Omega-3 fatty acids: synthesis, mechanism of action, health benefits, and foods

Omega-3 polyunsaturated fatty acids or omega-3 PUFAs or omega-3 fatty acids are unsaturated fatty acids that have a double bond three carbons from the methyl end of the carbon chain. For humans, the most important omega-3 PUFAs are:

  • alpha-linolenic acid or ALA or 18:3n-3, with 18 carbon atoms and 3 double bonds;
  • eicosapentaenoic acid or EPA or 20:5n-3, with 20 carbon atoms and 5 double bonds;
  • docosahexaenoic acid or DHA or 22:6n-3, that, with 22 carbon atoms and 6 double bonds, is the most complex.

EPA and DHA are termed long-chain polyunsaturated fatty acids or LC-PUFAs.
Animals cannot synthesize linoleic acid or LA and alpha-linolenic acid, the precursors to omega-6 polyunsaturated fatty acids and omega-3 PUFAs, respectively, due to the lack of two desaturases: delta-12 desaturase (EC 1.14.19.6) and delta-15 desaturase (EC 1-14.19.13). Such desaturases insert double bonds at positions 6 and 3 from the methyl end of the molecule, respectively. Linoleic acid and alpha-linolenic acid are therefore essential fatty acids. Humans and many other animals can produce, from dietary ALA, all the other omega-3 polyunsaturated fatty acids. Then, such omega-3 PUFAs become essential in the absence of dietary ALA, and for this reason they are termed conditionally essential fatty acids.
EPA and DHA are important structural components of cell membranes, where they are mainly found, especially in muscle and nerve tissues. Conversely, many other fatty acids are stored mainly in adipose tissue triglycerides.
DHA is the main component of cell membrane phospholipids of neural tissues of vertebrates, including photoreceptor of the retina, where it performs important functions. In addition to their structural functions, omega-3 PUFAs are substrates for the production of bioactive lipid mediators with anti-inflammatory action, such as eicosanoids, maresins, resolvins, and protectins.
Omega-3 polyunsaturated fatty acids are essential in neurological development of the fetus, and their intake during pregnancy is especially important in the third trimester of pregnancy, when significant brain growth occurs. In the course of life their intake has been associated with a reduction in the risk of developing many chronic diseases, particularly cardiovascular diseases.
The major dietary sources for humans are fishery products, especially those obtained from cold waters.

CONTENTS

Synthesis of omega-3 polyunsaturated fatty acids

Alpha-linolenic acid, the precursors to omega-3 polyunsaturated fatty acids, is produced from linoleic acid, an omega-6 PUFAs, only in the plastids of phytoplankton and vascular terrestrial plants, where delta-15 desaturase inserts a double bond between carbon 3 and 4 from the methyl end of LA. In turn, ALA undergoes desaturation reactions, catalyzed by delta-5 desaturase (EC 1.14.19.44) and delta-6 desaturase (EC 1.14.19.3), elongation reactions, catalyzed by elongase 5 (EC 2.3.1.199) and elongase 5 and/or by elongase 2 (EC 2.3.1.199), and a limited beta-oxidation in peroxisomes, to produce DHA. For more details see the article on DHA.

Synthesis and metabolism of omega-3 polyunsaturated fatty acids
Omega-3 Fatty Acid Metabolism

The enzymes that catalyze the conversion of ALA to DHA are shared with the synthetic pathways leading to the synthesis of omega-6, omega-7 and omega-9 PUFAs. Omega-3 PUFAs appear to be the preferred substrates for delta-5 desaturase and delta-6 desaturase. However, because in many Western diets there is a high intake of linoleic acid relative to alpha-linolenic acid intake, the omega-6 pathway would be preferred over the other pathways. This could be one of the explanations for the low conversion rate of alpha-linolenic acid into the other omega-3 PUFAs, although the synthesis of arachidonic acid or ARA from linoleic acid seems to be very low, too. Note that both the omega-3 and omega-6 families inhibit the synthesis of omega-9 polyunsaturated fatty acids.

