mercredi 28 février 2018
mardi 27 février 2018
mercredi 21 février 2018
Should we continue to fund large observational epidemiological studies?
Large epidemiological studies were the Graal of public health researchers notably after the WWII mainly because of the irruption of computers. Big is beautiful and bigger is more beautiful.Indeed the magnitude of studies hid biases of the findings and much more of their interpretations.
The major part of those studies is observational. Let us recall what are the limits and biases of observation of a large number of humans.
Causality: the rules.
The major part of those studies is observational. Let us recall what are the limits and biases of observation of a large number of humans.
Causality: the rules.
lundi 19 février 2018
The actual problem with this paper is apparently that sat fat effects on the brain needs sucrose...
https://www.sciencedirect.com/science/article/pii/S2212877817309389?via%3Dihub
"The present findings demonstrate that overconsumption of saturated fat (in combination with excess sugar) that leads to the development of DIO stimulates anxiodepressive behavior. "
Very ununderstandable abstract
"The present findings demonstrate that overconsumption of saturated fat (in combination with excess sugar) that leads to the development of DIO stimulates anxiodepressive behavior. "
 |
| Saturated high fat feeding is not high fat diet: 43% carbs, 50% fat and 7% of protein... |
Very ununderstandable abstract
Abstract
Objective
The incidence of depression is significantly compounded by obesity. Obesity arising from excessive intake of high-fat food provokes anxiodepressive behaviour and elicits molecular adaptations in the nucleus accumbens (NAc), a region well-implicated in the hedonic deficits associated with depression and in the control of food-motivated behaviour. To determine the aetiology of diet-induced depression, we studied the impact of different dietary lipids on anxiodepressive behaviour and metabolic and immune outcomes and the contribution of NAcimmune activity.
Methods
Adult C57Bl/6 mice were subjected to isocaloric high-fat/high-sucrose diets (HFD), enriched in either saturated or monounsaturated fat, or a control low-fat diet (LFD). Metabolic responses, anxiodepressive behaviour, and plasma and NAc inflammatory markers were assessed after 12 weeks. In separate experiments, an adenoviral construct inhibiting IKKβ, an upstream component of the nuclear factor kappa-b (NFkB) pathway, was a priori injected into the NAc.
Results
Both HFDs resulted in obesity and hyperleptinemia; however, the saturated HFD uniquely triggered anxiety-like behaviour, behavioural despair, hyperinsulinemia, glucose intolerance, peripheral inflammation, and multiple pro-inflammatory signs in the NAc, including reactive gliosis, increased expression of cytokines, antigen-presenting markers and NFкB transcriptional activity. Selective NAc IKKβ inhibition reversed the upregulated expression of inflammatory markers, prevented anxiodepressive behavior and blunted compulsive sucrose-seeking in mice fed the saturated HFD.
Conclusions
Metabolic inflammation and NFкB-mediated neuroinflammatory responses in the NAc contribute to the expression of anxiodepressive behavior and heightened food cravings caused by a diet high in saturated fat and sugar.
 |
| Leptin from adipocytes and ghrelin from GI tract |
jeudi 15 février 2018
mercredi 14 février 2018
Sulphites, fermentation, side effects
https://www.google.fr/amp/s/amp.theguardian.com/lifeandstyle/2009/feb/14/wine-sulphites
One example: cider
A lot of ciders provoke headaches which are of multiple origins. However, sulphites are one of the major cause as it acts as a vasodilator.
Added sulphites make a great difference in the final content of sulphites even if a small amount is the result of the fermentation process.
One example: cider
A lot of ciders provoke headaches which are of multiple origins. However, sulphites are one of the major cause as it acts as a vasodilator.
Added sulphites make a great difference in the final content of sulphites even if a small amount is the result of the fermentation process.
lundi 12 février 2018
Ketodiet and cancer: it is too early but we must keep watching
" If a tumor is unable to utilise ketone bodies, the use of KD may be an effective therapy for selective nutrient starvation of such tumors. However, numerous reports about inconsistent efficacies of this treatment broke the illusion about the possibility to cure cancer thoroughly with KD therapy."
http://www.jlr.org/content/early/2018/02/05/jlr.M082040.full.pdf+html
Mice study with HeLa tumour.
