans fats are unsaturated fatty acids with at least one a double bond in the trans or E configuration.
Carbon-carbon double bonds show planar conformation, and so they can be considered as plains from whose opposite sides carbon chain attaches and continues. “The entry” and “the exit” of the carbon chain from the plain may occur on the same side of the plain, and in this case double bond is defined in cis or Z configuration, or on opposite side, and in that case it is defined in trans configuration.

Examples of C18:1 cis/trans isomers, and of a saturated fatty acid
Fig. 1 – C18:1 cis/trans Isomers

Unsaturated fatty acids most commonly have their double bonds in cis configuration; the other, less common configuration is trans.
Cis bond causes a bend in the fatty acid chain, whereas the geometry of trans bond straightens the fatty acid chain, imparting a structure more similar to that of saturated fatty acids.


Properties of fats rich in trans fatty acids

Below, some distinctive characteristics of the fats rich in trans fats, that make them particularly suited for the production of margarines and vegetable shortening used in home and commercial cooking, and manufacturing processes.

  • Bent molecules can’t pack together easily, but linear ones can do it.
    This means that trans fatty acids contribute, together with the geometrically similar saturated fatty acids, to the hardness of the fats in which they are, giving them a higher melting point.
    Heightening the melting point of fats means that it is possible to convert them from liquid form to semi-solids and solids at room temperature.
    Note: trans fats tend to be less solid than saturated fatty acids.
  • They have:

a melting point, consistency and “mouth feel” similar to those of butter;
a long shelf life at room temperature;
a flavor stability.

  • They are stable during frying.

Sources of trans fatty acids

Dietary TFA come from different sources briefly reviewed below.

  • In industrialized countries, greater part of the consumed trans fatty acids, in USA about 80 percent of the total, are produced industrially, in varying amounts, during partial hydrogenation of edible oils containing unsaturated fatty acids (see below).
  • They are produced at home during frying with vegetable oils containing unsaturated fatty acids.
  • They come from bacterial transformation of unsaturated fatty acids ingested by ruminants in their rumen (see below).
  • Another natural source is represented by some plant species, such as leeks, peas, lettuce and spinach, that contain trans-3-hexadecenoic acid, and rapeseed oil, that contains brassidic acid (22:1∆13t) and gondoic acid (20:1∆11t). In these sources trans fatty acids are present in small amounts.
  • Very small amounts, less than 2 percent, are formed during deodorization of vegetable oils, a process necessary in the refining of edible oils. During this process trans fatty acids with more than one double bond are formed in small amounts. These isomers are also present in fried foods and in considerable amounts in some partially hydrogenated vegetable oils (see below).

Industrial trans fatty acids

Hydrogenation is a chemical reaction in which hydrogen atoms react, in the presence of a catalyst, with a molecule.
The hydrogenation of unsaturated fatty acids involves the addition of hydrogen atoms to double bonds on the carbon chains of fatty acids. The reaction occurs in presence of metal catalyst and hydrogen, and is favored by heating vegetable oils containing unsaturated fatty acids.

Partial hydrogenation of vegetable oils

The process of hydrogenation was first discovered in 1897 by French Nobel prize in Chemistry, jointly with fellow Frenchman Victor Grignard, Paul Sabatier using a nickel catalyst.
Partially hydrogenated vegetable oils were developed in 1903 by a German chemist, Wilhelm Normann, who files British patent on “Process for converting unsaturated fatty acids or their glycerides into saturated compounds”. The term trans fatty acids or trans fats appeared for the first time in the Remark column of the 5th edition of the “Standard Tables of Food Composition” in Japan.
During partial hydrogenation, an incomplete saturation of the unsaturated sites on the carbon chains of unsaturated fatty acids occurs. For example, with regard to fish oil, trans fatty acid content in non-hydrogenated oils and in highly hydrogenated oils is 0.5 and 3.6%, respectively, whereas in partially hydrogenated oils is 30%.

