
Subsections
- No-effect-level
- Additives in the European Food Law and the Codex Alimentarius
- Codex Alimentarius
- EU food additives regulations
- International Numbering System for Ingredients INS- Number
- E-Numbers
- Colorants
- E100 Turmeric
- E101 Lactoflavin
- E101a Phosphate-5-riboflavin
- Azo dyes
- Amaranthus betacyanin pigments as natural food colour
- Amarant as feed
- Invasive weeds
- E102 Tartrazin:
- POP colour as alternative to tartrazine
- Synthetic organic colours not azo dyes
- E104 Chinolin yellow
- E129 Allura red AC
- E154 brown FK
- Colorants found in nature:
- Chlorophyll in ripe fruits breakdown in NCCs which are strong
antioxidants
- Curcumin:
- Red beet Juice:
- E160a beta-Carotene,alfa Carotene,gamma-Carotene
- E160b Bixin, Norbixin,annatto,orleana
- E160c Capsanthin,Capsorubin
- E160d Lycopene
- E160e beta-Apo-8-carotenal
- E160f beta-Apo-8-ethyl ester of carotene acid
- E150a sugar colour
- E150b sulfite-sugar colour
- E150c ammonium sugar colour
- E150d ammonium sulfite-sugar colour
- E161 Xanthophyll
- E161a
Flavoxanthin
- E161b Lutein
- E161c
Kryptoxanthin
- E161d Rubixanthin
- E161e Violaxanthin
- Rhodoxanthin
- E161g Canthaxanthin
- E162 Red beet colour, betanin
- E163 Anthocyanin
- E170 calcium carbonate
- E171 Titanium dioxide
- E172 Iron oxides and hydroxides
- E579 Iron gluconate
- E17Aluminium
- E174 Silver
- E175 Gold
- E180 Rubin BK pigment
- E141 Copper chlorophyll complex
- E142 Brilliant green acid
- E239 Hexamethylene tetramine
- Natamycin
- Antioxidants
- Chemical preservatives
- E200 Sorbic acid
- E202 Potassium sorbate
- E203 Calcium sorbate
- E210 Benzoic acid
- E211 Sodium benzoate
- E212 Potassium benzoate
- E213 Calcium benzoate
- E214 Ethyl-p-hydroxi benzoate
- E215 PHB-ethyl ester sodium salt
- PHB-propyl ester
- E217 PHB-propyl ester
- E218 PHB- methyl ester
- E219 PHB-methyl ester,sodium salt
- E220 Sulphur dioxide
- E221 Sodium sulphide
- E222 Sodium hydrogen sulphite
- E223 Sodium metabisulfite
- E224 Potassium metabisulfite
- E226 Calcium sulphide
- E227 Calcium bisulphide
- E228 potassium bisulphide
- E230 Biphenyl
- E231 Ortophenylphenol
- E232 Sodium ortophenyphenol
- E233 Thiabendazol
- E234 Nisin
- E235 Natamycin
- E236 Formic acid
- E237 Sodium
formate
- E238 Calcium formate
- E242 Dimethyl
carbonate
- E249 Potassium nitrite
- E250 Sodium nitrite
- E251 Sodium nitrate
- E252 Potassium
nitrate
- E
270 Lactic acid
- E280 Propionic acid
- E281 Sodium propionate
- E282 Calcium propionate
- E283 Potassium propionate
- E284 Boric acid
- E285 Sodium tetraborate (borax)
- New preservative for meat products, non-alcoholic beverages energy
and sport drinks
- Safety concerns:
- Acidulants, acidity regulators
- E260 Acetic acid
- E261Potassium acetate
- E262 Sodium acetate
- E263 Calcium acetate
- Other ingredients:
- E325 Sodium lactate
- E326 Potassium lactate
- E327 Calcium lactate
- E290 Carbon dioxide
- E296 Malic acid
- E331 Sodium citrate i) Monosodium citrate, ii) disodium citrate,
iii) trisodium citrate
- E335 Sodium tartrate i) monosodium tartrate ii)
disodium tartrate
- E350 Sodium malate
- E351 Calcium malate
- E297Fumaric acid
- E300 Ascorbic acid
- E301 Sodium ascorbate
- E302 Calcium ascorbate
- E304 Fatty acid
esters from ascorbic acid, i) ascorbyl palmitate, II)ascorbyl stearate
- E306 Heavy tocopherol bearing
extracts
- E307 Alpha-tocopherol
- E308
Gama-tocopherol
- E309 Delta tocopherol
- E310 Propyl gallate
- E311 Octyl gallate
- E312 Dodecyl gallate
- E315 Isoascorbic
acid
- E316
Sodium isoascorbate
- E320 Butylhydroxyanisole (BHA)
- E321 Butylhydroxytoluene (BHT)
- Modified starch
- Emulsifier
- E322 Lecithin
- E442 Ammonium phosphatides
- E470a Sodium,potassium and calcium salts of fatty acids
- 470b Magnesium salt of edible fatty acids
- E471 Mono and diglycerides of fatty acids esterified with
organic acids
- Citric acid ester of mono- and di-glycerides replacing lecithin
in chocolate applications.
- Bulk sweeteners and intersity sweeteners
- Lack of association between saccharin, aspartame and other
sweeteners and the risk of several common neoplasms.
- Low-calorie sweeteners and obesity
- Smoke flavourings:
- Measuring the antioxidant activity of phytochemicals
- Safety and bioavailability of Vanadium, EFSA and FSA
assessment
- Enzymes
- Ezyme Commission number (EC number)
- UniProt
- SodiumBenzoate and certain colours increases hyperactivity in
children
- Sugar, anti-social behaviour and ADHD
- Sodium benzoate as source of benzene in soft drinks
- Benzene in foods without added benzoates
- Natural cure for meats
- Nitrites and nitrates in cured meat fruit and vegetable may
protect against heart attack
[58]
One of the most effective argument to play down the danger of cancer is to
classify the presence of a contaminant as not relevant because of the
no-effect-level.
According to that theory the reduction of the amount of
contaminants leads to a point where a carcinogenic activity only develops
after 100 to 150 years,that is after dying from other causes.
Unfortunately cancer comes up sooner, for the time being 25% of all human
beings die of cancer.
More as 50% of all cases are caused by ecological factors.
The theory of no-effect-level can only be applied on persons who wish not to
reproduce himself.
The genes who suffered mutations because of ecological factors should not be
passed on to following generations in order not to pass on the genetic
predisposition to cancer.
Carcinogenic activities are often analysed considering an isolated cause or a
single agent.
Today there are lots of chemicals with carcinogenic activity boosting the effects in a synergic way. Examples of
such synergic activities are:
Nitrosamines with PCB ,benzpyrene BHT and traces of mercury.
The international institute of cancer in Lyon, France has proved that damages on
the structure of chromosomes caused by toxic substances are passed on from
generation to generation.
The institute gave small dose of nitrosamines to pregnant mice. Typical tumours
were not only found on the mother but although on following
generations who had no contact with nitrosamines.
According to professor Schmähl,researcher on cancer in Heidelberg,Germany,
there is no dose , even being very small , that is free of danger to cause
cancer because of the effect of synergic addition of the effects.
The fact that a mouse can live with a small dose of carcinogen agents does not
prove anything.
The mouse does not smoke,it does not breathe sulphur dioxide,it does not take
medicine, it does not eat ham, smoked salmon or hamburgers. Therefore we have to
observe very critically all additives and all ingredients of our food.
The European food law is more stringent as the Codex Alimentarius. If a food or
any agricultural product meets European rules it is also fit for Codex. The Codex
used the principles of the EU food law. To instance, the E-Numbers of additives
from the European numbering system are being used by the Codex deleting the E in
front of the number.
The Regulation of food
additives in Europe changed. 1333/2008 will be in force. However, the lists of
additives of older directives (94/35/EC, 94/36/EC and 95/2/EC) remain valid
because new lists are not ready yet.
The article of the European
Commission on Food Additives and flavourings gives a summery of European food
law.
http://ec.europa.eu/food/fs/sfp/flav_index_en.html
The Regulation brings
together in a single legislative act all types of food additives including
colours and sweeteners.
http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2008:354:0016:0033:EN:PDF
Food enzymes are covered by Regulation (EC) No 1332/2008.
Whilst these lists cited as "Annexes" in
133/2008 are being drawn up, the Annexes of Directives 94/35/EC, 94/36/EC and
95/2/EC remain in force.
The "Codex General Standard for Food
Additives" (GSFA, Codex STAN 192-1995) sets forth the conditions under which
permitted food additives may be used in all foods, whether or not they have
previously been standardized by Codex.
http://www.codexalimentarius.net/gsfaonline/CXS_192e.pdf
http://www.codexalimentarius.net/gsfaonline/index.html?lang=en
http://www.codexalimentarius.net/gsfaonline/additives/index.html
The Codex Alimentarius Commission adopts standards, codes of
practices and other related texts that are prepared by specialised Codex
Committees and Ad hoc Task Forces. The 27 Member States of the European Union
are all members of the Codex Alimentarius Commission. In 2003, the European
Community (now the EU) also became a full member of the Codex Alimentarius
Commission and shares the competence with its Member States on the basis of
the level of harmonisation of the relevant legislation. Since the entry into
force of the Treaty of Lisbon on 1 December 2009 the European Union replaced
the European Community. The EU and its Member States elaborate EU position
papers on issues discussed in the Codex Alimentarius Commission, the various
Codex Committees and Task Forces.
http://ec.europa.eu/food/international/organisations/codex_en.htm
http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2003:309:0014:0021:EN:PDF
http://ec.europa.eu/food/fs/ifsi/eupositions/ccfa/index_en.html
All directives are available at:
http://eur-lex.europa.eu/RECH_naturel.do
Year and Number of the Directive: Old directives cite only the two
last digits of the year. New directives give four digits such as: 91/414 =
year 1991 Nr.414 and 2009/128 = year 2009 Nr.128
To search by one word: Just type a word, such as "pesticides"
http://eur-lex.europa.eu/RECH_mot.do
The Codex Alimentarius Commission was created in 1963 by FAO and WHO to develop
food standards, guidelines and related texts such as codes of practice under the
Joint FAO/WHO Food Standards Programme. The main purposes of this Programme are
protecting health of the consumers and ensuring fair trade practices in the food
trade, and promoting coordination of all food standards work undertaken by
international governmental and non-governmental organizations.
[2549]
- Current Standards: Here all Standards are available.
http://www.codexalimentarius.net/web/standard_list.do?lang=en
- Search system: Very efficient search engine of Codex
http://www.codexalimentarius.net/search/advancedsearch.do
- Codex database for limits of pesticides in foods
http://www.codexalimentarius.net/mrls/pestdes/jsp/pest_q-e.jsp
- Codex database for veterinary drugs residues in foods
http://www.codexalimentarius.net/mrls/vetdrugs/jsp/vetd_q-e.jsp
- Codex Food additives
http://www.codexalimentarius.net/gsfaonline/CXS_192e.pdf
http://www.codexalimentarius.net/gsfaonline/index.html?lang=en
Intensive farming bears the risk of overuse of antibiotics according the
National Consumer Council March 11 1998 in London.
The council blames in the words of his Director Ruth Evans the European Unions
common agricultural policy encouraging intensive farming.
Ruth Evans says:" The Common Agricultural policy is not just wasteful and
costly to consumers,it also encourages farming practices which raise serious
public health concerns.
Overintensive farming methods led to the BSE/CJD crisis.So long as we reward
high output rather than high quality of food further risks are likely"
The Council enumerates in his report the following areas of concern:
It is being used to treat , prevent and reduce disease and as a growth promoter
in animals. The residues can be toxic and cause hypersensitivity to
antibiotics in some humans.