Mice study with HeLa tumour cells and always this question: usually, human tumours do have a much higher rate of genomic variation and genetic variants than mice model especially HeLa
"Our results suggest that not a single HeLa cell line, or even a set of similar HeLa cell lines, exists. Rather, an indeterminate number of clones exist, each carrying large genomic differences that lead to different expression profiles. The HeLa cell recalls the main character of the novel by Pirandello (the Italian poet awarded the 1934 Nobel Prize in Literature): “One, no one, one hundred thousand”57: the HeLa cell line is thought to be a unique cell line (“one”), but it is clear that large differences exist between the tumour from which it was derived and the human genome (“no one”) and that an indeterminate number of HeLa cell lines are scattered in laboratories worldwide (“one hundred thousand” or more), each with a unique genomic profile."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613361/
http://www.jlr.org/content/early/2018/02/05/jlr.M082040.full.pdf+html
Mice study with HeLa tumour.
Mice study with HeLa tumour cells and always this question: usually, human tumours do have a much higher rate of genomic variation and genetic variants than mice model especially HeLa
"Our results suggest that not a single HeLa cell line, or even a set of similar HeLa cell lines, exists. Rather, an indeterminate number of clones exist, each carrying large genomic differences that lead to different expression profiles. The HeLa cell recalls the main character of the novel by Pirandello (the Italian poet awarded the 1934 Nobel Prize in Literature): “One, no one, one hundred thousand”57: the HeLa cell line is thought to be a unique cell line (“one”), but it is clear that large differences exist between the tumour from which it was derived and the human genome (“no one”) and that an indeterminate number of HeLa cell lines are scattered in laboratories worldwide (“one hundred thousand” or more), each with a unique genomic profile."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613361/
dimanche 11 février 2018
Food addiction: are cheeses very addictive?
http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0117959
The answer is no.
 |
| https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4487594/ |
vendredi 9 février 2018
mardi 6 février 2018
vendredi 2 février 2018
Lactalis: zero risk is not of this world
https://www.foodqualitynews.com/Article/2018/01/11/Retailers-failed-to-stop-sale-of-recalled-infant-formula-in-France?utm_source=newsletter_daily&utm_medium=email&utm_campaign=GIN_NId&c=dC5HnbRQjql3AFjSoX5a2d%2FsLfrxEkYo&p2=
http://www.lejdd.fr/societe/exclusif-le-patron-de-lactalis-sort-du-silence-dans-le-jdd-3545168
https://www.marianne.net/societe/lactalis-le-pdg-avoue-que-du-lait-contamine-pu-etre-donne-des-bebes-depuis-12-ans
http://www.lejdd.fr/societe/exclusif-le-patron-de-lactalis-sort-du-silence-dans-le-jdd-3545168
https://www.marianne.net/societe/lactalis-le-pdg-avoue-que-du-lait-contamine-pu-etre-donne-des-bebes-depuis-12-ans
3- and 2-monochloropropanediol (MCPD), and theirfatty acid esters, and glycidyl fatty acid esters in food
"2. Formation routes