The cis to trans isomerization of oleic acid to vaccenic acid
Fig. 2 – From Oleic Acid to Vaccenic Acid

But, most importantly, some of the remaining cis double bonds may be moved in their positions on the carbon chain, producing geometrical and positional isomers, that is, double bonds can be modified in both conformation and position.
Below, other changes that occur during partial hydrogenation are listed.

Partially hydrogenated vegetable oils were developed for the production of vegetable fats, a cheaper alternative to animal fats. In fact, through hydrogenation, oils such as soybean, safflower and cottonseed oils, which are rich in unsaturated fatty acids, are converted into semi-solid fats (see above).
The first hydrogenated oil was cottonseed oil in USA in 1911 to produce vegetable shortening.
In the 1930’s, partial hydrogenation became popular with the development of margarine.
Currently, per year in USA, 6-8 billion tons of hydrogenated vegetable oil are produced.

Ruminant trans fatty acids

Ruminant trans fats are produced by bacteria in the rumen of the animals, for example cows, sheep and goats, using as a substrate a proportion of the relatively small amounts of unsaturated fatty acids present in their feedstuffs, that is, feed, plants and herbs. And, considering an animal that lives at least a year, and has the opportunity to graze and/or eat hay, there is a season variability in unsaturated fatty acids intake, and trans fats produced. In fact, in summer and spring, pasture plants and herbs may contain more unsaturated fatty acids than the winter feed supply.
Then, TFA are present at low levels in meat and full fat dairy products, typically <5% of total fatty acids, and are located in the sn-1 and sn-3 positions of the triacylglycerols, whereas in margarines and other industrially hydrogenated products they appear to be concentrated in the sn-2 position of the triacylglycerols.
Ruminant trans fatty acids are mainly monounsaturated fatty acids, with 16 to 18 carbon atoms, and constitute a small percentage of the trans fatty acids in the diet (see below).

Isomers of dietary trans fatty acids

The most important cluster of trans fatty acids is trans-C18:1 isomers, that is, fatty acids containing 18 carbon atoms plus one double bond, whose position varies between Δ6 and Δ16 carbon atoms. In both sources, the most common isomers are those with double bonds between positions Δ9 and Δ11.
However, even if these molecules are present both in industrial and ruminant TFA, there is a considerable quantitative difference. For example, vaccenic acid (C18:1 Δ11t) represents over 60 percent of the trans-C18:1 isomers in ruminant trans fatty acids, whereas in industrial ones elaidic acid (C18:1Δ9t) comprises 15-20 percent and C18:1 Δ10t and vaccenic acid over 20 percent each others.

trans-C18:1 fatty acid isomers, the most important cluster of trans fatty acids
Fig. 3 – trans-C18:1 Isomers

Trans fatty acids: effects on human health

Ruminant trans fatty acids, in amounts actually consumed in diets, are not harmful for human health (see below).
Conversely, consumption of industrial trans fats has neither apparent benefit nor intrinsic value, above their caloric contribution, and, from human health standpoint they are only harmful, having adverse effects on:

  • serum lipid levels;
  • endothelial cells;
  • systemic inflammation;
  • other risk factors for cardiovascular disease.

Moreover, they are positively associated with the risk of coronary heart disease (CHD), and sudden death from cardiac causes and diabetes.

Note: further in the text, we will refer to industrial trans fatty acids as trans fats or trans fatty acids.

Trans fatty acids: effects at plasmatic level

Low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) plasma levels are well-documented risk markers for the development of coronary heart disease (CHD).

  • High LDL-C levels are associated with an increased incidence of ischemic heart disease.
  • High HDL-C levels are associated with a reduced incidence of the risk.

For this reason, the ratio between total cholesterol level and HDL-C is often used as a combined risk marker for these two components in relation to the development of heart disease: the higher the ratio, the higher the risk.