Uncontrolled use of antibiotics increase the resistance of certain bacteria to
these therapeutics. Salmonella and Escherichia coli are developing the capacity
to resist the medicine which treats diseases on humans and on animals.
The introduction of selected properties of an organism into another bears
unknown risks which cannot be estimated by risk analysis.
Hormones are used to promote animal growth.
This may lead to the development of sexual characteristics and certain
cancers.
In spite of being forbidden in the European Community many hormones are illegal
sold and used.
Nitrates are used to enrich the soil and promote growth to vegetable crops.
High use of nitrates are linked to the cyanosis called "blue baby Syndrome"
and to stomach cancer.
The maximum nitrate levels in vegetables and water which have been established
are sometimes exceeded.
Pesticides are used to protect crops and increase productivity.Exposure to
certain pesticides may weaken the immune system and reduce resistance to
cancer.
It has been noted that some pesticides are deposited in higher rates in the
interior of fruits and vegetables as in the skin. Peeling and washing has
therefore no effect in reducing the content of pesticides in food. According to
Mrs. Evans the EU should promote the reduction of the use of
antibiotics,pesticides and nitrates and strengthen the regulatory framework of
the industry, which has proved to be inadequate.
In 1988 began in United Kingdom a monitoring of pesticide residues in food.
Since then there were no detectable levels of residues found in around 70% of
examined samples.Only 1% exceeded the maximum residue levels.
Efforts however should be undertaken to achieve further reduction , because
there is no-effect-level.
The government of United Kingdom has made a statement that people who eat
average 90 grams of cooked red meat per day, or around 8 to 10 portions a week
need no reduction of red meat consumption.This includes beef, lamb and pork.
A lower consumption of red meat would probably reduce the risk of colon
rectal cancer.
However eating to little meat could cause iron deficiency.
In order to correct wrong behaviour related to food it is recommended to:
- Maintain a healthy body weight.
- Increase the amount and variety of fruits, vegetables and fibers.
- Be cautious about taking high dose of purified vitamin and mineral
supplements.They are not fully free of risks.
[2550]
Gastrointestinal cancer and methemoglobinemia risk in infants may be
increased by nitrates and nitrites in food. Hord, Tang an Bryan 2009, however,
claim that the risks and health benefits associated with consumption of
dietary nitrate and nitrite from fruits and leafy green vegetables should be
re-evaluated. The authors stress that nitrates and nitrites from fruits and
vegetables have a protective effect against coronary heart disease and
ischemic stroke risk.
80 per cent of dietary nitrates are derived from vegetable consumption. The
Dietary Approaches to Stop Hypertension (DASH) studies, using diets low in fat
dairy products and 8-10 servings, lowered blood pressure to an extent similar
to that achieved with medication. This was attributed to the high calcium,
potassium and low sodium concentrations.
Hord and colleagues, however, say that the nitrate contained in some fruit and
vegetables may be associated with the blood pressure reduction. Mammalian enzymes
were found to have nitrate reductase activity as well bacterial nitrate
reductases in mouth and gastrointestinal tract reduce nitrate to nitrite. The
authors found a variability on nitrate concentration in vegetables, fruit, juice
and fresh and processed meats, varying between 174 to 1222 mg in patterns of the
DASH diets.
Hord and colleagues say that infants under six months exposed to excess
nitrite may suffer from methhemoglobinemia and that infants fed home-prepared
food are probably my be harmed by high nitrates in foods. Cured and processed
meats with added nitrates have also a detrimental effect on health, but there
are little evidences of cancer risk associated with cured meat.
The authors stress that any health risk from nitrates in fruits and vegetables
are outweighed by their benefits, such as reduction of blood pressure. They
call to reconsider the acceptable daily intake (ADI) levels for nitrites
and nitrates and suggest to consider nitrates as nutrients.
[2541]
The regulation 1331/2008 [2542] lays down a common procedure for the
assessment and authorisation of food additives, food enzymes, food
flavourings. It is therefore important for the procedure of approval of food
additives, but not for the food industry and the consumer interested on
positive lists of additives. These are given in 1332/2008 [2543],
1333/2008 [2544] and 1334/2008 [2545] and the
annexes Directives 94/35/EC [], 94/36/EC [2548]and 95/2/EC
[2546]. Feed additives 429/ 2008 should also be considered by animal
breeders.
In accordance with article
30 of Regulation (EC) No 1333/2008, additives that are permitted in food under
Directives 94/35/EC, 94/36/EC and 95/2/EC and their conditions of use will be
entered the Community list of food additives in Annex II to the regulation. To
that end the compliance with their general and specific conditions of use must
first be reviewed. This review should be completed by January 2011.
The use of food additives already permitted in Directives 94/35/EC, 94/36/EC
and 95/2/EC will continue to be permitted until the review has been finalised
and the additives have been transferred in the Community list of food
additives in the Annex II of the new regulation. In the mean time, when
necessary, until the establishment of the Community list of food additives,
the annexes to the current directives can be amended based on a comitology procedure.
All colours which are allowed to be added to foods are included in positive
lists. Substances therein have been tested for their safety and meet specific
purity criteria.
The Colour Directive 94/36/EC gives
the actual permitted food colours. The safety of food colours and other food
additives is evaluated by the Scientific Committee on Food (SCF), an advisory
expert committee of the European Commission, located in Brussels.
The EU Commission Directive 95/45/EC of 26 July 1995 lays down specific purity
criteria concerning colours for use in foodstuffs with amendment Directives
1999/75/EC, 2001/50/EC and 2004/47/EC.
The European Commission regulations are binding to all member countries of the
EU, and have to be implemented into their national laws. Non-EU member states
food additives are regulated by their national authorities.
The WHO and the FAO members of the UN
have an advisory committee, the Joint WHO/FAO Expert Committee on Food Additives
(JECFA), The European SCF and JEFF A's toxicological evaluation, an ADI
(Acceptable Daily Intake) value, expressed in mg/kg body weight per day, is
allocated to the additive, or its use is not recommended.
The E numbers for colour additives range from E100 (curcumin) to E180
(lithorubine BK). Since a pigment derived from extraction may be differently
specified as the same pigment derived from chemical synthesis, it may be
characterised by a differentiated E number: beta- carotene extracts e.g. are
listed under E160ai (mixed carotenes), and synthetic beta-carotene under E
160aii (beta-carotene).
Food additive colours are defined in this regulation as: [2548]
"Substances which add or restore colour in a food, and include natural sources
which are normally not consumed as a foodstuff as such and not normally used as
a characteristic ingredient in food. Thereby, the Colour Directive excludes
colouring foodstuffs and food ingredients, which may be used in the preparation
of a final food, from the food additive regulation, such as tomato juice
(lycopene) or red beet juice (betanine) which is added to some foods, colouring
them.
According to the Colour Directive, the legal situation of such pigments
changes, when they are selectively extracted -relative to the nutritive or
aromatic constituents -from the original source material, and (in line with
Frame Directive 89/107 /EEC) intentionally added to foods for the purpose of
their colouration. [2551]
The global trade requires
harmonisation of food regulations on a world-wide basis in order to abolish
barriers of trade and to ensure that the economical and nutritional demands of
all nations are considered.
JECFA develops international standards for food additives considering
toxicology and elaborating purity criteria. These standards are the basis of
the standard for food colours of the General Standard for Food Additives from
the Codex Alimentarius. It is not legally binding, but influences food colour
regulations all over the world.
| Colour |
EC No |
Natural
occurrence |
Pigment |
| Re/blue |
E163 |
Black grapes, blackcurrants, cherries |
Anthocyanins |
| |
|
elderberries, red cabbage, strawberries |
|
| Pink |
E162 |
Beetroot |
Betanin |
| Red |
E120 |
Cochineal |
Carminik acid |
| Green |
E140 |
Alfafa grass, nettles, parley, spinach |
Chlorophylls |
| |
E141 |
|
Chlorophyllins |
| Carotinoids: |
|
|
|
| |
E160a (i) |
Annatto |
Mixed carotenes |
| |
E160a (ii) |
Carrots |
Beta-carotene |
| Yellow |
E160b |
Oranges |
Bixin, norbixin |
| Orange |
E160c |
Prawns |
Capsanthin, Capsorubin |
| Red |
E160d |
Red pepper |
Lycopene |
| |
E160e |
Tomatoes |
Apocarotenal |
| |
E160f |
Palm fruit |
Apocarotenal (ethyl ester) |
| |
E160b |
|
Lutein |
| |
E161g |
|
Canthaxanthin |
| Yellow |
E100 |
Turmeric |
Curcumin |
| Yellow |
E101 |
Eggs, milk, yeast |
|
| Black |
E153 |
Carbonised vegetable material |
Carbon black |
| Brown |
E150a-d |
Melanoidins (caramel) |
Melanoidins |
[2553]
Looking for alternatives to artificial food colours such as sunset yellow,
tartrazine and quinoline yellow Bermejo Ruperto, J. M. Alvarez-Pez and
colleagues studied the marine algae Porphyridium cruentum and its protein
B-ficoeritrina.
Phycoerythrin is a pigment of red algae and cyanobacteria. B-phycoerythrin and
R-phycocyanin in native state, were obtained by the authors using an
inexpensive and simple process from the red alga Porphyridium cruentum.
[2554] A new form of coloured coating is being suggested by D. Tyler McQuade and
colleagues. The coating is based on coloured calcium alginate hydrogels being
useful in food such as candies and dietary supplements, cosmetic, medicinal,
and textile uses and to wherever nontoxic, easily removable coloured coating is
desired.
Tests were made on artificial turf spraying aqueous solutions of gelling
agents: One layer of calcium chloride solution was followed by spraying
sodium alginate solution with one per cent red food colour. The sprayed
solutions then combined into a coloured thin film.
Gels with different physical properties were obtained varying the
concentrations of the gelling agent. Low concentration of 0.1 moles/l of
calcium chloride resulted in a brittle, easily removable film. High
concentration of 2.0 moles/l of gelling agent resulted in a film which adhered
well and was difficult to remove.
International Numbering System for Ingredients INS- Number
[2555]
Labelling often uses numbers instead of the common names of the
ingredients.These numbers differ from country to country. For international
use the Codex Alimentarius proposes an international numbering system which
largely uses the same numbers of the European Commission but without the E
[57]
As the European Market increases in importance throughout the world the
E-numbers of the allowed ingredients are getting important and are used by
the Codex Alimentarius for the International Numbering System INS. Therefore
they are listed below with a short comment.:
| E-number |
Ingredient |
| E100 |
turmeric |
| E101 |
lactoflavin |
| E101a |
riboflavin-5-phosphate |
| E102 |
tartrazin |
| E104 |
Chinolin yellow |
| E110 |
yellow orange S |
Colorants
Are used to improve the colour and the aspect of food being applied intern or
extern on the outer layer to promote appetite, selling.
In sweet products it
may fake a high content of fruit,in mayonnaise it suggests a high content of
egg yolk.
Colours are used in candies, soft drinks, puddings, ice creams,
liquors,margarine, cheese and seafood.
It is the natural colour of the root of turmeric (Curcuma longa).It is the
traditional ingredient of curry powder.
It may be obtained by synthesis. Its
colour is yellow.
E101 Lactoflavin
Azo dyes
Azo dyes are members of a chemical group comprising the following colours:
E102 tartrazin, E110 yellow-orange S, E122 Azorubine, E123 amaranth, E124 cochineal red red A, E151 brilliant black BN, E180 Lithol rubine BK, E128 red 2G, E155
brown HT.
Carcinogenic activity of azo colours were found in rats were due to impurities
of the colours used for the test and could not be confirmed further on. Calcium
deposits in the renal pelvis was found but it could not be put in relation to
the dosage of the colours.