The formation routes of 3-MCPD can be divided into three groups. The first pathway is the acid hydrolysis (used in HVP production), which is the reaction of hydrochloric acid with residual vegetable oil. The second route is the heat processing, which is independent of the presence of acid-HVP. In this way, 3-MCPD is formed from lipids and sodium chloride, which can be present in the material naturally or added during the processing. The heat can affect food not only during industrial production but also during domestic cooking, such as baking or frying. The two pathways were described in detail by Baer et al. in 2010. The third and recently most investigated pathway is the release of free 3-MCPD from its bound (esterified) form. 3-MCPD can occur as a mixture of mono- and diesters, usually of palmitic, oleic or stearic fatty acids. Until now, the formation mechanism of 3-MCPD esters has not been fully understood. The earlier hypothesis, published in 1991 by Collier et al., proposed the mechanism based on triacylglycerol reaction in which a key step is the nucleophilic substitution of the acyl group by the chloride anion at positions activated by neighbouring ester groups that results in chloropropanediol diester. According to a more recent assumption, the formation of 3- MCPD esters progresses through the cyclic acyloxonium ion as an intermediate, which derives from the elimination of hydroxyl groups from mono- and diacylglycerols (MAG and DAG) (Bakhiya et al., 2011). Rahn and Yaylayan (2011) provided further evidence for this hypothesis by monitoring this intermediate ion formation in palmitin systems using IR spectroscopy and isotope labelling technique. Both above assumptions take into consideration the presence of chloride ions, which seem to have the strong influence on 3-MCPD esters formation (Shimizu et al., 2013). 3-MCPD can be released from its esterified form via lipase catalysed hydrolysis in human gastrointestinal tract during digestion. In 2004, Robert et al. simulated the formation of chloropropanols using a model system consisting of mammalian, plant and fungal lipases, vegetable oil or fat, water and sodium chloride. Three years later, Seefelder et al. (2008) used a simple intestinal model to quantify the level of 3-MCPD release from the ester form. Monoesters and diesters were incubated with pancreatic lipase and porcine bile extract. The monoesters were almost completely hydrolysed after 1 min. The 3-MCPD release from diesters was slower, reaching 45% after 1 min, 65% after 2 min and almost 100% after approximately 1 hour. Also, the authors proposed that 3-MCPD esters have the same metabolic pathway as the one known for acylglycerols during human digestion, where pancreatic lipases release glycerol only from 1- and 3-monoacylglycerols. Triacylglycerols are hydrolysed to diacylglycerols, and incorporated in lipoproteins. However, this hypothesis appeared to be speculative, mainly because their studies have already proven a partial release of free 3-MCPD from diester form. Moreover, lipoproteins can be bioavailable through the lymphatic system (Chon et al., 2007). According to recent investigations on lipolytic enzymes, there are three enzymes that can completely hydrolyze triacylglycerols (Lass et al., 2011). Thus it can be assumed that these enzymes may release free 3-MCPD from diester form (Abraham et al., 2013). Until now, no in vivo research has been delivered to verify the aforementioned postulates, therefore, the assumption of 100% hydrolysis of 3-MCPD esters should be taken into account while assessing the human health risk. Besides the formation pathways of 3-MCPD described above, other routes were also proposed. Myszkowski and Zielinski (1965) assumed that monochloropropanediol can form from allyl alcohol, chlorine and water. Collier et al. (1991) reported the possibility of 3-MCPD formation from carbohydrates (pentosan and pectin) and hydrochloric acid. Cerbulis et al. (1984) demonstrated that small but significant amounts of 3-MCPD diesters were determined in raw goat s milk, so the authors assumed these compounds are naturally occurring in food. However, these postulates have not been proved in later studies."