TFA, as previously said, have adverse effects on serum lipids.
These effects have been evaluated in numerous controlled dietary trials by isocaloric replacement of saturated fatty acids or cis-unsaturated fatty acids with trans fats. It was demonstrated that such replacement:

  • raises LDL-C levels;
  • lowers HDL-C levels, in contrast to saturated fatty acids that increase HDL-C levels when used as replacement in similar study;
  • increases the ratio of total cholesterol to HDL-C, approximately twice that for saturated fatty acids, and, on the basis of this effect alone, trans fatty acids has been estimated to cause about 6% of coronary events in the USA.

Furthermore, trans fats:

  • produce a deleterious increase in small, dense LDL-C subfractions, that is associated with a marked increased in the risk of CHD, even in the presence of relatively normal LDL-C;
  • increase the blood levels of triglycerides, and this is an independent risk factor for CHD;
  • increase levels of Lp(a)lipoprotein, another important coronary risk factor.

But on 2004 prospective studies have shown that the relation between the intake of trans fatty acids and the incidence of CHD is greater than that predicted by changes in serum lipid levels alone. This suggests that trans fats influence other risk factors for CHD, such as inflammation and endothelial-cell dysfunction.

Trans fatty acids, inflammation and endothelial-cell dysfunction

The role of inflammation in atherosclerosis, and consequently in CHD, is burgeoned in the last decade.
Interleukin-6, C-reactive protein (CRP), and an increased activity of tumor necrosis factor (TNF) system are markers of inflammation.
In women greater intake of trans fatty acids is associated with increased activity of TNF system, and in those with a higher body mass index with increased levels of interleukin-6 and CRP. For example, the difference in CRP seen with an average intake of trans fats of 2.1% of the total daily energy intake, as compared with 0.9%, correspond to an increased risk of cardiovascular disease of 30%. Similar results have been reported in patients with established heart disease, in randomized, controlled trials, in in vitro studies, and in studies in which it has been analyzed membrane levels of trans fatty acids, a biomarker of their dietary intake.
So, trans fats promote inflammation, and their inflammatory effects may account at least in part for their effects on CHD that, as seen above, are greater than would be predicted by effects on serum lipoproteins alone.
Attention: the presence of inflammation is an independent risk factor not only for CHD but also for insulin resistance, diabetes, dyslipidemia, and heart failure.

Another site of action of TFA may be endothelial function.
Several studies have suggested the association between greater intake of trans fats and increased levels of circulating biomarkers of endothelial dysfunction, such as E-selectin, sICAM-1, and sVCAM-1.

Other effects of trans fatty acids

In vitro studies have demonstrate that trans fats affect lipid metabolism through several pathways.

  • They alter secretion, lipid composition, and size of apolipoprotein B-100 (apo B-100).
  • They increase cellular accumulation and secretion of free cholesterol and cholesterol esters by hepatocytes.
  • They alter expression in adipocytes of genes for peroxisome proliferator-activated receptor-γ (PPAR- γ), lipoprotein lipase, and resistin, proteins having a central roles in the metabolism of fatty acids and glucose.

Industrial trans fatty acids and CHD

Industrial trans fats are independent cardiovascular risk factor.
Since the early 1990s attention has been focused on the effect of trans fatty acids on plasma lipid and lipoprotein concentrations (see above).
Furthermore, four major prospective studies covering about 140,000 subjects, monitored for 6-14 years, have all found positive epidemiological evidence relating their levels in the diet, assessed with the aid of a detailed questionnaire on the composition of the diet, to the risk of CHD. These four studies are:

  • “The Health Professionals Follow-up study” (2005);
  • “The Alpha-Tocopherol Beta-Carotene Cancer Prevention Study” (1997);
  • “The Nurses’ Health Study” (2005);
  • “The Zutphen Elderly Study” (2001).