[2518]
Harold Corke and his co-workers from the University of Hong Kong report that
addition of betacyanin pigments from Amaranthus tricolour, led to pink-red
noodles with good colour stability, without affecting the cooking and textural
properties of cooked noodles. It also improved the protein content of the
noodles. Amaranth is an approved natural colorant in China, at levels of 0.1 and
0.5 per cent. Natural red pigments in use are anthocyanins, betalains, and
carotenoids sourced from berries and grapes, red beetroot, and red fruit,
vegetables and flowers, respectively. Natural red colours are betacyanins, and
betalains which are stable in low acid foods. The natural amaranth should not be
confused with a synthetic dye that has been named "amaranth" for its similarity
in color to the natural amaranth pigments known as betalains. This synthetic dye
is also known as Red No. 2 in North America and E123 in the European Union. The
Regulation 94/36 EC allows amarath only in bitter soda, aperitiv vines, spirit
drinks with less than 15% alcohol/volume and fish roe to be coloured with
amaranth E123. [2548]
[2519]
Alfaro and colleagues 2008 report that the amaranth plant could be a useful
resource for animal feeding. Dehydrated amaranth leaves and stalks in levels up
to 60%, were used to replace equal amounts of alfalfa leaf meal. The authors
found that amaranth leaf meal contained 17.8% protein and 12.4% crude fiber as
compared with the alfalfa leaf meal which contained 22.0% protein and 23.3%
crude fiber. The authors reported that amaranth leaf meal can efficiently
replace alfalfa leaf meal up to 15% of the total weight of the diet, whereas
growth retardation and interstitial nephrosis and edema, were observed at a 60%.
The authors stress that steam treatment improves the nutritive quality of the
amaranth meal.
[2520]
The following 9 species of Amaranthus are considered invasive and noxious weeds
in the U.S and Canada: A. albus, A. blitoides, A. hybridus, A. palmeri, A.
powellii, A. retroflexus, A. spinosus, A. tuberculatus, and A. viridis. A new
strain of the Palmer amaranth has appeared which is Glyphosate-resistant and so
cannot be killed by the widely used Roundup herbicide. Also, this plant can
survive in tough conditions. This could be of particular concern to cotton
farmers using Roundup Ready cotton. The species Amaranthus palmeri (Palmer
amaranth) causes the greatest reduction in soybean yields. Palmer amaranth is
among the "top five most troublesome weeds" in the Southeast and has already
evolved resistances to dinitroanilines and acetolactate synthase inhibitors
It is a synthetic substance highly allergenic.His use is restricted and even
forbidden in many European countries, such as Norway, Austria and UK. His
colour is yellow.
Synthetic colours such as tartrazin were found in some tests to cause behaviour
disturbance in overactive children. Success of therapy with colours free diet
were cited. High number of other tests could not confirm these results making
it controversial. Natural food such as haddock, strawberries, tomatoes, celery
and honey have higher allergy potentials as tartrazin. That is why tartrazin
is still allowed. [1288].
[1290]
The Institute for Agronomy Research (INRA) studies a by-product of the cider
industry as a natural alternative to tartrazine. The new colour is obtained
from apples and is called POP (phloridzine oxidation product)
Cider apples are rich in polyphenols forming colours as well as for the bitter
and astringent flavours of ciders.
Phloridzine is a polyphenol which during the production of apple juice and
cider is oxidised by polyphenoloxidase enzyme resulting in the yellow POP
colour which has antioxidant properties.
POP remains stable and resistant to the majority of food production processes.
It is yellow at acidity less than pH 5 and orange at pH 6. It does not stain
plastic packaging, unlike hydrophobic carotenoid pigments.
It is a group with different
chemical composition.
E131 patent blue V, E133
brilliant blue FCF, E
142 green S are members of the triarylmethan
group. All other colours have different composition and cannot be grouped
under a chemical terms:
E104 Chinolin yellow, E132 indigotin I E127 erythrosine, Erythrosine
bears iodine in its structure. This iodine is liberated in the body and acts
upon the thyroid gland which causes thyroid tumours on rats but not in other
animals. That is why some authors would like to see the allowance of this
colours withdrawn.
Synthetic substance harmless to rats and mice and dogs.The physiology in
humans is unknown.It is forbidden in food in USA.It has yellow colour.
E129 Allura red AC
E154 brown FK
Colorants found in nature:
E101
riboflavin, E101a riboflavin 5'-phosphate, E100 curcumin, turmeric
oleoresin, E120 carmine, E140 chlorophyll, E141 Chlorophyll-Cu, E163 Anthocyanin, E162 betanin, red beet
juice, 160a beta-carotene, alfa, gama-carotene, E160f beta-apo-8'-carotenal,
E160b Bixin,norbixin, capsanthin, capsorubin, E160d lycopene, E161b lutein
(xanthophyll), and E161g Canthaxanthin.
[2521]
According to Thomas Müller and colleagues the breakdown compounds of chlorophyll are strong antioxidants. The researchers found the reactions to be similar in leaves and in fruits. The first decomposition products are colourless, polar NCCs (nonfluorescing chlorophyll catabolytes), that contain four pyrrole rings which In ripe pears and apples, NCCs replace the chlorophyll, especially in the peel and the flesh immediately below it.
During the decomposition process chlorophyll is released from its protein
complexes becoming phototoxic. At this stage it can transfer energy to oxygen
which becomes highly destructive.
The NCCs compounds, on the contrary, are powerful antioxidants in plant and
humans.
[2522]
Stig Bengmark looking for therapeutic agents which can modulate the
inflammatory reaction , found that curcumin, a component of turmeric, to be
non-toxic, to have antioxidant activity, and to inhibit such mediators of
inflammation as NFB, cyclooxygenase-2 (COX-2), lipooxygenase (LOX), and
inducible nitric oxide synthase (iNOS).
According to Bengmark turmeric, an approved food additive, or its component
curcumin, has shown surprisingly beneficial effects in experimental studies of
acute and chronic diseases characterized by an exaggerated inflammatory
reaction.
When the concentrate of red beet is used
as food colour specifications need to be established. Because nitrate is a
component of beet red, it is necessary to ensure that levels of nitrate do not
exceed the specifications, keeping in mind the need to limit the nitrate
content of food produced for infants and young children.
E160a beta-Carotene,alfa Carotene,gamma-Carotene
It is the pigment of the annatto bush. The pigment is considered to be
harmless. His colour is orange.
E160c Capsanthin,Capsorubin
It is the pigment of the red tomato, being used as tomato powder. It is also
made synthetically.
E160e beta-Apo-8-carotenal
Is found in vegetables,in fruits, and in liver. there is also a synthetic
production of the pigment. It has yellow colour.
E150a sugar colour
E150b sulfite-sugar colour
E150c ammonium sugar colour
E150d ammonium sulfite-sugar colour
Natural colour found in many plants.It can also be obtained synthetically. It
is harmless.Its colour is orange/red.(It is removed from the positive List of
EU allowance.)
(It was removed from the positive List of EU allowance.)
E161b Lutein
(It is removed from the positive list of EU allowance.)
(It is
removed from the positive list of EU allowance.)
(It
is removed from the positive list of EU allowance.)
(It is
removed from the positive list of EU allowance.)
It is the pigment used to colour food. It is found in nature as red colour of
the flamingos, salmon which gets its pinkish colour from its shrimp diet,
farmed salmon however gets feed coloured with canthaxanthin in order to have
its flesh as pinkish as salmon in nature.
Broilers are although fed with canthaxanthin in order to give the skin and egg
yolks a brighter yellow colour. The colour of industrial egg yolk used for
large food production is standarised by adding canthaxanthin. It can be
obtained by synthesis. It is used in drugs for bronze colour of the skin to
avoid skin cancer by heavy exposure to sun.
A suspected link between canthaxanthin as feed additive and eyesight problems
led the European Commission to reduce the allowed levels of the additive from
80 mg canthaxanthin/Kg feed down to a maximum level of 25 mg/Kg feed for
salmon, trout and broilers and 8 mg/Kg feed for laying hens.
A high intake of E161g canthaxanthin produces an accumulation of pigments in
the retina, affecting the sight.
Natural colour of red beet.
Natural colour of the skin of red grapes.
E170 calcium carbonate
There is very little known about undesired reactions of this substance.It has
white colour.
Their colour vary from yellow,to red,to brown and to black.
Undesired reactions are unknown.The colours are yellow , red or black.
There are no arguments against intake by healthy people. In case of Alzheimer
disease aluminium should be avoided.
E174 Silver
Gold and silver in high dosage are toxic.However there is no danger of
poisoning because of the high price of gold and silver limiting in this way
its use.The colour is silvery and golden.
It is an azo pigment. There is very little known about its biochemical
activity.
This substance has green colour and is obtained by changing the magnesium
radical of chlorophyll with copper.It is a risk to patients with syndrome of
Wilson.An increase of the supply of copper is not
advisable.
It is a synthetic substance being relatively harmless.
It is a widely used substance, as medicine against gout and infections of the
urinary tract.It is also a vulcanization accelerator and is used in the
chemistry of explosives.In food it is a donator of formaldehyde.It was formerly
used as preservative .At the moment it is used only in some kind of cheese.
Natamycin(it is also called pimaricin) is an
antibiotic used in infections of mouth,foot and genitals. It is employed in
food industry to treat the shell of cheese. Resistance against this antibiotic
will soon be established in bacteria coming in contact with it.His use should
therefore be forbidden in food industry
Antioxidants are used to improve the shelf life of food
interfering in the reaction of oxygen with different components of food
avoiding their chemical decomposition. They are used in soups,sauces in powder,
chewing gum,dried products of potatoes in margarine, salad oil and icecream.
The chemical preservatives may prolong the shelf life of food retarding the
growth of bacteria and moulds.
The use of chemical preservatives enables the careless hygienic conditions by
the processing of food.
Chemical preservatives are used with fish products of all types, fruit juices,
soft drinks, pastries, salads, margarine, sauces, vines , dried fruits, citric
fruits, bananas, desiccated vegetables, sugar etc.
E200 Sorbic acid
E202 Potassium sorbate
Sorbic acid and his salts are considered as harmless because they are
metabolised in human body like fatty acids.
They may produce adverse taste in food, specially in bread.
E210 Benzoic acid
E211 Sodium benzoate
E212 Potassium benzoate
The benzoic acid and their salts causes frequent allergy (asthma, urticaria)
Cats are very sensible to benzoic acid. Even a very low concentration of 5
ppm may be mortal for cats (permitted in food are concentrations of sorbic
acid up to 2500 ppm in herring salads and up to 4000 ppm in salmon
products.Avoid to give these foods to your pets).
In combination with sorbic acid and E227 calcium hydrogen sulfit the
undesired reactions are potentiated.
E214 Ethyl-p-hydroxi benzoate
E215 PHB-ethyl ester sodium salt
PHB-propyl ester
E217 PHB-propyl ester
E218 PHB- methyl ester
The esters of PHB cause frequently allergies.They act as vascular dilating
and were indicated as anesthesics for frogs.
His antispastic action exceeds the action of sodium benzoate by one
hundred times.
In high dosage they retard the growing of rats.
E220 Sulphur dioxide
E221 Sodium sulphide
E222 Sodium hydrogen sulphite
E223 Sodium metabisulfite
E224 Potassium metabisulfite
E226 Calcium sulphide
E228 potassium bisulphide
. Dioxides and sulphites liberating sulfur dioxide may
cause headache and vomits.This is noted after drinking vine.They destroy
vitamin B1 and may produce asthma attack.Sulphur dioxide is a typical
pollution of nature being directly responsible for the dying of trees and
pseudocroup disease.