"3. Occurrence in food
During the past decade, the development of new analytical methods as well as renewed interest in chloropropanols as dangerous food toxicants caused that 3-MCPD was determined in a number of different foodstuffs. The investigated foods can be divided into three main groups, i.e. thermally-treated foods, edible oils and fats, and infant and baby foods (including human breast milk). Below, each groups has been described in detail in the consecutive paragraphs. 3.1 Thermally-treated foods Crews et al. were the first researchers who examined a large number of foodstuffs marketed in UK (2001). The main food group contaminated by 3-MCPD were cereal derived products; the highest concentration of monochloropropanediol was determined in toasted bread (0.088 mg/kg) and cream crackers (0.087 mg/kg). The same group of foodstuffs was analyzed by BreitlingUtzmann et al. (2003). The highest concentration of 3-MCPD was also found in toasts (over 0.500 mg/kg in a well-toasted bread) and breadcrumbs (over 0.400 mg/kg). It seems that the exposure to high temperatures is a key step in 3-MCPD formation in cereal-derived foods. Breitling-Utzmann et al. (2005) also tested the influence of bread ingredients on 3-MCPD formation. It appeared that the addition of fat and baking agent (consisting of sugar, flour, soy flour, calcium sulfate, mono- and diacylglycerols of edible fatty acids as emulsifiers) may influence the concentration of 3-MCPD in the final product, emulsifiers and sugar having the strongest effect. Regarding the precursors of 3-MCPD, Hamlet et al. used model dough systems to estimate the production of chloropropanols in leavened (Hamlet et al., 2004) and unleavened (Hamlet et al., 2004) doughs. In both cases, glycerol or compounds based on a glycerol skeleton such as, monoacylglycerols and phosphatidylglycerols were the main 3-MCPD precursors. Another foodstuffs in which heat treatment seems to have triggered 3-MCPD formation are malt-derived products such as, food-grade malted grains, malt flours and malt extracts (colour and flavour agents). The original components of these products can promote the formation of 3-MCPD, so there is no need for adding fat, acid or chloride. However, significant amounts of 3-MCPD in this type of foods were detected only in the dark brewing malt (0.247 mg/kg) [22]. The amount of free 3-MCPD present in beer is relatively low (10 μg/l) (IARC, 2000) but it seems that it may be bound to other beer components such as, acids, aldehydes and alcohol, which can significantly exceed the free form content (Divinová et al., 2007). Smoked foods also contain significant amounts of 3-MCPD (over 0.02 mg/kg). Kuntzer and Weisshaar (2006) analyzed the influence of food smoking on the formation of 3-MCPD in fermented sausages and ham. The smoking process appeared to be the main source of 3-MCPD, especially with regard to the type of wood and the duration of processing (Kuntzer and Weisshaar, 2006; FAO, WHO, 2007). In contrast to cereal- and malt-derived products, lipids are not considered the precursors of 3-MCPD in smoked foods, and the formation mechanism from 3-hydroxyacetone during cracking of cellulose was proposed instead. Apart from that, Reece (2005) suggested that the concentration of salt in the brine used in the smoking process may also be the influential factor in the formation of 3-MCPD. 3-MCPD was also determined in such heat-processed foodstuffs as coffee, particularly roasted coffee after prolonged roasting process, and instant coffee (Doležal et al., 2005); melted or grilled cheese prepared via domestic cooking (in which the most possible precursors are such abundant components as chloride ions and glycerol) (Crews et al., 2001); and meat such as salami, bacon and hamburgers, where glycerol does not seem to be the direct precursor (Baer et al., 2010). The survey of JECFA (2007) summarized the content of 3-MCPD in various foodstuffs consumed by adults and young children per body weight with regard to the estimates of exposure. Average dietary exposures ranged from 0.02 to 0.7 μg/ kg bw for a wide range of foods, including soy sauce and related foodstuffs in which the average concentration of 3-MCPD was the highest (8 mg/kg). The exposures estimated for young children, who constitute the highest percentage share among other consumer groups, ranged from 0.06 to 2.3 μg/ kg bw. Chung et al. (Chung et al., 2008) also reported a general overview on 3-MCPD concentration in foodstuffs marketed in Hong Kong which was based on the analysis of 318 samples of different food items; 101 types