These studies cover such different populations that the results very probably hold true for the populations as a whole.
A meta-analysis of these studies have shown that a 2% increase in energy intake from industrial TFA was associated with a 23% increase in the incidence of CHD. The relative risk of heart disease was 1.36 in “The Health Professionals Follow-up Study”, 1.14 in “The Alpha-Tocopherol Beta-Carotene Cancer Prevention Study”; 1.93 (1.43-2.61) in “The Nurses’ Health Study”, and 1.28 (1.01-1.61) in “The Zutphen Elderly Study”.
So,  there is a substantially increased risk even at low levels of intake: 2% of total energy intake, for a 2,000 Kcal diet is 40 Kcal or about 4-5 g of fat corresponding to a teaspoonful of fat!
Moreover, in three of the studies, the association between the intake of industrial trans fats and the risk of CHD was stronger than a corresponding association between the intake of saturated fatty acids and the risk of heart disease. In “The Zutphen Elderly Study”, this association was not investigated.
Because of the adverse effects of industrial trans fatty acids, for the same authors are unethical conducting randomized long-term trials to test their effects on the incidence of CHD.
So, avoidance of industrial trans fats, or a consumption of less 0.5% of total daily energy intake is necessary to avoid their adverse effects, far stronger on average than those of food contaminants or pesticide residues.

Further evidence
A study conducted in an Australia population with a first heart attack and no preceding history of CHD or hyperlipidemia has showed a positive association between levels of trans fatty acids in adipose tissue and the risk of nonfatal myocardial infarction.
It was shown that adipose tissue C18:1Δ7t, found in both animal and vegetable fats, was an independent predictor of a first myocardial infarction, that is, its adipose tissue level is still a predictor for heart disease after adjustment for total cholesterol. Again, it appears that only a minor part of the negative effects of trans fats occurs via plasma lipoproteins.
During the course of this study, mid-1996, TFA were eliminated from margarines sold in Australia (see below). This was a unique opportunity to investigate the temporal relationship between trans fat intake and their adipose tissue levels. It was demonstrated that trans fats disappear from adipose tissue of both case-patients and controls with a rate about 15% of total trans fats/y.
Another study conduct in Costa Rica have found a positive association between myocardial infarction and trans fatty acids.
Interestingly, in a larger, community-based case-control study, levels of trans fats in red blood cell membranes were associated, after adjustment for other risk factors, with an increase in the risk of sudden cardiac death. Moreover, the increased risk appeared to be related to trans-C18:2 levels, that were associated with a tripling of the risk, but not with cell membrane levels of trans-C18:1,  the major trans fatty acids in foods (see above).

Trans fatty acids and diabetes

In a prospective study covering 84,204 female nurses, from “The Nurses’ Health Study”, aged 34–59 y, analyzed from the 1980 to 1996, with no cancer, diabetes, or cardiovascular disease at base line, the intake of trans fatty acids was significantly related to the risk of developing type 2 diabetes. And, after adjustment for other risk factors trans fat intake was positively associated with the incidence of diabetes with a risk up to 39% greater.
Data from controlled intervention studies showed that TFA could impair insulin sensitivity in subjects with insulin resistance and type 2 diabetes (saturated fatty acids do the analogous response, with no significant difference between TFA and them) more than unsaturated fatty acids, in particular the isomer of conjugated linoleic acid (CLA) trans-10, cis-12-CLA. Be careful because some dietary supplements contain CLA isomers and may be diabetogenic and proatherogenic in insulin-resistant subjects.

No significant effect was seen in insulin sensitivity of lean, healthy subjects.