Omega-3 PUFA synthesis in humans

Humans, like many other animals, can convert alpha-linolenic acid to docosahexaenoic acid, a metabolic pathway found mainly in the liver and cerebral microcirculation of the hematoencephalic barrier, but also in the cerebral endothelium and astrocytes. It is common opinion that humans, like other terrestrial animals, have a limited capacity to synthesize LC-PUFAs, and therefore need an adequate intake of EPA and DHA from food.
It has been shown that the yield of the synthesis decreases along the pathway: the rate of conversion of alpha-linolenic acid to eicosapentaenoic acid is low, and the limiting factor seems to be the activity of delta-6 desaturase, and the rate of conversion to docosahexaenoic acid is extremely low. However recent studies have demonstrated the existence of a marked polymorphism in the fatty acid desaturase (FADS) gene cluster, especially for the contiguous genes FADS1 and FADS2 coding for delta-5 desaturase and delta-6 desaturase, respectively, which are present on chromosome 11q12.2. By analyzing genome-wide sequencing data from Bronze Age individuals and present-day Europeans, a  comprehensive overview was obtained of the changes in allele frequency of FADS genes. In European populations, the transition from a hunter-gatherer society to an agricultural society would have resulted in an increase in the intake of linoleic acid and alpha-linolenic acid, and a reduction in the intake of EPA and ARA. Natural selection would then have favored the haplotype associated with the increase in the expression of FADS1 and the decrease in the expression of FADS2. This pattern is opposite to that found in the Greenlander Inuit, where it is hypothesized that natural selection would have favored alleles associated with a decrease in the rate of conversion of linoleic acid and alpha-linolenic acid into LC-PUFAs, in order to compensate for their relatively high dietary intake in such population.

Do other animals need EPA and DHA?

Organisms lacking delta-15 desaturase cannot synthesize alpha-linolenic acid and hence the other omega-3 PUFAs, and, if needed, must obtain it from dietary sources. However, many animals do not need to get EPA and DHA from diet.
Terrestrial herbivorous vertebrates satisfy their need for long chain omega-3 polyunsaturated fatty acids by synthesizing them from alpha-linolenic acid obtained from the green parts of plants.
And there are animals that do not need EPA and DHA, and practically do not have them. These include terrestrial insects, that have very low levels of EPA. In such animals, EPA is synthesized from dietary alpha-linolenic acid and used for eicosanoid production.
Conversely, aquatic insects have high levels of EPA, whereas DHA is practically absent.
Some classes of phytoplankton, such as Cryptophyceae and Dinophyceae, are very rich in EPA and DHA, whereas Bacillariophyceae or diatoms are very rich in EPA. In general, microalgae are the primary producers of EPA and DHA, and then, aquatic ecosystems are the main source of omega-3 LC-PUFAs in the biosphere. EPA and DHA are then transferred from these microalgae along the food chain, from invertebrates to fish, and from fish to terrestrial animals, including humans. So, from microalgae to humans.

Benefits of omega-3 polyunsaturated fatty acids for humans

Omega-3 polyunsaturated fatty acids are essential components of a healthy and balanced diet. They are needed throughout development, starting from fetal life, and are associated with health improvements and reduced risk of disease. Indeed, many epidemiological studies have associated high intake of EPA and DHA with a lower cardiovascular mortality, especially for cardiac diseases, than predicted, probably due to the improvements in many risk factors such as plasma levels of triglycerides, HDL-cholesterol, C-reactive protein, blood pressure, both systolic and diastolic, and heart rate.
EPA and DHA have also been shown to be useful in the treatment of diseases such as rheumatoid arthritis, and could be useful in the treatment of other inflammatory conditions such as asthma, psoriasis or inflammatory bowel disease, due to their ability to modulate many aspects of the inflammatory processes.
Conversely, LC-PUFAs seem to have little or no effects on measures of glucose metabolism, such as insulin, insulin resistance, fasting glucose, and  glycated haemoglobin, or on type 2 diabetes.

Omega-3/omega-6 ratio

Epidemiological studies suggest that the consumption of a diet with a low omega-3/omega-6 ratio has had a negative impact on human health, contributing to the development, together with other risk factors such as sedentary life and smoking, of the main classes of diseases. Indeed, a lower incidence of cancer, autoimmunity and coronary heart disease has been observed in populations whose diet has a high omega-3/omega-6 ratio, such as Eskimos and Japanese, populations with a high fish consumption.
Despite these evidences, Western diet has become rich in saturated fatty acids and omega-6 polyunsaturated fatty acids, and poor in omega-3 polyunsaturated fatty acids, with an omega-3/omega-6 ratio between 1:10 and 1:20, then, far from the recommended ratio of 1:5.
The low value of the omega-3/omega-6 ratio is due to several factors, some of which are listed below.

  • Although wild plant foods are generally high in omega-3 PUFAs, crops high in omega-6 PUFAs have been much more successful in industrial agriculture than those high in omega-3 PUFAs.
  • Low consumption of fishery products and fish oils.
  • The high consumption of animals raised on corn-based feed, such as chickens, cattle, and pigs. Added to this is the fact that the omega-3 PUFA content of some farmed fish species is lower than that of  their wild counterparts.
  • The high consumption of oils rich in omega-6 PUFAs and poor in omega-3 PUFAs, such as safflower, sunflower, soybeans and corn oils.