of food contained 3-MCPD at the concentration range between 3 and 66 μg/ kg. 3.2 Edible oils and fats This group of foodstuffs is presented separately although it is processed at high temperatures during both industrial processing (refining process including seed roasting or deodorization) and domestic cooking, e.g. frying. In most cases, oils and fats, including lipid fractions of some foodstuffs, e.g. goat s milk (Rahn et al., 2011), potato fries, doughnuts or salty crackers (Hamlet et al., 2011) contain fatty acid esters of 3-MCPD. The bound form of 3-MCPD was determined for the first time in this group of foods by Gardner et al. (1983) in rapeseed oil (3800 μg/kg) in the presence of hydrochloric acid. Further investigations of edible oils were carried out by Zelinkova et al. (Zelinková et al., 2006) after analyzing 45 samples of crude and refined oils. Oils containing free 3-MCPD at the concentration range between <3 2007="" 2008="" 2010="" 2462="" 24="" 3-mcpd="" 400="" agency="" all="" almost="" amounts="" an="" analyzed="" and="" bound="" by="" chemical="" control="" different="" erman="" esterified="" exhibited="" fat="" fats="" finding="" food="" found="" from="" g="" higher="" highest="" in="" industry.="" intensive="" investigation="" kg="" levels="" much="" of="" oil="" oils.="" oils="" olive="" over="" refined="" resulted="" samples="" sector="" significant="" stuttgart="" test="" the="" this="" to="" varied="" veterinary="" virgin="" were="" which="" years="">4000 μg/kg) were determined in palm oils, whereas frying fat and margarine contained relatively high concentrations of 3-MCPD esters. Large amounts of 3-MCPD esters (540 4840 μg/kg) were also determined in the fat fraction of coffee creamers, cream aerosols and bouillon cubes (Karsulinova et al., 2007). Foodstuffs prepared by frying in palm oil such as, potato fries and potato chips also contained significant amounts of 3- MCPD esters (Zelinková et al., 2009). The overview on bound 3-MCPD determined in fats, oils and lipid fractions was presented by Weisshaar (2011). Undoubtedly, this group of foodstuffs needs to be investigated further with regard to the precursors and formation mechanism of 3- MCPD because it contributes to the overall food consumption and, consequently, to the daily intake of 3-MCPD by humans in a significant way. 3.3 Infant foods and human breast milk This group encompasses foods meant for consumption by infants. It is presented separately because of the small body weight of the consumers, which contributes significantly to the risk A assessment in relation to dietary exposure. Human breast milk can be used as a toxicity indicator of various compounds with regard to human tissues and biological fluids. Velisek et al. (2008) analyzed 12 samples of human breast milk. None of the samples contained free 3-MCPD at the concentration higher than LOD (3 μg/kg), however, all samples contained significant levels of esterified 3-MCPD. The average concentration of 3-MCPD was 1014 μg/kg isolated fat, which corresponds to 35.5 μg/kg milk. For comparison, samples of human breast milk collected after 14 76 days after childbirth contained 930 μg/kg isolated fat, which corresponds to 12 μg/kg milk. These results indicate that at the onset of lactation lipids are secreted into the breast milk together with toxicants in women who have digested contaminated food. Zelinková et al. (2009) analyzed 14 samples of infant foods which had composition similar to that of human breast milk. None of the samples contained significant amounts of free 3-MCPD however high levels of bound 3-MCPD were detected in all of them. The concentration level of bound 3-MCPD was 62- 588 μg/kg isolated fat, which corresponds to <300-2060 above="" amounts="" and="" as="" be="" because="" body="" can="" case="" consume="" content="" daily="" described="" determined="" each="" easily="" exceeded="" fact="" fat="" food.="" foods.="" further.="" g="" goes="" have="" in="" infant="" infants="" intake="" investigated="" it="" kg="" mentioned="" milk.="" needs="" of="" only="" p="" previously="" proportional="" saying="" small="" that="" the="" this="" to="" tolerable="" topic="" weight="" were="" without="">
DOI
10.1080/10408398.2013.829414
https://www.nutraingredients.com/Article/2018/01/11/EFSA-increases-safe-levels-for-contaminant-3-MCPD?utm_source=newsletter_daily&utm_medium=email&utm_campaign=12-Jan-2018&c=dC5HnbRQjqmgaiK0my3i8e6nfk44q4Az&p2=
https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2016.4426
Processed palm oil should not be on your table only virgin red palm oil...