Ruminant trans fatty acids and the risk of CHD

Four prospective studies have evaluated the relation between the intake of ruminant trans fatty acids and the risk of CHD: no significant association was identified.
In another study published on 2008 was analyzed data from four Danish cohort studies that cover 3,686 adults enrolled between 1974 and 1993, and followed for a median of 18 years. In Denmark, consumption of dairy products is relatively high and the range of ruminant trans fat intake is relatively broad, up to 1.1% of energy. Conversely, in the other countries, ruminant trans fatty acid consumption for most people is substantially lower than 1% of energy, in USA about 0.5% of energy. After adjustment for other risk factors, no significant associations between ruminant TFA consumption and incidence of CHD were found, confirming, in a population with relatively high intake of ruminant trans fatty acids, conclusions of four previous prospective studies.
So ruminant trans fats, in amounts actually consumed in diets, do not raise CHD risk.
The absence of risk of CHD with trans fats from ruminants as compared with industrial trans fatty acids  may be due to a lower intake. In the USA, greater part of trans fats have industrial origin (see above); moreover trans fat levels in milk and meats are relatively low, 1 to 8% of total fats.
The absence of a higher risk of CHD may be due also to the presence of different isomers. Ruminant and industrial sources share many common isomers, but there are some quantitative difference (see fig. 4):

  • vaccenic acid level is higher in ruminant fats, 30-50% of trans isomers;
  • trans-C18:2 isomers, present in deodorized and fried vegetable oils, as well as in some partially hydrogenated vegetable oils, are not present in appreciable amounts in ruminants fats.

Finally other, still unknown, potentially protective factors could outweigh harmful effects of ruminant trans fats.

Trans fatty acids: legislation regulating their content

Until 1985 no adverse effects of trans fatty acids on human health was demonstrated, and in 1975 a Procter & Gamble study showed no effect of trans fats on cholesterol.
Their use in fast food preparation grew up from 1980’s, when the role of dietary saturated fats in increasing cardiac risk began clear. Then, it was led a successful campaign to get McDonald’s to switch from beef tallow to vegetable oil for frying its French fries. Meanwhile, studies began to raise concerns about their effects on health. On 1985 Food and Drug Administration (FDA) concluded that TFA and oleic acid affected serum cholesterol level similarly, but from the second half of 1985 their harmful began clear, and the final proof came from both controlled feeding trials and prospective epidemiologic studies.
On 2003 FDA ruled that food labels, for conventional foods and supplements, show their content beginning January 1, 2006. Notably, this ruling was the first substantive change to food labeling since the requirement for per-serving food labels information was added in 1990.
On 2005 the US Department of Agriculture made a minimized intake of trans fatty acids a key recommendation of the new food-pyramid guidelines.
On 2006 American Heart Association recommended to limit their intake to 1% of daily calorie consumption, and suggested food manufacturers and restaurants switch to other fats.
On 2006 New York City Board of Health announced trans fat ban in its 40,000 restaurants within July 1, 2008, followed by the state of California in 2010-2011.

After June 1996 they were eliminated from margarine sold in Australia, that before contributed about 50% of their dietary intake.

On March 11, 2003 the Danish government, after a debate started in 1994 and two new reports in 2001 and 2003, decided to phase out the use of industrial trans fats in food before the end of 2003. Two years later, however, the European Commission (EC) asked Denmark to withdraw this law, which was not accepted on the European Community level, unfortunately. However, in 2007, EC decided to closes its infringement procedure against Denmark because of increasing scientific evidence of the danger of this type of fatty acids.
The Danish example was followed by Austria and Switzerland in 2009, Iceland, Norway, and Hungary in 2011, and most recently, Estonia and Georgia in 2014. So, about 10% of the European Union population, about 500 million people, lives in countries where it is illegal to sell food high in industrial trans fats.
Governments of other European Union countries instead rely on the willingness of food producers to reduce trans fatty acid content in their products. This strategy has proved effective only for Western European countries (see below).

Canada is considering legislation to eliminate them from food supplies, and, in 2005, ruled that pre-packaged food labels show their content.

Therefore, with the exception of the countries where the use of trans fats in the food industry was banned, the only way to reduce their intake in the other countries is consumer’s decision to choose foods free in such fatty acids, avoiding those known containing them, and always reading nutrition facts and ingredients because they may come from margarine, vegetable oil and frying. Indeed, for example in the USA, the producers of foods that contain less than 0.5 g of industrial trans fatty acids per serving can list their content as 0 on the packaging. This content is low but if a consumer eats multiple servings, he consumes substantial amount of them.