Note: there is no evidence that the omega-3/omega-6 ratio is important for prevention and treatment of type 2
diabetes mellitus.

Effects at the molecular level of EPA and DHA

In recent years, the molecular mechanisms underlying the functional effects attributed to omega-3 polyunsaturated fatty acids, especially to EPA and DHA, are being clarified, and most of these require their incorporation into membrane phospholipids.
Omega-3 PUFAs are structural components of cell membranes where they play an essential role in regulating fluidity. Due to this effect, omega-3, especially EPA and DHA, can modulate cellular responses that depend upon membrane protein functions. This is particularly important in the eye, where DHA allows for optimal activity of rhodopsin, a photoreceptor protein. The effect on membrane fluidity is essential for animals living in cold water, as EPA and DHA also have an antifreeze function.
EPA and DHA can modify the formation of lipid raft, microdomains with a specific lipid composition that act as platforms for receptor activities and the initiation of intracellular signaling pathways. By modifying lipid raft formation, they affect intracellular signaling pathways in different cell types, such as neurons, immune system cells, and cancer cells. In this way, EPA and DHA can modulate the activation of transcription factors, such as NF-κB, PPARs and SREBPs, and so the corresponding gene expression patterns. This is  central to their role in controlling adipocyte differentiation, the metabolism of fatty acids and triacylglycerols, and inflammation.
EPA, DHA, and ARA are substrates for the synthesis of bioactive lipid mediators, such as eicosanoids, that are involved in the regulation of inflammation, immunity, platelet aggregation, renal function, and smooth muscle contraction. Eicosanoids produced from arachidonic acid, that is the major substrate for their synthesis, have important physiological roles, but an excessive production has been associated with numerous disease processes. The increase in EPA and DHA content in membrane phospholipids is paralleled by a reduction in ARA content and associated with a decreased production of lipid mediators form ARA and an increased production of lipid mediators from the two omega-3. Moreover, among the molecules derived from EPA and DHA, there are eicosanoids analogous to those produced from ARA, but with lower activity, resolvins, and, from DHA, protectins and maresins. These molecules appear to be responsible for many of the immune-modulating and anti-inflammatory actions attributed to the omega-3 polyunsaturated fatty acids EPA and DHA.
EPA and DHA can also play a role in the non-esterified form, acting directly through receptors coupled to G proteins, modulating their activity.
Finally, they can reduce the intestinal absorption of omega-6 PUFAs, and, at the enzymatic level, competitively inhibit cyclooxygenase-1 or COX-1 (EC 1.14.99.1) and lipoxygenases, and compete with omega-6 PUFAs for acyltransferases.

Major sources of EPA and DHA for humans

In general, fish and aquatic invertebrates, such as molluscs and crustaceans, are the major sources of EPA and DHA for humans. These animals can get EPA and DHA from food, namely, from phytoplankton, or synthesize them from alpha-linolenic acid. Moreover, DHA is present in high concentrations in many fish oils, too, especially those from coldwater fish. However, it should be underscored that such oils are also high in saturated fatty acids. For those who do not eat fishery products, good sources of omega-3 LC-PUFAs are the liver of terrestrial animals and several birds of the order Passeriformes.
Regarding the recommended intake of omega-3 polyunsaturated fatty acids, it is not yet clear what it is. The following table shows the values suggested by Food and Agriculture Organization (FAO) of the United Nations and the European Food Safety Authority (EFSA).

Omega-3 polyunsaturated fatty acids and culinary treatments

As omega-3 polyunsaturated fatty acids are particularly susceptible to oxidation due to heating, cooking and other culinary treatments could reduce their content. However, this is only partially true. In food, EPA and DHA are not in free form but mainly esterified into membrane phospholipids and, in such form, are much less susceptible to oxidation.
Considering the content of EPA and DHA, to express it as a percentage of the total fatty acids instead of as absolute content, namely, mg/g wet weight, leads to erroneous conclusions. For example, a fatty fish like salmon has a high EPA + DHA content, ~8 mg/g wet weight, and expressed as a percentage of the total fatty acids ~20%; conversely Atlantic code has a low EPA + DHA content, ~3 mg/g of wet weight, but, if expressed as a percentage of the total fatty acids ~40%. Atlantic code has a high percentage of EPA + DHA because is a lean fish, whereas in fatty fish EPA + DHA content is diluted by the high fatty acid content of the adipose tissue of the animal.
And when EPA + DHA content is expressed in mg/g of product, no decrease in LC-PUFAs content is observed following most common culinary treatments.

