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:
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).
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.
The 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.
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;51:1080-87. 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;21:1983-92. [Abstract]
Definition and chemical structure of trans fatty acids
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. 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.
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.
a melting point, consistency and “mouth feel” similar to those of butter;
a long shelf life at room temperature;
a flavor stability.
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 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).
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.
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%.
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.
Cyclic monomers, as well as intramolecular linear dimmers, are also formed.
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 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).
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.
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;
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.
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.
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 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.
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).
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.
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.
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).
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).
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%.
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.
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.
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.
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.
Akoh C.C. and Min D.B. Food lipids: chemistry, nutrition, and biotechnology. 3rd Edition. CRC Press Taylor & Francis Group, 2008
Ascherio A., Katan M.B., Zock P.L., Stampfer M.J., Willett W.C. Trans fatty acids and coronary heart disease. N Engl J Med 1999;340:1994-8. doi:10.1056/NEJM199906243402511
Ascherio A., Rimm E.B., Giovannucci E.L., Spiegelman D., Stampfer M., Willett W.C. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States. BMJ 1996; 313:84-90. doi:10.1080/17482970601069094
Baylin A., Kabagambe E.K., Ascherio A., Spiegelman D., Campos H. High 18:2 trans-fatty acids in adipose tissue are associated with increased risk of nonfatal acute myocardial infarction in Costa Rican adults. J Nutr 2003;133:1186-91 doi:10.1093/jn/133.4.1186
Chow C.K. Fatty acids in foods and their health implication. 3rd Edition. CRC Press Taylor & Francis Group, 2008
Clifton P.M., Keogh J.B., Noakes M. Trans fatty acids in adipose tissue and the food supply are associated with myocardial infarction. J Nutr 2004;134:874-9 doi:10.1093/jn/134.4.874
Costa N., Cruz R., Graça P., Breda J., and Casal S. Trans fatty acids in the Portuguese food market. Food Control 2016;64:128-34. doi:10.1016/j.foodcont.2015.12.010
Eckel R.H., Borra S., Lichtenstein A.H., Yin-Piazza D.Y. Understanding the Complexity of Trans fatty acid reduction in the American diet. American Heart Association trans fat conference 2006 report of the trans fat conference planning group. Circulation 2007;115:2231-46. doi:10.1161/CIRCULATIONAHA.106.181947
Hu F.B., Manson J.E., Stampfer M.J., Colditz G., Liu S., Solomon C.G., and Willett W.C. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med 2001;345:790-7. doi:10.1056/NEJMoa010492
Hu F.B., Willett W.C. Optimal diet for prevention of coronary heart disease JAMA 2002;288:2569-78. doi:10.1001/jama.288.20.2569
Lemaitre R.N., King I.B., Raghunathan T.E., Pearce R.M., Weinmann S., Knopp R.H., Copass M.K., Cobb L.A., Siscovick D.S. Cell membrane trans-fatty acids and the risk of primary cardiac arrest. Circulation 2002;105:697-01. doi:10.1161/hc0602.103583
Lichtenstein A.H. Dietary fat, carbohydrate, and protein: effects on plasma lipoprotein patterns J. Lipid Res. 2006;47:1661-7. doi:10.1194/jlr.R600019-JLR200