Be careful: food labels are not obligatory in restaurants, bakeries, and many other retail food outlets.

Trans fatty acids and food reformulation

Public health organizations, including the World Health Organization in September 2006, have recommended reducing the consumption of industrial trans fatty acids; only in USA the near elimination of these fatty acids might avoid between 72,000 and 280,000 of the 1.2 million of CHD events every year.
Food manufacturers and restaurants may reduce industrial TFA use choosing alternatives to partially hydrogenated oils.
In Denmark, their elimination (see above) from vegetable oils did not increase consumption of saturated fatty acids because they were mostly replaced with cis-unsaturated fatty acids. Moreover, there were no noticeable effects for the consumer: neither increase in the cost nor reduction in availability and quality of foods.
In 2009, Stender et al. have shown that industrial trans fatty acids in food such as French fries, cookies, cakes, and microwave-oven popcorn purchased in USA, South Africa, and many European Country can be replaced, at similar prices, with a mixture of saturated, monounsaturated, and polyunsaturated fatty acids. Such substitution has even greater nutritional benefit than one-to-one substitution of industrial trans fats with saturated fatty acids alone. However, be careful because only in French fries with low industrial trans fats the percentage of saturate fatty acids remains constant, whereas in cookies and cakes is in average +33 percentage points and microwave-oven popcorn +24 percentage points: saturated fatty acids are less dangerous than industrial trans fats but more than mono- and polyunsaturated fatty acids.
The same research group, analyzing some popular foods in Europe, purchased in supermarkets, even of the same supermarket chain, and fast food, namely, McDonald’s and Kentucky Fried Chicken (KFC), from 2005 to 2014, showed that their TFA content was reduced or even absent in several Western European countries while remaining high in Eastern and Southeastern Europe.
In 2010 Mozaffarian et al. evaluated  the levels of industrial trans fats and saturated fatty acids in major brand-name U.S. supermarket and restaurant foods after reformulation to reduce industrial trans fatty acid content, in two time: from 1993 through 2006 and from 2008 through 2009. They found a generally reduction in industrial trans fat content without any substantial or equivalent increase in saturated fatty acid content.

Foods high in trans fatty acids: examples and values

Many foods high in trans fats are popularly consumed worldwide.
In USA greater part of these fatty acids comes from partially hydrogenated vegetable oils, with an average consumption from this source that has been constant since the 1960′s.
It should be noted that the following trans fatty acid values must be interpreted with caution because, as previously said, many fast food establishments, restaurants and industries may have changed, or had to change the type of fat used for frying and cooking since the analysis were done.
The reported values, unless otherwise specified, refer to percentage in trans fatty acids/ 100 g of fatty acids.


Among foods with trans fats, stick or hard margarine had the highest percentage of them, but levels of these fatty acids have declined as improved technology allowed the production of softer margarines which have become popular. But there are difference in trans fatty acid content of margarine from different countries. Below some examples.

  • The highest content, 13-16.5%, is found in soft margarine from Iceland, Norway, and the UK.
  • Less content is found in Italy, Germany, Finland, and Greece, 5.1%, 4.8%, 3.2%, and 2.9% respectively).
  • In Portugal, The Netherlands, Belgium, Denmark, France, Spain, and Sweden margarine trans fat content is less than 2%.

USA and Canada lag behind Europe, but in the USA, with the advent of trans fat labeling of foods and the greater knowledge of the risk associated with their consumption by the buyers, change is occurring. For this reason, at now, in the USA margarine is considered to be a minor contributor to the intake of TFA, whereas the major sources are commercially baked and fast food products like cake, cookies, wafer, snack crackers, chicken nuggets, French fries or microwave-oven popcorn (see below).

Vegetable shortenings

Trans fatty acid content of vegetable shortenings ranges from 6% to 50%, and varies in different country: in Germany, Austria and New Zealand it is less than France or USA.
However, like margarines, their trans fat content is decreasing. In Germany it decreased from 12% in 1994 to 6% in 1999, in Denmark is 7% (1996) while in New Zealand is about 6% (1997).