References

AbuMweis S., Jew S., Tayyem R. Agraib L. Eicosapentaenoic acid and docosahexaenoic acid containing supplements modulate risk factors for cardiovascular disease: a meta-analysis of randomised placebo-control human clinical. J Hum Nutr Diet 2018 31(1):67-84.  doi:10.1111/jhn.12493

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

Aron H. Uber den Nahvert (On the nutritional value). Biochem Z. 1918;92:211-233 (German)

Bergstroem S., Danielsson H., Klenberg D. and Samuelsson B. The enzymatic conversion of essential fatty acids into prostaglandins. J Biol Chem 1964;239:PC4006-PC4008.

Brown T.J., Brainard J., Song F., Wang X., Abdelhamid A., Hooper L. Omega-3, omega-6, and total dietary polyunsaturated fat for prevention and treatment of type 2 diabetes mellitus: systematic review and meta-analysis of randomised controlled trials. BMJ 2019;366:l4697. doi:10.1136/bmj.l4697

Buckley M.T., Racimo F., Allentoft M.E., et al. Selection in Europeans on fatty acid desaturases associated with dietary changes. Mol Biol Evol 2017;34(6):1307-1318. doi:10.1093/molbev/msx103

Calder P.C. Very long-chain n-3 fatty acids and human health: fact, fiction and the future. Proc Nutr Soc 2018 77(1):52-72. doi:10.1017/S0029665117003950

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

De Meester F., Watson R.R.,Zibadi S. Omega-6/3 fatty acids: functions, sustainability strategies and perspectives. Springer Science & Business Media, 2012

EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA). Scientific opinion on dietary reference values for fats, including saturated fatty acids, polyunsaturated fatty acids, monounsaturated fatty acids, trans fatty acids, and cholesterol. 2010. doi:10.2903/j.efsa.2010.1461

FAO. Global Recommendations for EPA and DHA Intake (As of 30 June 2014)

Gladyshev M.I.  and Sushchik N.N. Long-chain omega-3 polyunsaturated fatty acids in natural ecosystems and the human diet: assumptions and challenges. Biomolecules 2019;9(9):485. doi:10.3390/biom9090485

Oh D.Y., Talukdar S., Bae E.J., Imamura T., Morinaga H., Fan WQ, Li P., Lu W.J., Watkins S.M., Olefsky J.M. GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects. Cell 2010 142(5):687-698. doi:10.1016/j.cell.2010.07.041

Simopoulos A.P. The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med 2008;233(6):6746-88. doi:10.1016/S0753-3322(02)00253-6

Van D., Beerthuis R.K., Nugteren D.H. and Vonkeman H. Enzymatic conversion of all-cis-polyunsaturated fatty acids into prostaglandins. Nature 1964;203:839-841

Essential fatty acids: definition, synthesis, functions, and foods

Essential fatty acids or EFAs are fatty acids that cannot be synthesized by animals, and, like other essential nutrients, must be obtained from the diet. They are linoleic acid or LA or 18:2n-6, and alpha-linolenic acid or ALA or 18:3n-3.
Animals cannot synthesize these two fatty acids due to the lack of delta-12 desaturase (E.C. 1.14.19.6) and delta-15 desaturase (EC 1.14.19.25). These enzymes introduce cis double bonds beyond carbon 9, and are present in plants and microorganisms, such as some bacteria, fungi and molds. In particular, in plants:

  • delta-12 desaturase, present in the plastids, catalyzes the synthesis of linoleic acid from oleic acid, by introducing a double bond at delta-12 position, namely, between carbons 6 and 7 from the methyl end of the fatty acid;
  • delta-15 desaturase, present in the plastids and in the endoplasmic reticulum of phytoplankton and vascular terrestrial plants, catalyzes the synthesis of alpha-linolenic acid from linoleic acid by introducing a double bond at delta-15 position, namely, between carbons 3 and 4 from the methyl end of the fatty acid.
Synthesis of the essential fatty acids linoleic acid and alpha-linolenic acid
Synthesis of EFAs

Linoleic acid and alpha-linolenic acid are the precursors to omega-6 polyunsaturated fatty acids and omega-3 polyunsaturated fatty acids. Indeed, animals can synthesize, although with variable efficiency, the other omega-3 and omega-6 polyunsaturated fatty acids, molecules with 20, 22, or 24 carbon atoms, and up to 6 double bonds, such as arachidonic acid or ARA or 20:4n6 and docosahexaenoic acid or DHA or 22:6n3, due to the presence of desaturases that introduce double bonds at delta-5 and delta-6 positions and elongases that catalyze  the elongation of the carbon chain.
In the absence of dietary essential fatty acids, a rather rare condition, the other omega-3 and omega-6 fatty acids become essential, too. For this reason, they are defined by some as conditionally essential fatty acids.