Lichtenstein A.H., Ausman L., Jalbert S.M., Schaefer E.J. Effect of different forms of dietary hydrogenated fats on serum lipoprotein cholesterol levels. N Engl J Med 1999;340:1933-40. doi:10.1056/NEJM199906243402501
Lopez-Garcia E., Schulze M.B., Meigs J.B., Manson J.E, Rifai N., Stampfer M.J., Willett W.C. and Hu F.B. Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction. J Nutr 2005;135:562-66 doi:10.1093/jn/135.3.562
Masanori S. Trans Fatty Acids: Properties, Benefits and Risks J Health Sci 2002;48(1):7-13. [Abstract]
Mensink R.P., Katan M.B. Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects. N Engl J Med 1990;323:439-45. doi:10.1056/NEJM199008163230703
Mozaffarian D. Commentary: Ruminant trans fatty acids and coronary heart disease-cause for concern? Int J Epidemiol 2008;37(1):182-4. doi:10.1093/ije/dym263
Mozaffarian D., Katan M.B., Ascherio A., Stampfer M.J., Willett W.C. Trans fatty acids and cardiovascular disease. N Engl J Med 2006;354:1601-13. doi:10.1056/NEJMra054035
Mozaffarian D., Pischon T., Hankinson S.E., Joshipura K., Willett W.C., and Rimm E.B. Dietary intake of trans fatty acids and systemic inflammation in women. Am J Clin Nutr 2004;79:606-12 doi:https://doi.org/10.1093/ajcn/79.4.606
Oh K., Hu F.B., Manson J.E., Stampfer M.J., Willett W.C. Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the Nurses’ Health Study. Am J Epidemiol 2005;161(7):672-9. doi:10.1093/aje/kwi085
Okie S. New York to Trans Fats: You’re Out! N Engl J Med 2007;356:2017-21. doi:10.1056/NEJMp078058
Oomen C.M., Ocke M.C., Feskens E.J., van Erp-Baart M.A., Kok F.J., Kromhout D. Association between trans fatty acid intake and 10-year risk of coronary heart disease in the Zutphen Elderly Study: a prospective population-based study. Lancet 2001; 357(9258):746-51. doi:10.1016/S0140-6736(00)04166-0
Pietinen P., Ascherio A., Korhonen P., Hartman A.M., Willett W.C., Albanes D., VirtamO J.. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men: the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Epidemiol 1997;145(10):876-87. doi:10.1093/oxfordjournals.aje.a009047
Risérus U. Trans fatty acids, insulin sensitivity and type 2 diabetes. Scand J Food Nutr 2006;50(4):161-5. doi:10.1080/17482970601133114
Salmerón J., Hu F.B., Manson J.E., Stampfer M.J., Colditz G.A., Rimm E.B., and Willett W.C. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr 2001;73:1019-26 doi:10.1093/ajcn/73.6.1019
Stender S., Astrup A.,and Dyerberg J. A trans European Union difference in the decline in trans fatty acids in popular foods: a market basket investigation. BMJ Open 2012;2(5):e000859. doi:10.1136/bmjopen-2012-000859
Stender S., Astrup A., and Dyerberg J. Artificial trans fat in popular foods in 2012 and in 2014: a market basket investigation in six European countries. BMJ Open 2016;6(3):e010673. doi:10.1136/bmjopen-2015-010673
Stender S., Astrup A.,and Dyerberg J. Tracing artificial trans fat in popular foods in Europe: a market basket investigation. BMJ Open 2014;4(5):e005218. doi:10.1136/bmjopen-2014-005218
Stender S., Astrup A., Dyerberg J. What went in when trans went out?. N Engl J Med 2009;361:314-16. doi:10.1056/NEJMc0903380
Stender S., Dyerberg J., Astrup A. Consumer protection through a legislative ban on industrially produced trans fatty acids in Denmark. Scand J Food Nutr 2006;50(4):155-60. doi:10.1080/17482970601069458
Stender S., Dyerberg J., Astrup A. High levels of trans fat in popular fast foods. N Engl J Med 2006;354:1650-2. doi:10.1056/NEJMc052959
Willett W., Mozaffarian D. Ruminant or industrial sources of trans fatty acids: public health issue or food label skirmish? Am J Clin Nutr 2008;87(3): 515-6 doi:10.1093/ajcn/87.3.515
Green tea is an infusion of processed leaves of tea plant, Camellia sinensis, a member of the Theaceae family.
It is the most consumed beverages in Asia, particularly in China and Japan.
Western populations consume black tea more frequently than green tea. However, in recent years, thanks to its health benefits, it has been gaining their attention.
Currently, it accounts for 20% of the tea consumed worldwide.
“You can never get a cup of tea large enough or a book long enough to suit me.”C.S. Lewis
Processing and properties of green tea
As all other types of tea, it is produced from fresh leaves of Camellia sinensis.