E230 Biphenyl
E231 Ortophenylphenol
E232 Sodium ortophenyphenol
Are substances used as antifungal on citric fruitsand promote cancer of the bladder in animals, being very strong in
combination of E232 and E233. Thiabendazol is used in medicine and also in
agriculture as pesticide.It is being frequently used to impregnate paper used
to wrap up fruits. Avoid children playing with this paper or even putting
in contact with the mouth.
E234 Nisin
E235 Natamycin
(Not allowed as food ingredient.)
(Not allowed as food ingredient)
(Not allowed as food
ingredient) Formic acid and their salts may be metabolised in the
body.Undesired reactions only with high levels.
E242 Dimethyl
carbonate
E249 Potassium nitrite
E250 Sodium nitrite
E251 Sodium nitrate
E252 Potassium
nitrate
E
270 Lactic acid
. E270 stands for
both (left or right) optical active forms.
E280 Propionic acid
E281 Sodium propionate
E282 Calcium propionate
Propionic acid is a natural compound of food being found in very small
quantities.It produces cancer on the antestomach of rats.
According to the health authorities it is not significant to human because
we do not have an antestomach.Propionic acid and their salts are used as
preservative in bread.
Sorbic acid could become an ideal replacement for calcium propionate as mould
inhibitor, being thus a cost-saving method to keep bread fresh and mould-free
for a couple of weeks.
Sorbic acid can not generally be used as a suitable alternative as it destroys
yeast. The process works by coating the sorbic acid within an invisible
microfilm of vegetable fat to create a free flowing powder that can easily be
blended with dry ingredients prior to baking.
A controlled release mechanism ensures the sorbic acid is not released from its
encapsulate until the bread is baked past 60
, after the yeast has finished
working.
Preservatives in bread can be avoided as special care during production can
achieve a reasonable shelf life. Cost cutting on cleaning and maintenance of
the production line and reheating after packaging makes the use of
preservatives and obscure microencapsulated ingredients attractive. Bread
should be produced as natural as possible.
E284 Boric acid
E285 Sodium tetraborate (borax)
[3807]
The new preservative ethyl lauroyl arginate is
awaiting approval in March by the European Commission.
The application, Spain's Laboratorios Miret SA (LAMIRSA), originally proposed to
EFSA that the preservative be used in non alcoholic beverages made with fruit
juice, energy and sports drinks, and meat products, at a dosage of 115 to 225
ppm. However EFSA saw that this dosage would mean the potential exposure to the
chemical could be at or above the ADI of 0.5mg per kg of bodyweight per day.
Studies in different rat strains and sexes showed
that there was a consistent effect on white blood cell counts.
Experts speaking for LAMIRSA, the company the preservative, say that "the
data is toxicologically not significant since the observed effects are
inconsistent between the studies considered and did not demonstrate a
dose-effect relationship", and the effects on white blood cells were not
accompanied by changes to the tissue in any of the studies. Ethyl lauroyl
arginate has been generally recognised as safe (GRAS) in the US since 2005, at
levels up to up to 200 mg of the active ingredient ethyl-Nalfa-lauroyl-Larginate
HCl /kg. Last year JECFA recognised it as a food additive and allocated an ADI
of 0-4 mg/kg bw, and the additive was recently approved in Australia and New Zealand.
EFSA, however, maintains that the toxicological relevance of the findings could
not be assessed, since the mechanism of action is not clear. The ANS panel of the
EFSA concluded that the scientific evidence of a plausible mechanism for the
alterations in white blood cell counts has not been provided and that the
concerns and uncertainties related to white blood cell counts have not been
addressed.
Acidulants, acidity regulators
Acidulants and acidity regulators are used to give a sour taste to food and to
act as preservative.Some acidulants act as stabilisers, other help antioxidants
or emulsifiers.
Acidity regulators adjust the pH like phosphates and citrates, acids and
alkaline substances.
E260 Acetic acid
E261Potassium acetate
E262 Sodium acetate
Acetic acid(E260) is a harmless preservative. Acetic acid and his salts
(acetates) are synthetically produced from light benzine.
It is important for the production of leaven.The bread made with this
leaven is however of inferior quality.
E325 Sodium lactate
E326 Potassium lactate
E327 Calcium lactate
Lactic acid is obtained from starch under the activity
or bacteria.There are two types of lactic acids turning left and turning
right.European legislation permits both form. Small children cannot metabolise
the dextrorotatory Form.Its excessive ingestion may produce excessive blood
acid.Food with D- lactic acid should be labelled with an warning.
Its harmless and is found normally in air.
E331 Sodium citrate i) Monosodium citrate, ii) disodium citrate,
iii) trisodium citrate
During heating procedure
for infant formulae or follow-on formulae made from cow's milk the surplus of
ionised calcium results in denaturation and aggregation of proteins causing a
phase separation of fat and proteins. Sodium or potassium citrate, as well as
sodium and potassium phosphates are therefore used to complex free calcium ions
reducing denaturation and aggregation of formulae containing milk.
The use of sodium and potassium citrate is acceptable up to 2 g/l, either
single or in combination, in infant formulae and follow-on formulae for infants
and young children in good health and in FSMP. Sodium and potassium citrate are
permitted in weaning foods at quantum satis levels for pH adjustment only (
Directive 95/2/EC) and as source of nutrients in infant formula and follow-on
formula for infants and young children in good health (Directive 91/321/EEC)
[3808].
E335 Sodium tartrate i) monosodium tartrate ii)
disodium tartrate
E350 Sodium malate
E351 Calcium malate
Malic acid is present in many fruits.It exists as two types
( levorotatory form and dextrorotatory form )
Malic acid and its salts (malates) are being produced starting from fumaric
acid (E297 )
Fumaric acid can be obtained synthetically.It is also being used in the
production of plastics.
E300 Ascorbic acid
E301 Sodium ascorbate
E302 Calcium ascorbate
E304 Fatty acid
esters from ascorbic acid, i) ascorbyl palmitate, II)ascorbyl stearate
E306 Heavy tocopherol bearing
extracts
E307 Alpha-tocopherol
E308
Gama-tocopherol
E309 Delta tocopherol
E310 Propyl gallate
E311 Octyl gallate
E312 Dodecyl gallate
E315 Isoascorbic
acid
E316
Sodium isoascorbate
E320 Butylhydroxyanisole (BHA)
E321 Butylhydroxytoluene (BHT)
According to the European labeling legislation starch modified with enzymes
or with physical methods are not declared as "modified". These ingredients are
declared in the list of ingredients as "starch".
Modified starch has its chemical structure changed with inorganic
acids.Together with E339 disodium phosphate. E343 dimagnesium phosphate and E
450 orthophosphates modified starch can cause deposits of calcium in the
pelvic region.
Emulsifier are substances which make a mixture of water and oil possible. They
reduce the surface tension between both liquids, so that small droplet of oil
may swim in water. This emulsion is called "oil in water emulsion".
When water swims droplets are swimming in oil it is called "water in oil
emulsion".
In food technology there are many new organoleptic properties caused by
emulsions such as creamy,thickening,foaming.
Emulsifiers are used widely in
food such as margarine, in bakery in candies,puddings bred, soups.
Emulsifiers have great biological activity.They should not be employed
uncontrolled.There are very few toxicologic studies about emulsifiers and were
all made by their producers.In case of negative results they were not
published.Recent tests have not found adverse activities.It is however
believed that emulsifiers have a role in the development of diseases of
intestines and in allergies.
Emulsifiers modify the surface of the intestine making them permeable to
allergens,contaminants and other additives.
Lecithin is extracted from soya beans and colza.Enzymatic hydrolysis is
permitted.
They are obtained from oil of colza treated with ammonium.
Fatty acids are natural elements of fats and oils. Their salts are
obtained by treating them with alcaline substances in order to get soaps.
470b Magnesium salt of edible fatty acids
E471 reacts with tartaric acid,acetic acid or lactic acid.
Soy lecithin remains the most frequently used ingredient to lower the viscosity
of liquid chocolate masses during processing. non-GM (genetically modified) soy
lecithin with a full Identity Preserved (IP) status is, however, getting rare.
Recent developments of new types of citric acid esters of mono- and di-
glycerides from castor oil are replacing soy lecithin to overcome the shortage
of GM- free lecithin on the international market
Dosages of lecithin higher than 0.4 per cent increase the
yield value of the chocolate mass, making it necessary either to add extra
cocoa butter or PGPR (Polyglycerol Polyricinoleate E476 obtained from
ricinoleic acid and polyglycerol from canola) to the chocolate.
Citric acid ester of mono- and di-glycerides act also as a wetting agent in
instant chocolate drink powder an has an equivalent effect to soya lecithin
when tested in a milk system.
It is also used as an instantising agent for powdered food preparations and
instant chocolate drink powders intended for re-hydration in water or milk.
Possible name
in the list of ingredients is polyglycerol ester.
E477 Propylene glycol ester of fatty acids
[2524]
Aleogon, Frochot and Goff 2008 studied the effectiveness of propylene glycol
monostearate (PGMS) to inhibit ice recrystallization in ice cream and frozen
sucrose solutions. They found that 0.3 per cent of PGMS reduced ice crystal
sizes in such solutions when frozen in a scraped-surface freezer. The
crystal morphology was highly irregular. No effect was found in quiescently
frozen solutions, such as ice pop or ice lollies. The authors say that shear
during freezing is necessary to distribute PGMS around the ice and cover the
surface of the crystals. Danisco has a patent on this matter.
Propylene glycol monostearate esters of fatty acids (E477) are classified as
emulsifiers,the authors, however, found the emulsifying effect of PGMS to be
poor.
E479b Thermally oxidized soybean with mono- and diglycerides of
fatty acids
E481 Sodium stearyl-2-lactylate
E482 Calcium stearyl-2-lactylate
E483 Stearyl tartrate
E491 Sorbitan monostearate
E492 Sorbitan tristearate
E493 Sorbitan monolaurate
E494 Sorbitan monooleate
E495 Sorbitan monopalmitate
E330 Citric acid
E331 Sodium citrate
E332 Potassium citrate
Citric acid is present in many fruits,
mainly in Kiwi and lemon.
Citric acid is part of the biological cellular activity.By high levels of
citric acid in food, the intestines are forced to assimilate higher rates of
heavy metals and radionuclides.
Citric acid is won from sugar by bacterial activity.
E334 Tartaric acid
E335 Sodium tartrate
E336 Calcium tartrate
E337Sodium and potassium tartrate
E353 Metatartaric acid
Tartaric acid is a natural substance obtained from rests of wine reacting with
calcium milk (E526) with potassium tartrate (E336) and finally with sulphuric
acid.Only the harmless levorotatory form form (left turning form) is
allowed.
E338 Phosphoric acid
E339 Natrium phosphate i) monosodium phosphate, ii) disodium
phosphate, iii) trisodium phosphate
E340 Potassium phosphate, i) monopotassium phosphate, ii)
dipotassium phosphate, iii) tripotassium phosphate
E341 Calcium phosphate i) monocalcium phosphate, ii) dicalcium
phosphate, iii) tricalcium phosphate
Not allowed any more as food
ingredient.
E352 Calcium malate i) calcium malate ii) calcium
hydrogen malate
E355 Adipic acid
E356 Sodium adipate
E357 Potassium adipate
E363
E380 Triammonium citrate
E385 Calcium disodium
metylendiamine tetraacetate
E400 Alginic acid
E401 Sodium alginate
.
E402 Potassium alginate
E403 Ammonium alginate
E404 Calcium alginate
E405 Propylene glycol alginate
E406 Agar-Agar
E407Carrageenan
Carrageenan is obtained from red alga Irish Moss (Chondrus crispus) and is in
use as stabiliser or thickening agent and as an encapsulation agent.
New researches and experiments from the University Iowa (USA) with animals
rise the suspicion that this ingredient has carcinogenic potential. Low
molecular carrageenan was recognised long time ago as carcinogenic. That is the
reason to use only the long chain molecular types or carrageenan.