It should be pointed out that all essential fatty acids are polyunsaturated molecules, but not all polyunsaturated fatty acids are essential, such as those belonging to the omega-7 and omega-9 families.

CONTENTS

Discovery of essential fatty acids

The first evidence of their existence dates back to 1918, when Hans Aron suggested that dietary fat could be essential for the healthy growth of animals and that, in addition to their caloric contribution, there was a inherent nutritive value due to the presence of certain lipid molecules.
In 1927, Herbert M. Evans and George Oswald Burr demonstrated that, despite the addition of vitamins A, D, and E to the diet, a deficiency of fat severely affected both growth and reproduction of experimental animals. Therefore, they suggested the presence of an essential substance in the fat that they called vitamin F.
Eleven years after Aron work, in 1929, George Burr and his wife Mildred Lawson hypothesized that warm-blooded animals were not able to synthesize appreciable amounts of certain fatty acids. One year later, they discovered that linoleic acid was essential for animals, and it was they who coined the term essential fatty acid.
However, EFA deficiency in humans was first described by Arild Hansen et al. only in 1958, in infants fed a milk-based formula lacking them.
And in 1964, thanks to the research of Van Dorp et al. and Bergstroem et al., one of their biological functions was discovered: being the precursors for the synthesis of prostaglandins.

Functions of EFAs and their PUFA derivatives

EFAs and their polyunsaturated fatty acid derivatives play important biological functions.

  • They are structural components of cellular membranes, modulating, for example, their fluidity, particularly DHA.
  • They are essential for the development and functioning of the nervous system, particularly ARA and DHA.
  • They are involved in signal transduction, particularly omega-6 polyunsaturated fatty acids, such as ARA.
  • They are involved in the regulation of genes encoding lipolytic and lipogenic enzymes, being strong inducers of fatty acid oxidation, as well as inhibitors of their synthesis and that of triglycerides, at least in animal models.
    They act, for example, as:

    • activators of the peroxisome proliferator-activated receptor α (PPAR-α) that stimulates the transcription of genes encoding lipolytic enzymes as well as mitochondrial and peroxisomal beta-oxidation enzymes, and inhibitors of transcription of genes encoding enzymes involved in lipogenesis;
    • inhibitors of sterol responsive element binding protein-1c (SREBP-1c) gene transcription, a transcription factor required for liver fatty acid and triglyceride synthesis induced by insulin.
      Note: PUFAs also increase SREBP-1c mRNA degradation as well as SREBP-1 degradation.
  • They are precursors for signaling molecules, with autocrine and paracrine action, that act as mediators in many cellular processes, such as eicosanoids
  • They are essential in the skin, especially linoleic acid in sphingolipids of the stratum corneum, where they contribute to the formation of the barrier against water loss.
  • They have a crucial role in the prevention of many diseases, particularly coronary heart disease, acting as antihypertensive, antithrombotic, and triglyceride-lowering agents.
  • Noteworthy, their energy storage function is quantitatively unimportant.

Foods rich in essential fatty acids

Linoleic acid is the most abundant polyunsaturated fatty acid in the Western diet, and accounts for 85-90% of dietary omega-6 polyunsaturated fatty acids.
The richest dietary sources are vegetable oils and seeds of many plants, such as:

  • safflower oil, ~ 740 mg/g;
  • sunflower oil, ~ 600 mg/g;
  • soybean oil, ~ 530 mg/g;
  • corn oil, ~ 500 mg/g;
  • cottonseed oil, ~ 480 mg/g;
  • walnuts, ~ 340 mg/g;
  • brazil nuts, ~ 250 mg/g;
  • peanut oil, ~ 240 mg/100 g;
  • rapeseed oil, ~ 190 mg/g;
  • peanuts, ~140 mg/g;
  • flaxseed oil, ~ 135 mg/g.

Linoleic acid is present in fair amounts also in animal products such as chicken eggs or lard, because it is present in their feed.
It should be noted that some of the major sources of linoleic acid, such as walnuts, flaxseed oil, soybean oil, and rapeseed oil are also high in alpha-linolenic acid.

Some of the richest dietary sources of alpha-linolenic acid are:

  • flaxseed oil, ~ 550 mg/g
  • rapeseed oil, ~ 85 mg/g
  • soybean oil, ~ 75 mg/g

Other foods rich in ALA include nuts, ~ 70 mg/g, and soybeans, ~ 10 mg/g.