The peculiar properties of the beverage depend on the type of processing that the leaves undergo. In fact, they are processed in such a way as to minimize both enzymatic and chemical oxidation processes of the substances contained in them, in particular catechins.
Therefore, among the different types of tea, it undergoes the lowest degree of oxidation during processing.
At the end of the processing, tea leaves retain their green color, thanks to the little chemical modifications/oxidations they have undergone. The infusion shows off a yellow-gold color.
Finally, the processing of tea leaves ensures that green tea flavor is more delicate and lighter than black tea.
The three main steps in the processing of tea leaves
After harvesting, tea leaves are exposed to the sun for 2-3 hours and withered/dried; then, the real processing starts.
It consists of three main steps: heat treatment, rolling and drying.
Heat treatment, short and gentle, is the crucial step for the quality and properties of the beverage.
It occurs with steam (the traditional Japanese method) or by dry cooking in hot pans (a large wok, the traditional Chinese method). Heat treatment has the purpose of:
inactivate the enzymes present in the tissues of the leaves, thus stopping enzymatic oxidation processes, particularly of polyphenols;
eliminate the grassy smell in order to stand out tea flavor;
evaporate part of the water present in the fresh leaf (water constitutes about 75% of the weight of the leaf), making it softer, so as to make the next step easier.
The rolling step follows the heat treatment of the leaves; this step has the purpose of:
facilitate the next stage of drying;
destroy the tissues of the leaves in order to favor, later, the release of aromas, thus improving the quality of the product.
The drying is the last step, which also leads to the production of new compounds and improves the appearance of the product.
Green tea polyphenols
All types of tea are rich in polyphenols, compounds that are also present in fruits, vegetables, extra virgin olive oil, and red wine.
Fresh tea leaves are rich in water-soluble polyphenols, especially catechins (or flavanols) and glycosylated catechins (both belonging to the class of flavonoids), molecules which are believed to be the responsibles of the benefits of green tea.
The major catechins in green tea are epigallocatechin-3-gallate (EGCG), epigallocatechin, epicatechin-3-gallate, epicatechin, epicatechin, but also catechin, gallocatechin, catechin gallate, and gallocatechin gallate are present, even if in lower amount. These polyphenols account for 30%-42% of the dry leaf weight (but only 3%–10% of the solid content of black tea).
Green tea caffeine accounts for 1,5-4,5% of the dry leaf weight.
How to maximize the absorption of catechins
In vitro studies have shown the high antioxidant power of catechins, greater than that of vitamin C and vitamin E. In vitro, EGCG is generally considered the most biologically active catechin. In vivo studies and several epidemiologic studies have shown the possible preventive effects of green tea catechins, especially EGCG, in preventing the development of:
cardiovascular disease, such as hypertension and stroke;
some cancers, such as lung cancer (but not among smokers) and oral and digestive tract cancers.
For these reasons, it is essential to maximize the intestinal absorption of catechins. Catechins are stable in acidic environment, but not in non-acidic environment, as in the small intestine; also for this reason, after digestion, less than 20% of the total remains.
Studies with models of the digestive tract of rat and man, that simulate digestion in stomach and small intestine, have shown that the addition of citrus juice or vitamin C to green tea significantly increases the absorption of catechins.
Among tested citrus juices, lemon juice is the best, followed by orange, lime and grapefruit juices. Citrus juices seem to have a stabilizing effect on catechins that goes beyond what would be predicted solely based on their ascorbic acid content.