The formation routes of 3-MCPD can be divided into three groups. The first pathway is the acid hydrolysis (used in HVP production), which is the reaction of hydrochloric acid with residual vegetable oil. The second route is the heat processing, which is independent of the presence of acid-HVP. In this way, 3-MCPD is formed from lipids and sodium chloride, which can be present in the material naturally or added during the processing. The heat can affect food not only during industrial production but also during domestic cooking, such as baking or frying. The two pathways were described in detail by Baer et al. in 2010. The third and recently most investigated pathway is the release of free 3-MCPD from its bound (esterified) form. 3-MCPD can occur as a mixture of mono- and diesters, usually of palmitic, oleic or stearic fatty acids. Until now, the formation mechanism of 3-MCPD esters has not been fully understood. The earlier hypothesis, published in 1991 by Collier et al., proposed the mechanism based on triacylglycerol reaction in which a key step is the nucleophilic substitution of the acyl group by the chloride anion at positions activated by neighbouring ester groups that results in chloropropanediol diester. According to a more recent assumption, the formation of 3- MCPD esters progresses through the cyclic acyloxonium ion as an intermediate, which derives from the elimination of hydroxyl groups from mono- and diacylglycerols (MAG and DAG) (Bakhiya et al., 2011). Rahn and Yaylayan (2011) provided further evidence for this hypothesis by monitoring this intermediate ion formation in palmitin systems using IR spectroscopy and isotope labelling technique. Both above assumptions take into consideration the presence of chloride ions, which seem to have the strong influence on 3-MCPD esters formation (Shimizu et al., 2013). 3-MCPD can be released from its esterified form via lipase catalysed hydrolysis in human gastrointestinal tract during digestion. In 2004, Robert et al. simulated the formation of chloropropanols using a model system consisting of mammalian, plant and fungal lipases, vegetable oil or fat, water and sodium chloride. Three years later, Seefelder et al. (2008) used a simple intestinal model to quantify the level of 3-MCPD release from the ester form. Monoesters and diesters were incubated with pancreatic lipase and porcine bile extract. The monoesters were almost completely hydrolysed after 1 min. The 3-MCPD release from diesters was slower, reaching 45% after 1 min, 65% after 2 min and almost 100% after approximately 1 hour. Also, the authors proposed that 3-MCPD esters have the same metabolic pathway as the one known for acylglycerols during human digestion, where pancreatic lipases release glycerol only from 1- and 3-monoacylglycerols. Triacylglycerols are hydrolysed to diacylglycerols, and incorporated in lipoproteins. However, this hypothesis appeared to be speculative, mainly because their studies have already proven a partial release of free 3-MCPD from diester form. Moreover, lipoproteins can be bioavailable through the lymphatic system (Chon et al., 2007). According to recent investigations on lipolytic enzymes, there are three enzymes that can completely hydrolyze triacylglycerols (Lass et al., 2011). Thus it can be assumed that these enzymes may release free 3-MCPD from diester form (Abraham et al., 2013). Until now, no in vivo research has been delivered to verify the aforementioned postulates, therefore, the assumption of 100% hydrolysis of 3-MCPD esters should be taken into account while assessing the human health risk. Besides the formation pathways of 3-MCPD described above, other routes were also proposed. Myszkowski and Zielinski (1965) assumed that monochloropropanediol can form from allyl alcohol, chlorine and water. Collier et al. (1991) reported the possibility of 3-MCPD formation from carbohydrates (pentosan and pectin) and hydrochloric acid. Cerbulis et al. (1984) demonstrated that small but significant amounts of 3-MCPD diesters were determined in raw goat s milk, so the authors assumed these compounds are naturally occurring in food. However, these postulates have not been proved in later studies."