References

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

Bergstroem S., Danielsson H., Klenberg D. and Samuelsson B. The enzymatic conversion of essential fatty acids into prostaglandins. J Biol Chem 1964;239:PC4006-PC4008

Burr G. and Burr M. A new deficiency disease produced by the rigid exclusion of fat from the diet. J Biol Chem 1929;82:345-367

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

Evans H. M. and G. O. Burr. A new dietary deficiency with highly purified diets. III. The beneficial effect of fat in the diet. Proc Soc Exp Biol Med 1928;25:390-397. doi:10.3181/00379727-25-3867

Smith W., Mukhopadhyay R. Essential fatty acids: the work of George and Mildred Burr. J Biol Chem 2012;287(42):35439-35441. doi:10.1074/jbc.O112.000005

Van Dorp. D.A., Beerthuis R.K., Nugteren D.H. and Vonkeman H. Enzymatic conversion of all-cis-polyunsaturated fatty acids into prostaglandins. Nature 1964;203:839-841. doi:10.1038/203839a0

Nutrition for athletes: strategies for training and competition

The right diet is one of the basic foundations for achieving the best athletic performance.
Unfortunately, there aren’t special diets or “magic” foods.Nutrition for Athletes
Athletes, as the rest of the population, should follow a Mediterranean-type diet, so providing an adequate intake of energy, of mineral salts, vitamins, antioxidants, fiber and water, keeping at the same time  good  balance  of caloric intake by wisely splitting it during the day.
Finally, they should avoid as much as possible industrial foods or fast foods.

Nutrition for athletes and the distribution of meals and calories

Still more than sedentary man, because of his greater caloric intake, athlete will have to consume more meals during the day to avoid concentrating an excessive amount of calories (and food) in one meal.
In this way, he will:

  • avoid reaching lunch-time and especially dinner-time with an excessive hunger;
  • digest foods more easily, not engaging the digestive system with too much abundant meals.
  • avoid any increases in blood chemistry parameters associated with an increased risk of cardiovascular disease, such as hypertriglyceridemia and hypercholesterolemia.

Of course, in nutrition for athletes, the distribution of the meals will have to consider also training and competition times. The best distribution might be: breakfast, lunch and dinner plus two snacks, one in the morning and the other in the afternoon.

Breakfast

It is of one of most important and often underestimated meals of the day, that should never be skipped.
Typical breakfast foods are milk and/or yogurt, fruit juice (better if freshly squeezed seasonal fruit; when you buy a packaged fruit juice, select it without added sugar/sweeteners and with a caloric content of about 45 kcal/100 g), freshly made tea,bread, dry cookies without cream (however moderately), corn flakes without addition of syrup, honey, fresh/dry fruit, chocolate, and jam/honey (the last three in moderation).
Breakfast will be consumed considering the time when physical activity, and still more the competition, is made.
In nutrition for athletes, as for sedentary population,the breakfast should represent about 15% of the daily caloric intake, to pass to 20% without mid-morning snack.

Lunch

It should represent the meal in which the major part of complex carbohydrates is taken up that is pasta, rice, barley, cous-cous, oats, millet, etc (better if “al dente” with a light seasoning), based on personal preferences.
To limit glycemic increase it is advisable to eat, after a dish rich in carbohydrates, vegetables, fresh or cooked (in the latter when possible, better if steamed), but avoiding potatoes, cooked carrots and onions (foods with an high glycemic index). Bread, if present, should be eaten moderately.
At the end of the lunch a fruit can be eaten as well (if it doesn’t cause feelings of bloating when eaten at the end of the meal; in the case, fruit may be eaten during snacks) and/or a dessert without cream.
Seasonal fruit and vegetable will ensure an adequate intake of mineral salts, vitamins, fiber and water.
It is advisable having lunch at least two-three hours before the start of training sessions/competition, in order to allow a complete digestion, normalization of postprandial glycemic peaks and of insulin response before starting workout.
In nutrition for athletes, the lunch should represent 25-30% of the daily caloric intake.

Dinner

In this meal, it is advisable to give priority to proteins rather than carbohydrates, hence fish, white or red meat (the last one lean and less frequently) or legumes (rich in slow absorption carbohydrates, fiber and mineral salts) will be present, with seasonal vegetables, fresh or cooked, (recommended is also a vegetable soup, that will help in restoring liquids), moderate bread, and fruit (if it doesn’t cause feelings of bloating when eaten at the end of the meal, as seen for lunch).
It is advisable to eat legumes at dinner to avoid bothersome bloating during training.
In nutrition for athletes, the dinner should represent 25-30% of the daily caloric intake.