Clifford M.N., van der Hooft J.J.J., and Crozier A. Human studies on the absorption, distribution, metabolism, and excretion of tea polyphenols. Am J Clin Nutr 2013;98:1619S-1630S [Abstract]
Dwyer J.T. and Peterson J. Tea and flavonoids: where we are, where to go next. Am J Clin Nutr 2013;98:1611S-1618S [Abstract]
Green R.J., Murphy A.S., Schulz B., Watkins B.A. and Ferruzzi M.G. Common tea formulations modulate in vitro digestive recovery of green tea catechins. Mol Nutr Food Res 2007;51(9):1152-1162 [Abstract]
Huang W-Y., Lin Y-R., Ho R-F., Liu H-Y., and Lin Y-S. Effects of water solutions on extracting green tea leaves. ScientificWorldJournal 2013;Article ID 368350 [Abstract]
Sharma V.K., Bhattacharya A., Kumar A. and Sharma H.K. Health benefits of tea consumption. Trop J Pharm Res 2007;6(3):785-792 [Abstract]
Tea drinking, particularly green tea, has always been associated, at least in East Asia cultures (mainly in China and Japan) with health benefits. Only recently, the scientific community has begun to study the health benefits of tea consumption, recognizing its preventive value in many diseases.
Green tea benefits in preventing cancer
Several epidemiological and laboratory studies have shown encouraging results with respect to possible preventive role of tea, particularly green tea and its catechins, a subgroup of flavonoids (the most abundant polyphenols in human diet) against the development of some cancers like:
oral and digestive tract cancers;
lung cancer among those who have never smoked, not among smokers.
Tea polyphenols, the most active of which is epigallocatechin-3-gallate (EGCG), seem to act not only as antioxidants, but also as molecules that, directly, may influence gene expression and diverse metabolic pathways.
Green tea and cardiovascular disease
Cardiovascular disease is the main cause of deaths worldwide, particularly in low- and middle-income countries, with an estimate of about 17 million deaths in 2008 that will increase up to 23.3 million by 2030.
Daily tea consumption, especially green tea, seems to be associated with a reduced risk of developing cardiovascular disease, such as hypertension and stroke.
Among the proposed mechanisms, the improved bioactivity of the endothelium-derived vasodilator nitric oxide (NO), due to the action of tea polyphenols that enhance nitric oxide synthesis, and/or decrease superoxide-mediated nitric oxide breakdown seem to be important.
Green tea and antioxidant properties
Tea polyphenols may act, in vitro, as free radical scavengers.
Since radical damage plays a pivotal role in the development of many diseases such as atherosclerosis, rheumatoid arthritis, cancer, or in ischemia-reoxygenation injury, tea polyphenols, particularly green teacatechins, may have a preventive role.
Green tea benefits in weight loss and weight maintenance
Green tea, but also oolong tea, that is, catechins and caffeine rich teas, has a potential thermogenic effect. This has made them a potential tool for:
weight loss, by increasing energy expenditure and fat oxidation;
weight maintenance, ensuring a high energy expenditure during the maintenance of weight loss.
Indeed, it has been shown that green tea and green tea extracts are not an aid in weight loss and weight maintenance, since:
they are not able to induce a significant weight loss in overweight and obese adults;
they are not helpful in the maintenance of weight loss.
Green tea and preventing dental decay
Animal and in vitro studies have shown that tea, and in particular its polyphenols, seems to possess:
antibacterial properties against pathogenic action of cariogenic bacteria, as Streptococcus mutans, particularly green tea EGCG;
inhibitory action on salivary and bacterial amylase (it seems that black tea thearubigins and theaflavins are more effective than green teacatechins);
it is able to inhibit acid production in the oral cavity.
All these properties make green tea and black tea, beverages with potential anticariogenic activity.