Vegetable oils

At now, non-hydrogenated vegetable oils for salad and cooking contain no or only small amounts of trans fats.
Processing of these oils can produce minimal level of them, ranged from 0.05g/100 food for extra virgin oil to 2.42 g/100 g food for canola oil. So, their contribution to trans fat content of the current food supply is very little.
One exception is represented by Pakistani hydrogenated vegetable oils whose TFA content ranges from 14% to 34%.

Prepared soups

Among foods with trans fats, prepared soups contain significant amount of them, ranging from 10% of beef bouillon to 35% of onion cream. So, they contribute great amount of such fatty acids to the diet if frequently consumed.

Processed foods

Thanks to their properties (see above), trans fatty acids are used in many processed foods as cookies, cakes, croissants, pastries and other baked goods. And, baked goods are the greatest source of these fats in the North American diet. Of course, their trans fat content depends on the type of fat used in processing.


Mayonnaise, salad dressings and other sauces contain only small or no-amounts of trans fats.

Human milk and infant foods

Trans fat content of human milk reflects the trans fat content of maternal diet in the previous day, is comprised between 1 and 7%, and is decreasing from 7.1% in 1998 to 4.6% in 2005/2006.
Infant formulas have trans fat values on average 0.1%-4.5%, with a brand up to 15.7%.
Baby foods contain greater than 5% of trans fats.

Fast foods and restaurant’s foods

Vegetable shortenings high in trans fats are used as frying fats, so fast foods and many restaurant’s foods may contain relatively large amounts of them. Foods are fried pies, French fries, chicken nuggets, hamburgers, fried fish as well as fried chicken.
In articles published by Stender et al. from 2006 to 2009, it is showed that for French fries and chicken nuggets their content varies largely from nation to nation, but also within the same fast food chain in the same country, and even in the same city, because of the cooking oil used. For example, oil used in USA and Peru outlets of a famous fast food chain contained 23-24% of trans fats, whereas oil used in many European countries of the same fast food chain contained about 10%, with some countries, such as Denmark, as low as 5% and 1%.
And, considering a meal of French fries and chicken nuggets, in serving size of 171 and 160 g respectively, purchased at McDonald‘s in New York City, it contained over 10 g of TFA, while if purchased at KFC in Hungary they were almost 25 g.
Below, again from the work of Stender et al. it can see a cross-country comparison of trans fat contents of chicken nuggets and French fries purchased at McDonald ‘s or KFC.

Chicken nuggets and French fries from McDonald’s:

  • less than 1 g only if the meals were purchased in Denmark;
  • 1-5 g in Portugal, the Netherlands, Russia, Czech Republic, or Spain;
  • 5-10 g in the United States, Peru, UK, South Africa, Poland, Finland, France, Italy, Norway, Spain, Sweden, Germany, or Hungary.

Chicken and French fries from KFC:

  • less than 2 g if the meals were purchased UK (Aberdeen), Denmark, Russia, or Germany (Wiesbaden);
  • 2-5 in Germany (Hamburg), France, UK (London or Glasgow), Spain, or Portugal;
  • 5-10 in the Bahamas, South Africa, or USA;
  • 10-25 g in Hungary, Poland, Peru, or Czech Republic.


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Relationship between potassium intake, blood pressure and hypertension

High dietary potassium (K+) intakes and blood pressure are inversely related: animal studies, observational epidemiological studies, clinical trials, and meta-analyses of these trials support this.
Furthermore, the prevalence of hypertension tends to be lower in populations with high K+ intakes than in those with low intakes.
Finally, an increase in potassium intake (2.5-3.9 g/d) reduces blood pressure in normotensive and hypertensive, and to a greater extent in blacks than in whites.