Researches in the University of Iowa have shown that carrageenan is broken in
small molecules during processing and during digestion. These small parts can
enter the bloodstream.[2525]- Carrageen is largely sourced
from the Philippines and Indonesia.
Thomas Karbowiak and colleagues found that adding high melting point fat to
form an emulsified film can reduce the transfer of water and enhance moisture
barrier properties. This is important in the development of composite foods
where Karbowiaks research can lead to edible films and coatings applied between
the different phases of this food.
Blends of iota-carrageenan hydrocolloid matrix and fat developed by the
researchers reduce the water transfer between compartments of different water
activities in the same food. Increased shelf-life can thus be obtained.
The authors conclude that carrageenan can be used for application such as
encapsulation of active substances incorporated in biopolymer coatings or films
for food packaging.
Degraded carrageen
[2526]
Joanne Tobacman reviewing experimental data pertaining to carrageenan's effects
found that exposure to undegraded as well as to degraded carrageenan was
associated with the occurrence of intestinal ulcerations and neoplasms. This
association may be attributed to contamination of undegraded carrageenan by
components of low molecular weight, spontaneous metabolism of undegraded
carrageenan by acid hydrolysis under conditions of normal digestion, or the
interactions with intestinal bacteria.
Chemically degraded form of carrageen have lower molecular weight. factors such
as bacterial action, stomach acid and food preparation may transform undegraded
carrageenan into the more dangerous degraded type.
The safety of carrageenan has recently been reviewed in 2001 by the Joint
FAO/WHO Expert Committee on Food Additives (JECFA). The experts on this
Committee did not find evidence to suggest that the levels of carrageenan in
foods posed any hazard to health. [2527] [2528]
During the course of the re-evaluation, the JECFA specifically reviewed the
matter of the potential for gastrointestinal effects from ingestion of
carrageenan. This included an evaluation of the effects of stomach flora on
carrageenan, food processing conditions on carrageenan and the degradation of
carrageenan in the stomach. Throughout the course of the re-evaluation, the
JECFA considered genotoxicity studies, metabolism, reproduction and
developmental toxicity, and short term and long-term mammalian feeding studies
(including a 7.5 year feeding study in monkeys).
The JECFA also considered
information about the current understanding of the concept of cell
proliferation and promotion of tumors.[2527] [2528]
The fact that proliferative effects were seen at 2.6% in the diet is not being
considered as relevant, because the estimated carrageenan consumption is
below the threshold concentration for these effects. Further, the JECFA also
noted that at 5% in the diet of rats, carrageenan did not act as at tumor
promotor. Effects seen at exceptionally high levels of exposure to carrageenan
were determined to be caused by altered toxicokinetics. [2527]
[2528]
Overall, the JECFA concluded that there was no concern to the continued
consumption of carrageenan. It allows for the use of the additive at the level
necessary to achieve the technical or functional effect in food, also referred
to as the level of Good Manufacturing Practices (GMP). The complete report of
this review was made publicly available in 2003 and therefore post dates the
review by Dr. Tobacman. [2527] [2528]
E407a Processed Euchema algae
E410 Carob seed
Also known as locust bean gum is allowed in follow-on formulae at a maximum level of 1g/l, and in
weaning foods at a maximum level of 10g/kg under Directive 92/2/EC. Locust bean
gum is refined from the endosperm of the carob tree Ceratonia siliqua.
It contains tannins. The carbohydrate component is a galactomannan polymer
consisting of linked D-mannose units with side chains of D-galactose. It is
used as a stabiliser and thickening agent.
E412 Guar gum
E413 Tragacanth
E414 Gum arabic
Gum arabic, acacia gum E414 is won from acacia trees in Sudan and Nigeria.
Gum arabic is a complex mixture saccharides and glycoproteins, which gives it
one of its most useful properties: it is perfectly edible. Other substances
have replaced it in situations where toxicity is not an issue, as the
proportions of the various chemicals in gum arabic varies widely and make its
reliable performance troublesome. Still, it remains an important ingredient in
soft drinks, syrups, hard gummy candies like gumdrops, and in marshmallows.
[2529]
Corn fibre gums replacing acacia gum:
Madhav P. Yadav and colleagues, in a study, extracted two different types of
corn fiber gum from the corn kernel pericarp and/or endosperm fiber. The
researchers found that the emulsifying properties of corn fibre gums, an
arabinoxylan (hemicellulose), were better than native and modified acacia gums
and could domestically produced gum with a dependable supply and consistent
quality replacing acacia gums.[2530]
E415 Xanthan
E416 Karaya gum
E417 Tara seed
E418 Gellan
E425 Konjac
Konjac is approved by WHO, US Food and Drug Administration and the European
Union with up to one per cent of the final product. It is used for gel
strength, viscosity in confectionery,as dietary fiber,edible films, improves
mouthfeel.
It is also called glucomannan being a hydrocolloidal
polysaccharide obtained from the tuber of Amorphophallus Konjac, K.Koch,
growing in East Asia. The chain of the molecules of the nonionic glucomannan is
built mainly of mannose and glucose in a ratio of 1.6 : 1.0 the molecular
weight is between 200,000 and 2,000,000 daltons. There are acetyl groups which
are responsible for water solubility.
There were rumours linking konjac with certain death cases after ingestion of
jelly minicups and fruit gel sweets containing konjac.
[2531]
Hydrocolloids are increasingly needed in the production of foods as
stabilisers, thickeners, emulsifiers and gelling agents, papermaking, textile
and cosmetic industries.
Steffan Willför and colleagues stress that mannans used as
guar gum, Konjac glucomannan, locust bean gum, tara gum, and fenugreek gum are used, but
mannans from wood are neglected. The researchers found that the process
waters in mechanical pulp mills processing Norway spruce is
high in dissolved O-acetylgalactoglucomannans (AcGGM). This hydrocolloid represents about 50
per cent of the dissolved matter in the process water.
Sugar, sorbitol, maltitol, isomalt, mannitol,
erytritol, lactitol.
Saccharin, aspartame, acesulfame K,
sucralose and cyclamate.
E420 Sorbitol, ii) sorbitol syrup
Sorbitol is widely used in diabetic
foods. Can cause gastric disturbances.
Sorbitol in chewing gum and sweets may
cause serious weight loss
[2532] Sorbitol is a
"sugar-free" sweetener found in chewing gum and sweets. The safety of
sorbitol has been thoroughlylyols must be labelled with the statement,
"Excessive consumption may produce laxative effects."
According to Juergen Baudits and colleagues 2008 serious weight loss and
diarrhoea were caused by excessive sorbitol consumption. In the two reported
cases the daily consume of sorbitol was abaut 20 to 30 grams. The authors
stress that the side effects of sorbitol are usually found only within the
small print on foods containing sorbitol, consumers may be unaware of its
laxative effects and fail to recognise a link with their gastrointestinal
problems. The industry would be well advised to print the warning
concerning the laxative effect in 0,6 mm letters or higher.
Sorbitol is a sugar alcohol derived from corn starch that is widely used in a
range of food products, including confectionery, baked goods, jams and
preserves, ice cream and diabetic foods. Sorbitol is hailed as noncariogenic,
it has humectant and texturising properties and is used in food products such
as snack foods and beverages.
The range of corn-derived sweeteners comprises glucose syrup, maltose syrup,
high fructose corn syrup, crystallized glucose and maltodextrin and sorbitol,
which is being sold as bulk reduced calorie sweetener.
Polyols such as sorbitol, xylitol, lactitol, mannitol, maltitiol and isomalt
have been approved by the Scientific Committee for Food (SCF) for use in
foodstuffs and fall under the "additives" label. In the sorbitol has achieved
GRAS (Generally Recognised As Safe) status.
E421 Mannit
E422 Glycerin
E432 Polyoxyethylen-sorbitan monolaurat (Polysorbate 20)
E433 Polyoxyethylen-sorbitan monooleat (Polysorbate 80)
E434 Polyoxyethylen-sorbitan monopalmitate (Polysorbate 40)
E435 Polyoxyethylen-sorbitan monostearate (Polysorbate 60)
E436 Polyoxyethylen-sorbitan tristearate (Polysorbate 65)
E440 Pectine
E444 Sacharoseacetate isobutyrate
E445 Glycerinester of root resin
Phosphates which are
allowed as food ingredients: i) disodiumdiphosphate, ii)
trisodiumdiphosphate, iii)tetrasidiumdiphosphate, iv) dipotassiumdiphosphate,
v) tetrapotassiumdiphosphate, vi) dicalciumdiphosphate, vii)
calciumdihydrogendiphosphate.
E451 Triphospohate:
Allowed triphosphates are:i) Pentasodium triphosphate, ii) pentapotassium triphosphate.
E452 Polyphosphates:
Allowed
polyphosphates are: i) sodium polyphosphate, ii) potassium polyphosphate, iii)
sodium calcium polyphosphate, iv) calcium polyphosphate.
E460 Cellulose:
i) Cellulose microcristaline ii)Cellulose powder.
E461 Methylcellulose
E463 Hydroxymethyl cellulose
E464 Hydroxypropylmethyl cellulose
E465 Ethylmethyl cellulose
E466 Carboxymethyl cellulose
It is not
allowed any more.
E541 Sodium aluminum phosphate
Not allowed any more,
Phosphates in food are a great group of
substances. They were often commented in the press.They are not as dangerous as
public opinion
According official classifications the calcium ortophosphate ( E341 ) is
harmless.Nevertheless it is being used as insecticide.The activity of
phosphates in case of hyperactivity of children is still unknown.
Polyphosphates can alterate the metabolytic activity in humans.In addition
to modified starch they may cause calcification of the pelvic region in rats.
Polyphosphates intensify the activity of heavy metals making them easier to
cross the intestine wall.
Polyphosphates may contain a lot of impurities.
In Japan a group of children were intoxicated with arsene as impurity of
ortophosphate used in food.
Other impurities are uranium and cadmium. In Europe the
following maximal contents of impurities are allowed in food:
- Fluor 3 mg/Kg
- Lead 50 mg/Kg
- Copper 10 mg/Kg
- Zinc 50 mg/Kg
[2533]
The use of phosphates in foods increased from 470mg per day in the average
adult diet in 1990s, to as much as 1000mg per day for present time. Phosphates
are added to increases water retention and improve texture in meats, sausages,
cheeses, beverages and bakery goods.
Dr Myung-Haing Cho and colleagues found that feeding K-rasLA1 mice with a diet
containing 1.0% inorganic phosphates for 4 weeks, increased the size of the
tumours and stimulated growth of the tumours, compared with lower or none
phosphate supplementation.
High dietary inorganic phosphate strongly activates Akt signaling, which plays
an important role in the lung tumorigenesis. The authors stress that the
results of their study suggest that elevated phosphates may activate the Akt
signaling in the normal lungs and increase lung tumorigenesis.
According to the authors disruption of Akt signaling pathways in lung tissues can
confer a normal cell with malignant properties. They call for a careful
regulation of dietary inorganic phosphates for lung cancer prevention as well as
treatment.
E551 Silicon dioxide
E552 Calcium silicate
E553a i)Magnesium silicate, ii) Magnesium trisilicate
E553b Talcum
E554 Sodium aluminum silicate
E555 Potassium aluminium silicate
E556 Calcium aluminium silicate
E558 Betonit:Fluor silicic acid
E559 Aluminium silicate (kaolin)
E570 Fatty acids
E574 Gluconic acid
Gluconic acid is present in small quantities in honey.It is used as acidulant
in soft drinks and as anticorrosive in tin can of sprays.
E575 Glucono delta-lactone
Used in sausages to enhance the
action of nitrate in order to get a red colour.It is used as acid regulator.
In low levels it is harmless.