"3. Occurrence in food
During the past decade, the development of new analytical methods as well as renewed interest in chloropropanols as dangerous food toxicants caused that 3-MCPD was determined in a number of different foodstuffs. The investigated foods can be divided into three main groups, i.e. thermally-treated foods, edible oils and fats, and infant and baby foods (including human breast milk). Below, each groups has been described in detail in the consecutive paragraphs. 3.1 Thermally-treated foods Crews et al. were the first researchers who examined a large number of foodstuffs marketed in UK (2001). The main food group contaminated by 3-MCPD were cereal derived products; the highest concentration of monochloropropanediol was determined in toasted bread (0.088 mg/kg) and cream crackers (0.087 mg/kg). The same group of foodstuffs was analyzed by BreitlingUtzmann et al. (2003). The highest concentration of 3-MCPD was also found in toasts (over 0.500 mg/kg in a well-toasted bread) and breadcrumbs (over 0.400 mg/kg). It seems that the exposure to high temperatures is a key step in 3-MCPD formation in cereal-derived foods. Breitling-Utzmann et al. (2005) also tested the influence of bread ingredients on 3-MCPD formation. It appeared that the addition of fat and baking agent (consisting of sugar, flour, soy flour, calcium sulfate, mono- and diacylglycerols of edible fatty acids as emulsifiers) may influence the concentration of 3-MCPD in the final product, emulsifiers and sugar having the strongest effect. Regarding the precursors of 3-MCPD, Hamlet et al. used model dough systems to estimate the production of chloropropanols in leavened (Hamlet et al., 2004) and unleavened (Hamlet et al., 2004) doughs. In both cases, glycerol or compounds based on a glycerol skeleton such as, monoacylglycerols and phosphatidylglycerols were the main 3-MCPD precursors. Another foodstuffs in which heat treatment seems to have triggered 3-MCPD formation are malt-derived products such as, food-grade malted grains, malt flours and malt extracts (colour and flavour agents). The original components of these products can promote the formation of 3-MCPD, so there is no need for adding fat, acid or chloride. However, significant amounts of 3-MCPD in this type of foods were detected only in the dark brewing malt (0.247 mg/kg) [22]. The amount of free 3-MCPD present in beer is relatively low (10 μg/l) (IARC, 2000) but it seems that it may be bound to other beer components such as, acids, aldehydes and alcohol, which can significantly exceed the free form content (Divinová et al., 2007). Smoked foods also contain significant amounts of 3-MCPD (over 0.02 mg/kg). Kuntzer and Weisshaar (2006) analyzed the influence of food smoking on the formation of 3-MCPD in fermented sausages and ham. The smoking process appeared to be the main source of 3-MCPD, especially with regard to the type of wood and the duration of processing (Kuntzer and Weisshaar, 2006; FAO, WHO, 2007). In contrast to cereal- and malt-derived products, lipids are not considered the precursors of 3-MCPD in smoked foods, and the formation mechanism from 3-hydroxyacetone during cracking of cellulose was proposed instead. Apart from that, Reece (2005) suggested that the concentration of salt in the brine used in the smoking process may also be the influential factor in the formation of 3-MCPD. 3-MCPD was also determined in such heat-processed foodstuffs as coffee, particularly roasted coffee after prolonged roasting process, and instant coffee (Doležal et al., 2005); melted or grilled cheese prepared via domestic cooking (in which the most possible precursors are such abundant components as chloride ions and glycerol) (Crews et al., 2001); and meat such as salami, bacon and hamburgers, where glycerol does not seem to be the direct precursor (Baer et al., 2010). The survey of JECFA (2007) summarized the content of 3-MCPD in various foodstuffs consumed by adults and young children per body weight with regard to the estimates of exposure. Average dietary exposures ranged from 0.02 to 0.7 μg/ kg bw for a wide range of foods, including soy sauce and related foodstuffs in which the average concentration of 3-MCPD was the highest (8 mg/kg). The exposures estimated for young children, who constitute the highest percentage share among other consumer groups, ranged from 0.06 to 2.3 μg/ kg bw. Chung et al. (Chung et al., 2008) also reported a general overview on 3-MCPD concentration in foodstuffs marketed in Hong Kong which was based on the analysis of 318 samples of different food items; 101 types of food contained 3-MCPD at