Snacks

In nutrition for athletes, to ensure adequate distribution of calories, often much higher than in the sedentary man and avoid an excessive accumulation at major meals, at least two snacks must be present, one at mid-morning and the other at mid-afternoon. Assume preferably fruit (moderately also dry fruit, advisable walnuts and almonds), yogurt/milk, dry cookies or a sandwich with lean sliced salami (e.g. lean raw ham or cured raw beef), cottage cheese (soft fresh cheese) or simply with extra-virgin olive oil and tomato or other vegetables (always choose seasonal vegetables).
The snack should represent 10-15% of the daily caloric intake.

Daily caloric intake

In nutrition for athletes, caloric intake must be matched to energy consumption that, in turn, depends on:

  • sex;
  • age;
  • growing phase;
  • physical structure;
  • level of physical activity (training plane, competition, recovery);
  • even possible pathological states.

Athlete’s diet must consider energy consumption due to workload sustained during training sessions.
In fact, if there are sports (as swimming, running, rowing or cross-country skiing) whose training sessions cause an increase of energy requirement in excess of 50% compared to needs referred to a moderately active lifestyle, in other sports (as artistic or rhythmic gymnastics, shooting etc.) the consumption related to the activity may be modest.
So, the only difference in nourishment between a sedentary or moderately active man and an athlete engaged in sports causing a large increase of energy requirement will be of quantitative type: the greater is the energy expenditure linked to physical activity, the greater will be the caloric intake.

References

Jeukendrup A.E. Nutrition for endurance sports: marathon, triathlon, and road cycling. J Sport Sci 2011:29;sup1, S91-S99. doi:10.1080/02640414.2011.610348

Invert sugar: definition, production, and uses

Invert sugar (also known as inverted sugar) is sucrose partially or totally cleaved into fructose and glucose (also known dextrose) and, apart from the chemical process used (see below), the obtained solution has the same amount of the two carbohydrates.

Honey has a fructose and glucose composition almost equal to that of 100% invert sugar
Moreover, according to the product, not cleaved sucrose may also be present.

Invert sugar production

The breakdown of sucrose may happen in a reaction catalyzed by enzymes, such as:

  • sucrase, active at our own intestinal level;
  • invertase, an enzyme secreted by honeybees into the honey and used industrially to obtain invert sugar.

Another process applies acid action, as it happens partly in our own stomach and as it happened in the old times, and still happens, at home-made and industrial level. Sulfuric and hydrochloric acids was used, heating the solution with caution for some time; in fact the reaction is as fast as the solution is acid, regardless of the type of acid used, and as higher the temperature is. The acidity is then reduced or neutralized with alkaline substances, as soda or sodium bicarbonate.

A chemical process as described occurs when acid foods are prepared; i.e. in the preparation of jams and marmalades, where both conditions of acidity, naturally, and high temperatures, by heating, are present. The situation is analogous when fruit juices are sweetened with sucrose.
The reaction develops at room temperature as well, obviously more slowly.
What is the practical outcome of that?
It means that, during storage, also sweets and acid foods, even those just seen, go towards a slow reaction of inversion of contained/residue sucrose, with consequent modification of the sweetness, since invert sugar at low temperatures is sweeter (due to the presence of fructose), and assumption of a different taste profile.

Properties and uses

It is principally utilized in confectionery and ice-cream industries thanks to some peculiar characteristics.

  • It has an higher affinity for water (hydrophilicity) than sucrose (see fructose) therefore it keeps food more humid: e.g. cakes made with invert sugar dry up less easily.
  • It avoids or slows down crystal formation (dextrose and fructose form less crystals than sucrose), property useful in confectionery industries for icings and coverage.
  • It has a lower freezing point.
  • It increases, just a bit, the sweetness of the product in which it has been added, as it is sweeter than an equal amount of sucrose (the sweetness of fructose depends on the temperature in which it is present).
  • It may take part to Maillard reaction (sucrose can’t do it) thus contributing to the color and taste of several bakery products.

It should be noted that honey, lacking in sucrose, has a fructose and glucose composition almost equal to that of 100% invert sugar (fructose is slightly more abundant than glucose). So, diluted honey, better if not much aromatic, may replace industrial invert sugar.