Diet high in potassium, blood pressure, and ictus

Controlled feeding studies, such as “The Dietary Approaches to Stop Hypertension (DASH) Study” and “OmniHeart Trial”,  have highlighted the role of a good potassium intake, along with other minerals and fiber, in blood pressure reduction.
These studies have shown that a dietary pattern rich in fruits, vegetables, and low-fat dairy products, with whole grains, poultry, fish and nuts but poor in fats, red meat, sweets, and sugar-containing beverages reduces blood pressure. And such dietary patterns are characterized by foods high in potassium, as well as magnesium, calcium and fiber, but poor in total fat, saturated fat and cholesterol. The best result on lowering blood pressure are with black participants than white participants.
In another study, a systematic review of the literature and meta-analyses has been conducted on potassium intake in apparently healthy adults and children without renal impairment. The study showed that, in adult with hypertension, an increased potassium intake reduced systolic blood pressure by 3.49 mm Hg and diastolic blood pressure by 1.96 mm Hg. No effect was seen in adult without hypertension and in children. In addition, there was no effect of increased potassium intake on blood lipids, or catecholamine concentrations in adults, whereas an inverse statistically significant association was seen between its intake and the risk of incident stroke. Hence, this study suggests that, in people without impaired renal function, increased potassium intake is potentially beneficial for the prevention and control of elevated blood pressure and stroke.

Potassium, sodium and blood pressure

The effects of potassium on blood pressure depend on the concurrent intake of sodium and vice versa:

  • an increased intake of K+ has:

a greater blood pressure-lowering effect when sodium intake is high;

a lesser blood pressure-lowering effect when sodium intake is low;

  • on the other hand, the blood pressure reduction from a lowered sodium intake is greatest when potassium intake is low.

An high K+ intake also increases urinary excretion of sodium, the so-called natriuretic effect.
In the generally healthy population with normal kidney function the recommended potassium intake level is 3.1 g/day. But, in the presence of impaired urinary potassium excretion, a K+ intake less than 3.1 g/day (120 mmol/d) is appropriate, because of adverse cardiac effects (arrhythmias) from hyperkalemia, that is, blood potassium level higher than normal.

Mediterranean Diet and K+ intake

As already pointed out, the best strategy to increase K+ intake is to consume legumes, and fruits and vegetables in season, i.e. foods high in  potassium, that is also accompanied by a variety of other nutrients. No supplements are needed.Potassium
Therefore, it is sufficient to follow a  Mediterranean dietary pattern, for:

  • meet the daily requirements of the mineral;
  • consume K+ intake in adequate amounts to ensure its blood pressure-lowering effect.

Potassium content in some foods

High content: >250 mg/100 g of product

  • Dried legumes (chickpeas, beans, lentils, peas and soybeans) and fresh beans;
  • garlic, chard, cauliflower, cabbage, Brussels sprouts, broccoli, artichokes, cardoons, fennel, mushrooms, potatoes, tomatoes, spinach, zucchini;
  • avocados, apricots, bananas, fresh and dried chestnuts, watermelon, kiwi, melon, hazelnuts;
  • sweet dried fruits (apricots, dates, figs, prunes, raisins etc..) and oily dried fruits (peanuts, almonds, walnuts, pine nuts, pistachios, etc.);
  • oat flour, whole wheat flour and spelt;
  • ketchup;
  • roasted coffee;
  • milk powder (also rich sodium);
  • yeast;
  • cocoa powder.

Medium content: 150-250 mg/100 g of product

  • asparagus, beets, carrots, chicory, green beans, fresh broad beans, endive, lettuce, peppers, fresh peas, tomatoes, leeks, radishes, celery, tomato and carrot juice, pumpkin;
  • pineapple, oranges, raspberries, blueberries, loquats, pears, peaches, grapefruit, grapes;
  • meat and fish products, both fresh and preserved (the latter, however, should be avoided because of their high sodium content).

Note: cooking methods tend to reduce the K+ content of the food.
To reduce potassium loss, avoid boiling in plenty of water, for more than an hour, vegetables cut into small pieces (this increases the “exchange area” with water).


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