the concentration range between 3 and 66 μg/ kg. 3.2 Edible oils and fats This group of foodstuffs is presented separately although it is processed at high temperatures during both industrial processing (refining process including seed roasting or deodorization) and domestic cooking, e.g. frying. In most cases, oils and fats, including lipid fractions of some foodstuffs, e.g. goat s milk (Rahn et al., 2011), potato fries, doughnuts or salty crackers (Hamlet et al., 2011) contain fatty acid esters of 3-MCPD. The bound form of 3-MCPD was determined for the first time in this group of foods by Gardner et al. (1983) in rapeseed oil (3800 μg/kg) in the presence of hydrochloric acid. Further investigations of edible oils were carried out by Zelinkova et al. (Zelinková et al., 2006) after analyzing 45 samples of crude and refined oils. Oils containing free 3-MCPD at the concentration range between <3 2007="" 2008="" 2010="" 2462="" 24="" 3-mcpd="" 400="" agency="" all="" almost="" amounts="" an="" analyzed="" and="" bound="" by="" chemical="" control="" different="" erman="" esterified="" exhibited="" fat="" fats="" finding="" food="" found="" from="" g="" higher="" highest="" in="" industry.="" intensive="" investigation="" kg="" levels="" much="" of="" oil="" oils.="" oils="" olive="" over="" refined="" resulted="" samples="" sector="" significant="" stuttgart="" test="" the="" this="" to="" varied="" veterinary="" virgin="" were="" which="" years="">4000 μg/kg) were determined in palm oils, whereas frying fat and margarine contained relatively high concentrations of 3-MCPD esters. Large amounts of 3-MCPD esters (540 4840 μg/kg) were also determined in the fat fraction of coffee creamers, cream aerosols and bouillon cubes (Karsulinova et al., 2007). Foodstuffs prepared by frying in palm oil such as, potato fries and potato chips also contained significant amounts of 3- MCPD esters (Zelinková et al., 2009). The overview on bound 3-MCPD determined in fats, oils and lipid fractions was presented by Weisshaar (2011). Undoubtedly, this group of foodstuffs needs to be investigated further with regard to the precursors and formation mechanism of 3- MCPD because it contributes to the overall food consumption and, consequently, to the daily intake of 3-MCPD by humans in a significant way. 3.3 Infant foods and human breast milk This group encompasses foods meant for consumption by infants. It is presented separately because of the small body weight of the consumers, which contributes significantly to the risk A assessment in relation to dietary exposure. Human breast milk can be used as a toxicity indicator of various compounds with regard to human tissues and biological fluids. Velisek et al. (2008) analyzed 12 samples of human breast milk. None of the samples contained free 3-MCPD at the concentration higher than LOD (3 μg/kg), however, all samples contained significant levels of esterified 3-MCPD. The average concentration of 3-MCPD was 1014 μg/kg isolated fat, which corresponds to 35.5 μg/kg milk. For comparison, samples of human breast milk collected after 14 76 days after childbirth contained 930 μg/kg isolated fat, which corresponds to 12 μg/kg milk. These results indicate that at the onset of lactation lipids are secreted into the breast milk together with toxicants in women who have digested contaminated food. Zelinková et al. (2009) analyzed 14 samples of infant foods which had composition similar to that of human breast milk. None of the samples contained significant amounts of free 3-MCPD however high levels of bound 3-MCPD were detected in all of them. The concentration level of bound 3-MCPD was 62- 588 μg/kg isolated fat, which corresponds to <300-2060 above="" amounts="" and="" as="" be="" because="" body="" can="" case="" consume="" content="" daily="" described="" determined="" each="" easily="" exceeded="" fact="" fat="" food.="" foods.="" further.="" g="" goes="" have="" in="" infant="" infants="" intake="" investigated="" it="" kg="" mentioned="" milk.="" needs="" of="" only="" p="" previously="" proportional="" saying="" small="" that="" the="" this="" to="" tolerable="" topic="" weight="" were="" without="">
DOI
10.1080/10408398.2013.829414
https://www.nutraingredients.com/Article/2018/01/11/EFSA-increases-safe-levels-for-contaminant-3-MCPD?utm_source=newsletter_daily&utm_medium=email&utm_campaign=12-Jan-2018&c=dC5HnbRQjqmgaiK0my3i8e6nfk44q4Az&p2=
https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2016.4426
Processed palm oil should not be on your table only virgin red palm oil...
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