Arab L., Khan F., and Lam H. Tea consumption and cardiovascular disease risk. Am J Clin Nutr 2013;98:1651S-1659S doi:10.3945/ajcn.113.059345
Dwyer J.T. and Peterson J. Tea and flavonoids: where we are, where to go next. Am J Clin Nutr 2013;98:1611S-1618S doi:10.3945/ajcn.113.059584
Goenka P., Sarawgi A., Karun V., Nigam A.G., Dutta S., Marwah N. Camellia sinensis (Tea): implications and role in preventing dental decay. Phcog Rev 2013;7:152-6 doi:10.4103/0973-7847.120515
Grassi D., Desideri G., Di Giosia P., De Feo M., Fellini E., Cheli P., Ferri L., and Ferri C. Tea, flavonoids, and cardiovascular health: endothelial protection. Am J Clin Nutr 2013;98:1660S-1666S doi:10.3945/ajcn.113.058313
Hursel R. and Westerterp-Plantenga M.S. Catechin- and caffeine-rich teas for control of body weight in humans. Am J Clin Nutr 2013;98:1682S-1693S doi:10.3945/ajcn.113.058396
Hursel R., Viechtbauer W. and Westerterp-Plantenga M.S. The effects of green tea on weight loss and weight maintenance: a meta-analysis. Int J Obesity 2009;33:956-961 doi:10.1038/ijo.2009.135
Jurgens T.M., Whelan A.M., Killian L., Doucette S., Kirk S., Foy E. Green tea for weight loss and weight maintenance in overweight or obese adults. Editorial group: Cochrane Metabolic and Endocrine Disorders Group. 2012:12 Art. No.: CD008650 doi:10.1002/14651858.CD008650.pub2
Lagari V.S., Levis S. Phytoestrogens for menopausal bone loss and climacteric symptoms. J Steroid Biochem Mol Biol 2014;139:294-301 doi:10.1016/j.jsbmb.2012.12.002
Lambert J.D. Does tea prevent cancer? Evidence from laboratory and human intervention studies. Am J Clin Nutr 2013;98:1667S-1675S doi:10.3945/ajcn.113.059352
Lethaby A., Marjoribanks J., Kronenberg F., Roberts H., Eden J., Brown J. Phytoestrogens for menopausal vasomotor symptoms. Cochrane Database Syst Rev 2013:10;12 Art. No.: CD001395 doi:10.1002/14651858.CD001395.pub4
Levis S., Strickman-Stein N., Ganjei-Azar P., Xu P., Doerge D.R., Krischer J. Soy isoflavones in the prevention of menopausal bone loss and menopausal symptoms: a randomized, double-blind trial. Arch Intern Med 2011:8;171(15):1363-9 doi:10.1001/archinternmed.2011.330
Lorenz M. Cellular targets for the beneficial actions of tea polyphenols. Am J Clin Nutr 2013;98:1642S-1650S doi:10.3945/ajcn.113.058230
Sharma V.K., Bhattacharya A., Kumar A. and Sharma H.K. Health benefits of tea consumption. Trop J Pharm Res 2007;6(3):785-792 [Abstract]
Yang Y-C., Lu F-H., Wu J-S., Wu C-H., Chang C-J. The protective effect of habitual tea consumption on hypertension. Arch Intern Med 2004;164:1534-1540 doi:10.1001/archinte.164.14.1534
Yuan J-M. Cancer prevention by green tea: evidence from epidemiologic studies. Am J Clin Nutr 2013;98:1676S-1681S doi:10.3945/ajcn.113.058271
Carotenoids belong to the category of bioactive compounds taken up with diet, that is, molecules able to provide protection against many diseases such as cardiovascular diseases, cancer and macular degeneration. They are also important for the proper functioning of the immune system.
Among the mechanisms that seem to be at the basis of their human health-promoting effects have been reported (Olson, 1999, see References):
the capability to quench singlet oxygen (see above);
the scavenging of peroxyl radicals and reactive nitrogen species;
the modulation of carcinogen metabolism;
the inhibition of cell proliferation;
the enhancement of the immune response;
a filtering action of blue light;
the enhancement of cell differentiation;
stimulation of cell-to-cell communication
Carotenoids and antioxidant activity
Carotenoids, with the adaptation of organisms to aerobic environment, and therefore to the presence of oxygen, have offered protection against oxidative damage from free radicals, particularly by singlet oxygen, a powerful oxidizing agent (see also below). Carotenoids stabilize singlet oxygen acting both chemical and physical point of view:
chemical action involves the union between the two molecules;
in physical action, the radical transfers its excitation energy to the carotenoid. The result is a low energy free radical and an excited carotenoid; later, the energy acquired by the carotenoid is released as heat to the environment, and the molecule, that remains intact, is ready to carry out another cycle of stabilization of singlet oxygen, and so on.