E576 Sodium gluconate
E577 Potassium gluconate
E578 Calcium gluconate
E579 Iron-II gluconate
E585 Iron-II lactate
E471 Mono and diglycerids from edible fatty acids:
They are used as emulsifier for margarine, fine food, and
many other products. Moslems and Jews which are looking for halaal or koscher
foods are often exchanging E- Numbers or references of emulsifiers such as E
471 and E472.
The E-Number or their chemical name in the list of
ingredients give no information about the origin of the fatty acids used. Their
origin may be vegetable, such as palm oil from the palm Elaeis
guineensis, cocoa oil from Cocos nucifera as well as hydrated oils and fats from soy beans Soy bean (Glycine
maxima), cottonseed oil from Gossipium barbadense and
Gossipium hirsutum.
Mono- and diglycerids E471 may also have their origin from bovine tallow and
what is relevant to moslems and Jews: from lard from pigs. The specifications
given by the producer of the emulsifier must specify the origin as it
cannot be seen by the declaration of the list of ingredients. In each case
it must be cleared by the producer.
E472a Acetic esters of mono- and diglycerides of edible fatty acids
E472b Lactic acid esters of mono- and diglycerides of edible fatty acids
E472c Citric acid esters of mono- and diglycerides of edible fatty acids
E472d Tartaric acid esters of mono- and diglycerides of edible fatty acids
E472e Mono- and diacetyl tartaric acid ester of mono- and diglycerides of edible fatty acids
E472f Mixture of tartaric and acetic acid ester of mono- and diglycerides of edible fatty acids
E473 Sucrose ester of edible fatty acids
E474 Sucroglyceride
It is used in backery,effervescent drinks,as acid regulator in baby food and
cheese.It is harmless for adults. For children it is necessary to consider the
amount of sodium from salt in food which must be added to the sodium of
Sodium carbonate.
It is being employed in the treatment of cocoa and as an acidity regulator in
sauces like Maggi in addition to chloridric acid.
Potassium carbonate is being employed in the production of raisins. It is being
considered as harmless.
Ammonium carbonate is toxic when eating directly, because of the amount of
ammonium being liberated.As ammonium is removed during heating in a furnace
its use for bakeries is harmless.
It is used in the production of cocoa and drinking water,chewing gum and
kitchen salt to avoid clotting.
It is used in the production of sugar from corn starch and as acid hydrolysis
of proteins to obtain Maggi.His use is harmless because no acidity is present
in final products.
It is used to substitute kitchen salt in case of hipersensibility to
sodium.It is also used in combination with gelling agents.
It is being used in combination with specific gelling agents. It acts against
the hardness of water in the production of beer.
In the production of cheese calcium chloride is being used in order to get a
higher rate of albumin.
It is harmfull.In animals and in humans there were found modifications or
bones,modification of the haemogram,alterations of the hypophysis and renal
gland. According to World Health Organisation ammonium chloride produces
weight loss in during pregnancy,vomits, loss of appetite and
hiperventilation.
It is being used in special types of candies and in drinking water, a maximum
of 0,6 mg ammoniac/liter had been allowed.(It is removed from the positive
list of EU allowance.)
indexSulphuric acid
It is used in the treatment of drinking water and in the production of
sugar. It is harmless as long the concentration in food is low so that there
cannot be caused acid lesions.
E514 Sodium sulphate, ii) Sodium hydrogen sulfate
Sodium sulphate is being used as strong laxative.In food it
adjusts colours in very little concentrations so that it may be considered as
harmless.
E515 Potassium sulphate, ii) Potassium hydrogen sulphate
E517 Ammonium sulphate
E520 Aluminium sulphate
E521 Aluminium sodiumsulphate
E522 Aluminium potassium sulphate
E523 Aluminium ammoniumsulphate
It is gypsum, being used to stabilise bread and is used in addition to
thickening agents.It is also used as colour. It is used to treat water for the
production of beer.
It is being used extern in the production of pretzel, in the production of
cocoa,in treatment of drinking water.
E525 Potassium hydroxide
Calcium milk is being used in the preservation of eggs.
Ammoniac is permitted to treat cocoa, and drinking water.As a free substance
it is cell toxic.
E528 Magnesium hydroxide
It is used in treating drinking water.
IndexMagnesium oxide
E535 Sodium ferrocyanide
E536 Potassium ferrocyanide
(It is removed from the positive list of EU allowance.)
E541 Sodium aluminium phosphate
E900 Dimethyl polysiloxane
E901 Beeswax
E902 Candelilla wax
E903 Carnauba wax
E904 Shellac
E912 Montan ester
E914 Polyethylen waxoxidate
E927 Carbamid
E938 Argon
E939 Helium
E941 Nitrogen
E950 Acesulfame K
It is an artificial sweetener. "K" stands for the chemical sign of
potassium,as salt.It is stable at high temperatures.An old nomenclature was
acetusulfame. The European Commission has approved
acesulfame K in June 1990 with an ADI (Acceptable Daily Intake) of 9
milligram/kilogram body weight. This ADI should not be surpassed.
E951 Aspartame
Aspartame is a low-calorie artificial sweetener which was approved by the FDA
in 1981 and by EU Commission since June 1990.
It is built by two amino acids: Phenylalanine and asparagine acid and methanol
which are linked together to form the new substance aspartame.
In the stomach the aspartame is broken down into methanol and the two amino
acids which are than digested as any other amino acids furnishing 4 Kcal/gram.
Aspartame is considered to be safe with exception in cases of phenylketonuria
(PKU) which is a rare disorder caused by a defective
gene which regulates metabolism of the amino acid phenylalanine. An
intermediary toxic metabolite builds up in the blood damaging brains. A
special diet low in phenylalanine must be continued the whole life. Because of
that aspartame must be labelled with: "contains a source of phenylalanine",
as a warning for patients with phenylketonuria.
A good information about safety of aspartame is given by www.cancer.org. Please
search for "Aspartame". Fanatics claim the methanol being released in the
body is converted to formic acid and formaldehyde Thermal decomposition of
aspartame is told to origin DKP, a substance with cancer activity. See at
www.dorway.com.
Remember the end of Introduction of www.ourfood.com: "Be careful not to fall
into sectarian thinking-allow always arguments of the other side." Aspartame was
approved by FDA, EU Commission and other international governmental
institutions which are guarantors for a neutral decision regarding safety of
aspartame.
[2534]
Sodium saccharin causes urinary bladder tumors in male rats.
While it cannot While some have argued that those tumors are irrelevant to
humans, such arguments are flawed. While it cannot be proved that sodium
saccharin's causation of bladder tumors in male rats is relevant to humans,
neither can it be assumed to be irrelevant.
[2535]
Lambertini an colleagues demonstrated, that aspartame causes a statistically
significant, dose-related increase in lymphomas and leukaemias in female rats
at dose levels very near those to which humans can be exposed.
The authors say that this could be related to methanol, a metabolite of
aspartame, which is metabolised to formaldehyde and then to formic acid, both in humans and rats.
The authors conclude that the results of the study call for urgent
re-examination of permissible exposure levels of aspartame in both food and
beverages, especially to protect children.
Animal studies of the 1970s, linking saccharine to bladder cancer were not reproduced in humans.
Researchers at Ramazzini's cancer research centre in Italy caused a stir in 2005 by claiming that
their study indicated that aspartame consumption by rats leads to increase in lymphomas and leukaemias in females at dose levels "very near those to which humans can be exposed"
[2536]
Researchers examined the relationship between aspartame intake and 1,888 lymphomas or leukemias and 315 malignant brain cancers among the participants of the NIH-AARP Diet and Health Study from 1995 until 2000. Development of these cancers was not associated with estimated aspartame consumption, refuting a recent animal study with positive findings for lymphomas and leukemias and also contradicting claims regarding brain cancer risk.
[2536]
The US National Cancer Institute study found no
statistically significant link between aspartame-containing beverage consumption and leukemias, lymphomas or brain tumors in man or women.
[2537]
The European Food Safety Authority issued its opinion last may, that there is no need for a further safety review of aspartame nor a revision of the acceptable daily intake (40 mg/kg body weight).
According to Panel the kinetic data in humans indicate that dose levels around
the acceptable daily intake (ADI) (40 mg/kg bw/d), even when taken as a bolus
dose, do not lead to systemic exposure to aspartame. Furthermore, exposure to any of its breakdown products, including methanol or formaldehyde, is negligible.
The Panel considers that no significant new data have emerged since 2002 on aspects other than carcinogenicity and there is therefore no reason to review the previous SCF opinion on aspartame.
The Panel concludes, on the basis of all the evidence currently available from the ERF study, other recent studies and previous evaluations that there is no reason to revise the previously established ADI for aspartame of 40 mg/kg bw.
[2538]
Dr Silvano Gallus and colleagues considered data from a network of
case-controlled studies conduced in Italy between 1991 and 2004. A significant inverse trend in risk for increasing categories of total sweeteners was found for breast and ovarian cancer, and a direct one for laryngeal cancer. The authors concluded that there is a lack of association between saccharin, aspartame and other sweeteners and the risk of several common neoplasms.
These findings confirm foregoing researches, such as the US National Cancer
Institute study which found no statistically significant link between aspartame-containing beverage consumption and leukemias, lymphomas or brain tumors in man or women.
Aspartame-acesulfame-salt E962
[2539] It is a new
sweetener built of acesulfame K which has substituted the sodium ion from the
aspartame creating thus a chemical link between both sweeteners. This new
sweetener is supposed to have handling advantages. It is about to be approve by
the EU Commission.
Sucralose (E955)
[2539]
It is a new sweetener which is about to be approved by the EU Commission.It is
non-caloric an is 600 times sweeter than sugar. Sucralos
(trichlorogalactosucrose) is being made by
chlorinating saccharose. The ADI is 15 mg/Kg body weight. It is resistant to
heat and can be used for cooking and backing.
Sucralose: National Institute of Health [2540]
Food industry tries to substitute sugar for cheap alternatives and follows a
trend towards sugar-free and low-calorie products. Altern is a
low-calorie tabletop sweetener containing sucralose. It is being blamed of
infringing on intellectual property of Tate & Lyle company, which has a 1976
patent on a similar sucralose product branded Splenda.
The patent expired but
Tate & Lyle holds on its process patents. Altern product is sold at a 30%
discount and is believed to be a direct copy of Splenda, which it had supplied
to a manufacturing customer who had then sold it to the US retail giant.
E952 Cyclamate and its Na- and Ca- salts
It is an artificial non-caloric non-cariogenic sweetener. Its chemical name is
sodium or calcium cyclohexylsulfamate. Cyclamate is about 1/10 sweeter than saccharin and 30
times than sugar. An AID of 11 mg/Kg body weight can easily exceeded when
soft drinks are largely consumed in summer. It has no wrong taste in high
concentrations. AID is therefore easily exceeded in kitchen formulations.
Cyclamate is heat resistant and can be used for cooking and backing. Cyclamate
is not digested by most persons, only a small number can do it.
Cyclamate is often used in combination with other sweeteners enhancing each
other so that final taste is sweeter as the sum of the individual sweeteners. 5
mg of saccharin together with 50 mg cyclamate are equivalent to 125 mg
cyclamate and 12.5 mg saccharin. Cyclamate is also used in combination with
aspartame, sucralose and acesulfame K.
Cyclamate was banned in the United States in 1970 following the result of a
test on rats which developed bladder cancer with very high dose of cyclamate in
addition to saccharin. A current petition to reaprove cyclamate is before the
FDA.
Cyclamate and its major metabolites cyclohexylamine are not considered as
carcinogenic according to numerous animal test failing to confirm the original
findings of 1969. Meanwhile cyclamate is approved in more than 55 countries
around the world.