References

Belitz .H.-D., Grosch W., Schieberle P. “Food Chemistry” 4th ed. Springer, 2009

Bender D.A. “Benders’ Dictionary of Nutrition and Food Technology”. 8th Edition. Woodhead Publishing. Oxford, 2006

Jordan S. Commercial invert sugar. Ind Eng Chem 1924;16(3):307-310. doi:10.1021/ie50171a037

Stipanuk M.H., Caudill M.A. Biochemical, physiological, and molecular aspects of human nutrition. 3rd Edition. Elsevier health sciences, 2012

Body weight: what to do not to increase it

In order to maintain your body weight, energy intake with foods must match your individual needs, depending on age, sex and level of physical activity; calories exceeding needs accumulate in form of fat that will deposit in various parts of the body (typically in men, as in postmenopausal women, the accumulation area for excellence is abdomen).Body Weight: Adjust Caloric Intake According to Consumption
An example: let’s assume an energy requirement of 2000 kcal with an intake of 2100 kcal. The extra 100 kcal could result from 30 g of pasta or 35 g of bread or a 25 g package of crackers or 120 g of potatoes or 10 g of oils from any source etc., not a particularly large amount of food. This modest calories surplus, if performed daily for one year leads us to take:
100 kcal x 365 days = 36500 kcal/year extra calories compared to needs.
Since a kilogram of body fat contains approximately 7000 kcal, if we assume that 36500 kcal in excess accumulate exclusively in form of fat (very plausible approximation), we obtain: 36500/7000 = about 5 kilogram of body fat.
So, even a modest daily calorie surplus, over a year, can lead to a substantial body weight gain in the form of fat mass.
This example shows the importance of estimating with accuracy our daily energy requirements.

Split daily caloric intake into multiple meals

Let’s assume that daily caloric requirement to maintain body weight is equal to 2000 kcal.
Is it the same thing if they are consumed in just two meals, maybe dividing them in half between lunch and dinner, or is it advisable to take three to five meals during a day?
In order to mantain body weight, the best choice  is to divide calories into five meals: breakfast, lunch and dinner, the most abundant, plus two snacks, one on mid-morning and the other on mid-afternoon. Why? There are various reasons.

  • Consuming only two meals during the day, lunch and dinner or breakfast and dinner, it is likely to approach both meals with a hunger difficult to control; we eat what we have on our plate already thinking about what else to eat, having the feeling of not being able to satisfy the hunger. We eat, but there is always room for more food. Among the reasons for this there are too many hours between meals. Two examples:

dinner at 8:00 p.m. and, the next day, lunch at 1:00 p.m.: the interval is 17 hours, more than 2/3 of a day;

breakfast at 7:00 a.m. and dinner to 8:00 p.m., 13 hours have passed, most of which are spent in working activities and therefore more energy-consuming than hours of sleep.

Then, drops in blood sugar levels (glycemia) can also occur: liver glycogen stores, essential for maintaining normal glycemia, with time intervals between meals previously seen, can easily reach values close to depletion.

Therefore, by splitting the daily caloric intake into two meals, it is most likely difficult to meet the target of assuming 2000 kcal (the suggested daily calorie intake).

  • The concentration of too many calories in a single meal may promote the increase of plasma triglycerides, the excess of which is linked to the onset of cardiovascular disease.
  • When accumulating almost all or all of the calories in just two meals we are likely to grow stout, have feelings of bloating and getting real digestive problems due to excess of ingested food, not to mention that could occur even a postprandial sleepiness or difficulties in getting asleep.

Exercise regularly

Physical activity has a central role both in maintaining the reached body weight and in the loss of fat mass.
Make physical activity on a regular basis has several advantages.

  • If exercise is conducted on a regular basis and is structured in the proper way, is possible that, even without appreciable changes in weight, a redistribution of fat occurs between fat mass, which drops, and free fat mass, which, on the contrary, increases. Such a result can’t obviously be reached by simple walk; we need a specific training program, better if planned by a professional, and a proper diet, always of Mediterranean type.
  • We protect muscle mass (and as suggested in point 1. we can also increase it).
  • We maintain a high metabolism.
  • Muscle burn energy during and especially after exercise.
  • The body is toned.
  • Appetite is controlled more easily.
  • Making physical activity on a regular basis makes the prevention of weight gain easier, due to the inevitable “escapades” (indulging in a bit of chocolate, an ice cream etc..).

References

Haskell W.L., Lee I.M., Pate R.R., Powell K.E., Blair S.N., Franklin B.A., Macera C.A., Heath G.W., Thompson P.D., Bauman A..Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Med Sci Sports Exerc 2007;39(8):1423-1434. doi:10.1249/mss.0b013e3180616b27

Shils M.E., Olson J.A., Shike M., Ross A.C.: “Modern nutrition in health and disease” 9th ed. 1999

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