The capability of carotenoids to quench singlet oxygen is due to the conjugated double-bond system present in the molecule, and the maximum protection is given by those molecules that have nine or more double bonds (moreover, the presence of oxygen in the molecule, as in xanthophylls, seems to have a role). Carotenoids are involved not only in singlet oxygen quenching, but also in the scavenging of other reactive species both of oxygen, as peroxyl radicals (therefore contributing to the reduction of lipid peroxidation) and nitrogen. These reactive molecules are generated during the aerobic metabolism but also in the pathological processes.
Lycopene, xanthophylls and human health
Lycopene, a carotene, canthaxanthin and astaxanthin, two xanthophylls present in foods of animal origin, are better antioxidants than beta-carotene but also than zeaxanthin that, with lutein, is involved in prevention of age-related macular degeneration.
Lycopene, in addition to act on oxygen free radicals, acts as antioxidant also on the radicals of vitamin C and vitamin E, that are generated during the antioxidant processes in which these vitamins are involved, “repairing them”.
Finally, lycopene exerts its antioxidant action also indirectly, inducing the synthesis of enzymes involved in the protection against the action of oxygen free radicals and other electrophilic species; these enzymes are quinone reductase, glutathione S-transferase and superoxide dismutase (they are part of the enzymatic antioxidant system).
Vitamin A and human health
Vitamin A, whose deficiency affects annually more than 100 million children worldwide, causing more than a million deaths and half million cases of blindness, is a well-known carotenoid derivative with many biological actions, being essential for reproduction, growth, vision, immune function and general human health.
In the human diet, the major sources of vitamin A are the preformed vitamin, which is found in foods of animal origins (meat, milk, eggs, etc), and provitamin A carotenoids, present in fruits and vegetables. In economically deprived countries, fruits and vegetables are the main source of vitamin A being less expensive than food of animal origin.
Of the more than 750 different carotenoids identified in natural sources, only about 50 have provitamin A activity, and among these, beta-carotene (precisely, all-trans-beta-carotene isomer) is the main precursor of the vitamin A.
Among the other carotenoids precursors of vitamin A, alpha-carotene, gamma-carotene, beta-cryptoxanthin, alpha-cryptoxanthin, and beta-carotene-5,6-epoxide have about half the bioactivity of beta-carotene.
Spinach, carrots, pumpkins, sweet potatoes (yellow) are example of vegetables rich in beta-carotene and other provitamin A carotenoids. Acyclic carotenes, such as lycopene (the main carotenoid in the human diet), and xanthophylls, except those mentioned above (beta-cryptoxanthin, alpha-cryptoxanthin, and beta-carotene-5,6-epoxide), cannot be converted to vitamin A.
de la Rosa L.A., Alvarez-Parrilla E., Gonzàlez-Aguilar G.A. Fruit and vegetable phytochemicals: chemistry, nutritional value, and stability. 1th Edition. Wiley J. & Sons, Inc., Publication, 2010
Olson, J.A. 1999. Carotenoids. p. 525-541. In: Shils M.E., Olson J.A., Shike M., Ross A.C. “Modern nutrition in health and disease” 9th ed., by Lippincott, Williams & Wilkins, 1999
Ross A.B., Thuy Vuong L., Ruckle J., Synal H.A., Schulze-König T., Wertz K., Rümbeli R., Liberman R.G., Skipper P.L., Tannenbaum S.R., Bourgeois A., Guy P.A., Enslen M., Nielsen I.L.F., Kochhar S., Richelle M., Fay L.B., and Williamson G. Lycopene bioavailability and metabolism in humans: an accelerator mass spectrometry study. Am J Clin Nutr 2011;93:1263-73. doi:10.3945/ajcn.110.008375
Studies conducted on Greenland Eskimos, which consume large amount of fish or marine mammals rich in omega-3 fatty acids and have a low incidence of cardiovascular disease or CVD, have suggested a protective effects of such fatty acids against these disease. Results of other epidemiological studies, randomized trials and animal investigations, have also suggested that omega-3 fats, and in particular long-chain omega-3 fatty acids, eicosapentaenoic aci or EPA and docosahexaenoic acid or DHA have cardiovascular effects. These studies indicate that they have anti-inflammatory, antiatherogenic, and antiarrhythmic effects, which are considered plausible mechanisms for reducing the risk of cardiovascular disease.