Cyclamate and the EU Directive 2003/115/EC amending Sweeteners
Directive 94/35/EC:
The Directive 2003/115/EC, taking account of the
opinion of the Scientific Committee on Food on cyclamic acid and its sodium and calcium salts (cyclamate) restricts the use of
cyclamate in water, milk and fruit juice based drinks as well as energy-reduced
and non-added sugar drinks and a range of confectionery products, including
sugar-free chewing gum and breath-freshening sweets.
Formulations with blending of cyclamate and acesulfame are trying to compensate
the reduction of cyclamate.
E954 Saccharin and its Na- and Ca-
salts
[2491]Saccharin is a
artificial sweetener Saccharin is 300 times sweeter than sugar. Due to the
water solubility the sodium salt is most frequently used. Saccharin is high
temperature and cooking and backing resistant.
Saccharin high dose was charged of causing bladder cancer, this could not be
confirmed. In small amount saccharin is considered to be safe. In some
industrial recipes sugar is being substituted because to bring down cost of
ingredients.
Don't use a higher concentration as 5% to 8% sugar substitution= maximum
0.02% saccharine in food as a metallic taste will be present in higher
concentrations.
All artificial sweeteners reduce their sweetening power when a certain dose is
exceeded. The combination of two sweeteners such as saccharin/acesulfame K or
saccharin/cyclamate or cyclamate/aspartame increases the sweetening power.In
kitchen and in industrial production saccharin/cyclamate in relation 1 to 10 is
therefore frequently used.
[2490]
According to Marco Scheurer and colleagues 2009 artificial sweeteners are not
removed in waste water treatment.
All sweeteners used in the EU are approved and safe, however they pose an
environmental problem because they pass sewage treatment plants. They were
found in surface water and may cause sweet taste in tap water.
The researchers used a new method to analyse drinking water. The method
focussed on the simultaneous detection of cyclamate, acesulfame, saccharine,
aspartame, neotame, neohesperidin dihydrochalcone and sucralose in German waste
and surface water.
Samples from sewage treatment plants and from a soil aquifer treatment site
that treats secondary effluent from a sewage treatment plant showed that
artificial sweeteners are incompletely eliminated by the treatment process.
The authors found levels of 190 microgram/l, 40 microgram/l for acesulfame and
saccharine, and under 1microgram/l for sucralose in influents of German
sewage treatment plants. In surface waters acesulfame concentrations exceeded
2 microgram/L, being of primary concern.
The authors suggest the use of sucralose and acesulfame as tracers for
anthropogenic contamination
E957 Thaumatin
[2491]
It is won from the fruit of the west African shrub Ketemfe
Thaumatococcus daniellii. It is a mixture of
proteins (a polypeptide chain of 207 amino acids). It is 2000 times sweeter
than saccharose.
It is non-cariogenic and has 4.2 Kcal/g and contributes no
calories when used in low levels. It is considered as safe and has no maximum
ADI (Allowable Daily Intake). It is not resistant to heat, therefore not
indicated for cooking and backing.Thaumatin can also be produced by bacteria
using genetic engineering.
E959 Neohesperidin DC
eohesperiden DC[2491]
It is won from different types of Bromelia fruits, like pineapple.and
grapefruit. It is a sweetening agent with very intensive taste,
dihydrochalcone C
H
O
, a glycosidic flavonoid. It is also a
bitterness suppressor. Blends of Neohesperidin with polyols, aspartame and
acesulfame K and Saccharine are used. It is 1500 times sweeter than
saccharose.The ADI of neohesperidin is 5 mg/Kg body weight.
Neotame E961. New artifical sweetener in Europe
[2492]
Neotame is a highly intense sweetener with a sweetness potency ranging from 7
000 to 13 000 times that of sucrose. It may be used as a replacement for
sucrose or other sweeteners in a broad range of products. Neotame can be used
alone or with other sweeteners. In addition, neotame can modify the flavour of
foods and beverages. The sweetener was developed by The NutraSweet Company in
the US and is a derivative of aspartame.
It is used to mask bitter or harsh notes, such as may be present when potassium
choloride is used in salt substitutes, or the beany taste of soy. The approval
is an amendment to directive 94/35/EC.
Allowed are up to 20 mg/Kg of Neotame for non-alcoholic drinks. Deserts and
similar, and milk- and derivates- based products may use up to 32mg/Kg.
Confectionaries and others vary from 12 mg/Kg to 200 mg/Kg.
Erythritol
[2493]
Erythritol is a natural sugar alcohol (a type of sugar substitute). It is a
non-caloric sveetener. It has been approved for use in the United States and
throughout much of the world and in the EU. It was included in the positive
list with amendment of the EC Directive 94/35/EC.
It is 70% as sweet as table sugar and excellent-tasting, yet it is virtually
non-caloric, does not affect blood sugar, does not cause tooth decay, and is
absorbed by the body, therefore unlikely to cause gastric side effects unlike
other sugar alcohols. Under U.S. Food and Drug Administration (FDA) labeling
requirements, it has a caloric value of 0.2 calories per gram (95% less than
sugar and other carbohydrates), but other countries such as Japaqn label it at
0 calories.
Erythritol has been certified as toothfriendly. The sugar alcohol cannot be
metabolized by oral bacteria, and so does not contribute to tooth decay.
Interestingly, erythritol exhibits some, but not all, of the tendencies to
"starve" harmful bacteria like xylitol does. Unlike xylitol, erythritol is
actually absobed into the bloodstream after consumption but before excretion;
however it is not clear if the effect of starving harmful bacteria occurs
systemically at this stage. [998]
Erythritol occurs naturally in a wide variety of fruits, vegetables and
fermented foods. It has a crystalline appearance, taste and functionality
similar to sucrose, yet without the calories.
[999]
Replacing sugar with low-calorie sweeteners is a common strategy for
facilitating weight control. However, arguments arise saying that intense
sweeteners increase appetite for sweet foods, promote overeating, and may even
lead to weight gain. Bellisle and Drewnowski in a review published in 2007
related to studies focused on energy density, satiety and the control of food
intake stress that weight loss is best achieved by a combination of reducing
caloric intake, lowering energy density of the diet, increasing physical
activity, and sweeteners may help a lot.
The authors concluded that low-calorie (or no-calorie)sweeteners may be of
help in resolving the obesity problem. However, new studies reopens the
discussion related to the effect of sweeteners:
[1000]
Energy-containing beverages have been implicated in the increasing incidence
and prevalence of overweight and obesity. In 2006 Dr. R.D. Mattes from the
University of Purdue wrote that epidemiological data indicates that caloric
beverage consumption is positively associated with energy intake and body mass
index. Caloric beverages elicit weak satiety and compensatory dietary
responses, this being attributed to the components of beverages (e.g.,
carbohydrate form). Other theories say that the limited appetitive and dietary
responses hold across beverage types.
Dr. Mattes concludes that the fluid medium rather than energy form or nutrient
composition is responsible. He recommends moderate consumption of energy from
beverages for example, substitution of one energy-yielding beverage for
another may be less effective than reducing intake or switching to lower or non-energy sources.
[1001]
Swithers and Terry Davidson observed in rats increased body weight gain,
energy intake, adiposity, decreases in core body temperature, and blunted
caloric compensation for sweet-tasting calories. This study was published in February 2008.
Animals may use sweet taste to predict the caloric contents of food. Eating
sweet noncaloric substances may degrade this predictive relationship, leading
to positive energy balance through increased food intake and/or diminished energy expenditure.
They concluded that consumption of products containing artificial sweeteners
may lead to increased body weightand obesity by interfering with fundamental
homeostatic, physiological processes.
A study on artificial sweeteners published in 2004 by Swithers and Davidson at
Purdue University suggested that artificial sweeteners may disrupt the body's
natural ability to "count" calories, and that sweetness in non-caloric or
low-caloric foods leads to a disregulation of food intake in humans. The
authors hypothesised hat experience with these foods interferes with the
natural ability of the body to use sweet taste and viscosity to gauge caloric
content of foods and beverages [1002]
The 2004 Purdue study was strongly criticised by the National Soft Drink
Association. The group cited researches conducted by Blackburn, Birch et al
(1989) and Anderson et al (1989) that found replacing sugar with a high
intensity sweetener in foods or beverages does not affect food intake or hunger in children.
[1003]
Beth Hubrich from the Calorie Control Council says that the study 2008
Purdue study oversimplifies the causes of obesity. She blames increasing
portion sizes of foods, decreasing physical activity and increased overall
calorie intake for the increasing obesity epidemic.
[1004]
Several studies claim that artificial non-caloric and low-caloric sweeteners
promote weight gain as they disrupt the calorie prediction of the body and
its capability to react accordingly to the nutritional intake. According to
Tracy Hampton low-calorie sweeteners may promote weight gain.
Bellisle, Drewnowsku, 2007 in a review of studies about the effect of
low-calorie sweeteners presented inconclusive results.
[1005]
[1006]
Guido K.W. Frank and colleagues found that brain response distinguishes the
caloric from the non-caloric sweetener, however, the conscious mind could not
notice the caloric difference.
[1007]
According to Swithers and Davidson 2008 sweet taste of sugar is a predictor
of the caloric or nutritive consequences of eating. It evokes physiological
responses that underlie tight regulation. The authors say that non-caloric
sweeteners disrupt the validity as a caloric predictor, and contribute to
deficits in the regulation of energy.
They concluded that artificial sweeteners may lead to increased body weight
and obesity by interfering with positive energy balance through increased food
intake and/or diminished energy expenditure.
Non-caloric sweeteners such as saccharin, aspartame and sucralose and
low-caloric sweeteners such as sorbitol,mannitol and maltitol, should be avoided
in weight reduction diets. Intensive sweet tasting foods promote weight gain.
These recent findings support general nutritional rules which call for a change
of the nutritional habits. Changing from sweetened artificial flavoured foods
and beverages to fruits, vegetables and low fat foods together with exercise
will improve weight regulation and general health condition.
[1008]
Rodearmel and colleagues 2007 assessed two groups of the America on the Move
trial. One group was asked to walk an additional 2000 steps per day above
baseline measured by pedometers and to eliminate 420 kJ/day (100 kcal/day)
from their typical diet by replacing dietary sugar with a noncaloric
sweetener. A self-monitoring second group group was asked to use pedometers
to record physical activity but were not asked to change their diet or
physical activity level.
Both groups of children showed significant decreases in BMI for age. However,
the noncaloric sweetener group had a significantly higher reduction of BMI
compared with the self-monitor group.
The authors concluded that the small-changes approach advocated by America on
the Move could be useful for addressing childhood obesity.
E967 Xilit
E999 Quillaia extract
E1105 Lysozyme
E1200 Polydextrose
E1201 Polyvinylpyrrolidon
E1202 Polyvinylpropylpyrrolidon
Modified starch
: The name used for the ingredients list is "modified starch".
: The name used for the ingredients list is "modified starch".
: The name used for the ingredients list
is " modified starch".
Distarch phosphate has been requested for use up to 10g/l (reconstituted dry
powders) and 22g/l (liquids) in infant formulae and follow-on formulae for
infants and young children in good health and in FSMPs.
In its 1992 opinion the SCF recommended distarch phosphate should not be
permitted in infant formulae because the Committee would prefer to see direct
evidence indicating that infants can tolerate the 2.5% level of modified
starches then requested. The current request is for use up to 2.2%.
A concern was also raised that infants could develop fermentative diarrhoea or
modification of the gut flora. No new information on these aspects have been
found. Furthermore, the Committee is not persuaded there is a need for use
of distarch phosphate in instant formulae generally. The Committee does not
consider that the use of distarch phosphate is acceptable in infant formulae,
follow-on formulae for infants and young children in good health and in FSMP.
[3514]
: The name used for the ingredients list is " modified starch".
: The name used for the ingredients list is " modified starch".