Omega-3 fatty acid supplements and secondary prevention of CVD
In a study published on Archives of Internal Medicine a research team, using a meta-analysis of randomized, double-blind, placebo-controlled trials, has evaluated the preventive effect of omega-3 fatty acid supplements (omega-3 fatty acid supplements for at least 1 year, with a daily dose of EPA or DHA ranged from 0.4 to 4.8 g/d, and a follow-up period ranged from 1.0 to 4.7 years) in the secondary prevention of cardiovascular disease, i.e. among patients with a history of cardiovascular disease (not in healthy individuals).
The study involved 20485 patients, male or female aged ≥18 years, 10259 randomized to a placebo group and 10226 randomized to an intervention group. Placebo groups received vegetable oils (sunflower oil, olive oil, and corn oil), mixed fatty oil, and other “inert” or ill-defined substances (aluminum hydroxide and unspecified placebo).
The meta-analysis showed insufficient evidence of a secondary preventive effect of omega-3 fatty acid supplements against overall cardiovascular events, which include peripheral vascular disease, angina and unstable angina, transient ischemic attack and stroke, fatal and nonfatal myocardial infarction, sudden cardiac death, cardiovascular death, congestive heart failure, and nonscheduled cardiovascular interventions (i.e., coronary artery bypass surgery or angioplasty).
Moreover, no significant preventive effect was observed in subgroup analyses by the following: history of cardiovascular disease, concomitant medication use (lipid lowering agents, no lipid-lowering agents, or antiplatelet agents only), country location (Western Europe, Northern Europe, United States, or Asia), inland or coastal geographic area, methodological quality of the trial, duration of treatment, type of placebo material in the trial (oil vs nonoil), dosage of EPA or DHA, or use of fish oil supplementation only as treatment.
The study showed insufficient evidence of a secondary preventive effect of omega-3 fatty acid supplements against overall cardiovascular events among patients with a history of cardiovascular disease.
Kwak S.M., Myung S-K., Lee Y.J., Seo H.G., for the Korean Meta-analysis Study Group. Efficacy of omega-3 fatty acid supplements (eicosapentaenoic acid and docosahexaenoic acid) in the secondary prevention of cardiovascular disease. A meta-analysis of randomized, double-blind, placebo-controlled trials. Arch Intern Med 2012;172(9):686-694. doi:10.1001/archinternmed.2012.262
In a study published on British Medical Journal a research team has conducted a systematic review of the literature and meta-analyses on potassium intake and health in apparently healthy adults and children without renal impairment that might compromise its handling.
Eleven cohort studies (127038 participants) reporting all cause mortality, stroke, cardiovascular disease, or coronary heart disease in adults and twenty-two randomized controlled trials (1606 participants) reporting blood lipids, blood pressure, renal function, and catecholamine concentrations were included in the study.
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 (however, the studies were of relatively short duration and did not consider the effect that increased potassium intake may have over time) and in children (there is a lack of data in children: only three controlled studies with 156 partecipants).
There was no adverse effect of increased 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 (a 24% lower risk).
In healthy adult there was no significant adverse effect on renal function.
This study suggests that, in people without impaired renal function, increased potassium intake (at least 90 mmol/day) is potentially beneficial for the prevention and control of elevated blood pressure and stroke.
How to increase K+ intake
It should be noted that an increased potassium intake can be achieved following the largely plant-based Mediterranean Diet, which is characterized by the consumption of large quantities of fresh fruit, vegetable, legumes and unrefined cereals, all rich in potassium (that is also accompanied by a variety of other nutrients).
Aburto N.J., Hanson S., Gutierrez H., Hooper .L, Elliott P., Cappuccio F.P. Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses. BMJ 2013;346:f1378. doi:10.1136/bmj.f1378
Biochemistry and Nutrition