The name used for the ingredients list is " modified starch".
The name used for the ingredients list is " modified starch".
The name used for the ingredients list is " modified starch".
The name used for the ingredients list is " modified starch".
The name used for the ingredients list is " modified starch".
[3515]
Lockwood, King and Labonte studied the starch of white- and orange-fleshed
Beauregard sweet potato and the effects of amino acid additives, aspartic
acid, leucine, lysine, and methionine, on their pasting and thermal characteristics.
The authors found that starch from orange-fleshed sweet potato could easier be
cooked, had a lower retrogradation and stability during heating than the
white-fleshed sweet potato starch.
The addition of charged amino acids, aspartic acid and lysine, altered pasting
characteristics of the 2 starches more than the neutral amino acids, leucine and methionine.
The positively-charged amino acid, lysine and negatively charged aspartic
acid, decreased the viscosity of starch paste of orange-fleshed sweet potatoes
improving the cooking time.
Lysine increased the stability of orange-fleshed sweet potato starch during
cooking.
Aspartic acid had similar effects on both starches, reduced the cooking
stability and lowered retrogradation.
The authors concluded that the addition amino acids can be used to alter
properties of sweet potato starches can be altered. Blends of sweet potato
starches with amino acids may avoid the use of modified starches such as oxidyzed
starches, phosphate starches, or acetylated starches.
E1505 Triethyl citrate
E1518 Glyceryl triacetate
Vitamins are essential substances which act in very small quantities.
Under- or oversupply of vitamins bears serious dangers.To avoid misuse in food
production there were limits established by each country.
Germany has a limit for vitamin A of 1000 and for vitamin D 2,5
microgramms/100g food.
As sun incidence and the amount of natural vitamins in different geographical
regions throughout the world vary, each country has its own regulations.
France being nearer to the Equator and having thus a higher sun incidence as
Germany has a limit of vitamin A which is very low. Vitamin D is there not
allowed in order to avoid an oversupply.
[3516]
Michael Holick and colleagues found that vitamin D2 daily was as effective as
the same amount of vitamin D3 in maintaining serum 25-hydroxyvitamin D
levels and did not negatively influence serum 25-hydroxyvitamin D3 levels.
Therefore, vitamin D2 is equally as effective as vitamin D3 in maintaining
25-hydroxyvitamin D status. This study was performed in response to two
reports suggested that vitamin D2 is less effective than vitamin D3 in maintaining vitamin D status.
The European Union advises not to exceed 1000 mg of complementary vitamin C in
a daily personal feeding.
Other specific legislations exists and should be observed for each vitamin and
each kind of food.
[3517]
According to US surveys the intake of vitamin D is insufficient. Additional
food fortification as well as dietary and supplement guidance are needed for
the general population.
Vitamin D status differs by latitude and race and variation of the sunlight
during seasons, especially the winter month. Individuals with more skin
pigmentation are at increased risk of deficiency. It is synthesised in the body
on exposure to sunlight. Food can not supply sufficient amounts.
To reduce cancer risk, exposure to sunlight or artificial UVR sources should be
accompanied by abundant fruit and vegetables intake and/or antioxidants, not
smoking in order to help combat the free radicals generated from UVR exposure.
[3518]
According to the study published by Garland, a scientist of the University of
California Moores Cancer Centre, the vitamin D status differs by latitude and
race, with residents of the northeastern United States and individuals with
more skin pigmentation being at increased risk of deficiency.
The increased skin pigmentation of African-Americans reduces their ability to
synthesize vitamin D, turning them more susceptible to breast cancer, colon,
prostate and ovarian cancers as white women.
Vitamin D fortified foods are consumed to reduce the risk of osteoporosis. The
cancer risk reduction may become another important reason for the demand of
this vitamin The authors suggest that efforts to improve vitamin D status,
for example by vitamin D supplementation, could reduce cancer incidence and
mortality at low cost, with few or no adverse effects.
[]
Harald Dobnig and colleagues 2008 say that low 25-hydroxyvitamin D and
1,25-dihydroxyvitamin D levels are independently associated with all-cause and
cardiovascular mortality.
Thes authors write that these findings base on the correlation of low
25-hydroxyvitamin D levels of inflammation indicators (C-reactive protein
and interleukin 6 levels), oxidative burden (serum phospholipid and
glutathione levels), and cell adhesion (vascular cell adhesion molecule 1 and
intercellular adhesion molecule 1 levels).
The authors point out that urbanization, demographic shifts, decreased
outdoor activity, air pollution and global dimming, and decreases in the
cutaneous production of vitamin D with age may account for 50% to 60% of
people to have low vitamin-D status.
The minimum desirable serum level of 25-hydroxyvitamin D has been suggested to
be 20 to 30 ng/mL, and levels lower than this are clearly related to
compromised bone-mineral density, falls, and fractures and more recently have
also been linked to cancer and immune dysfunction, as well as cardiovascular
disease, hypertension, and metabolic syndrome, the authors report.
The study used data from the Ludwigshafen Risk and Cardiovascular Health
(LURIC) study which investigated the effect of genetic polymorphisms and
plasma biomarkers on cardiovascular health status.
[3519]
However, they stress that aside of the effect of low vitamin D status, other
factors may be associated with mortality including matrix metalloproteinases.
[3533]
Edward Giovannucci and colleagues in a study in 2008 found an association of low
levels of 25(OH)D with higher risk of myocardial infarction.
[3520]
Foregoing vitamin D studies said it could only reduce fracture risk in
combination with calcium. However, according to Heike A. Bischoff-Ferrari and
colleagues 2009 the prevention of nonvertebral fractures with vitamin D is
dose-dependent for individuals aged 65 years or older. The authors found that
a high supplemental vitamin D dose (482-770 IU/d) should reduce nonvertebral
fractures by at least 20% and hip fractures by at least 18%. The use of
low-dose vitamin D with or without calcium in the prevention of fractures
among older individuals is not being recommended by the authors, and greater
benefits may be achieved if vitamin D supplementation starts earlier.
[3521]
Bruce Ames and Joyce McCann in a critical review write that there is evidence
to suggest an important role for vitamin D in brain development and function.
The authors comment previous studies in both human and animal models which
indicate that inadequate levels of vitamin D may also produce cognitive or
behavioural consequences, although the evidence is not conclusive for the moment.
The authors conclude that despite residual uncertainty, recommendations for
vitamin D supplementation of at-risk groups, including nursing infants, the
elderly, and African-Americans appear warranted to ensure adequacy.
[]
Marian Evatt and colleagues 2008 report that Fifty-five per cent of patients
with Parkinson's disease had insufficient levels of plasma 25-hydroxyvitamin D
(25[OH]D). The authors wrote that low vitamin D levels may contribute to the
risk of developing Parkinson's disease.
The group with Parkinson's disease in this study presented a vitamin D serum
level of 31.9 ng/ml compared with 34.8 ng/ml of a group of Alzheimer's
disease and 37.0 ng/ml of healthy groups. The authors concluded that vitamin
D insufficiency may have a unique association with Parkinson's.
The researchers continue their study to see if a dietary supplement, or increased
exposure to sunlight may help alleviate symptoms or even retard progression of
the disease.
[3523]
Llewellyn and colleagues 2010 studied the connection between cognitive decline
and low levels of serum 25-hydroxyvitamin D (25[OH]D) using data of the
InCHIANTI study [3524] conducted in Italy between 1998 and 2006.
The Mini-Mental State Examination (MMSE) [3525] was used
to evaluate cognitive decline. Severe serum 25(OH)D deficiency were found
with levels
25 nmol/L), levels
25 to
50 nmol/L were considered as
insufficient, whereas levels of 25(OH)D
/=75 nmol/L were considered as
sufficient.
Evaluating their data, the authors state that low levels of vitamin D are
associated with substantial cognitive decline in the elderly population, and
status of vitamin D should be considered en treatment and prevention.
Data from the Third National Health and Nutrition Survey (NHANES III)
[3526] also show that vitamin D deficiency is associated with
an increased risk for cognitive impairment in older persons. According to Dr.
Llewellyn vitamin D seems to play a role in processes that may be important
for dementia risk, including vascular health and amyloid clearance from the brain.
Controversies
McGrath and colleagues 2007 also using data from NHANES III did not find an
association between vitamin D levels and cognitive performance. Llewelly says
that results of McGrath study may be related to methodology which used only
delayed verbal memory from the Mini-Mental State Examination (MMSE) and the
East Boston Memory Test. [3527]
Andrew Grey, MD, and Mark Bolland, in an editorial comment the study of
Llewellyn and colleagues, pointing out that it is unlikely that a single
vitamine could play such a substantial role in preventing diseases. The
authors say that it is more likely that low vitamin D is not the cause, but
only a marker of overall poor health, low sunlight exposure, low physical
activity, high adiposity. [3528]
[3529]
Overall, individuals with
1000 IU/day oral Vitamin D had 50% lower
incidence of colorectal cancer compared to reference values. Cedric F. Garland
urges for a prompt public health action to increase intake of Vitamin D
to 1000 IU/day, and to raise 25-hydroxyvitamin D by encouraging a modest
duration of sunlight exposure.
[3530]
A study leaded by Esther M. John found that the risk of prostate cancer was
reduced by 50 percent in men who had high levels of sun exposure during their
lifetimes, compared with men who had low lifetime levels. The findings of this
study support the hypothesis that sun exposure and vitamin D receptor (VDR)
polymorphisms together play important roles in the aetiology of prostate cancer.
The best source of vitamin D is from 20-30 minutes sun exposure. Long sun
exposure is discouraged due to the risk of skin cancer. Other authors find 5 to
10 minutes sun exposure on our face and arms during the summer time sufficient
to obtain the required daily amount of Vitamin D.
[3539]
Vitamin D supplementation in winter necessary
[3534] [3535]
[3539]
Dr Julie Wallace and researchers from the Northern Ireland Centre for Food and
Healthtogether with with colleagues from University College Cork to
investigate what level of dietary vitamin D is needed in winter.
According to Dr. Wallace higher levels of vitamin D fortification and
supplementation are needed. Large population groups are at risk of having not
sufficient supply of vitamin D. Foods which are good sources of vitamin D like
oily fish are not consumed regularly. The best source could be from fortified
foods and supplements.
Some authors point out that Asian children suffer insufficient levels of
vitamin D with , risk of osteoporosis.
Vitamin D2 is as effective as vitamin D3
Michael Holick and colleagues found that vitamin D2 daily was as effective as
the same amount of vitamin D3 in maintaining serum 25-hydroxyvitamin D
levels and did not negatively influence serum 25-hydroxyvitamin D3 levels.
Therefore, vitamin D2 is equally as effective as vitamin D3 in maintaining
25-hydroxyvitamin D status. This study was performed in response to two
reports suggested that vitamin D2 is less effective than vitamin D3 in
maintaining vitamin D status.
[3540]
Gordon and colleagues 2008 found that a low degree of vitamin D insufficiency
is widespread in US. The authors also stress that breastfed infants in winter
who did not receive vitamin D supplementation were the most severely vitamin D deficient.
The authors enforce the recommendations for health care providers and parents
to ensure that breastfed infants receive daily vitamin D supplementation for
the duration of breastfeeding
In this study older age, winter season, higher body mass index, black
race/ethnicity, and elevated parathyroid hormone concentrations were also
associated with lower vitamin D status. One-third of vitamin D-deficient
participants exhibited demineralization.
[3541]
Rovner and O'Brien 2008 found that there
is still insufficiency on vitamin D in children in the United States. The
authors efforts call for efforts to improve the vitamin D status of children.
[3542]
According to Kremer and colleagues 2010 vitamin D insufficiency
(25-hydroxyvitamin D) is linked to increased muscle fat and decreased muscle
strength. Approximately 59% of subjects were 25OHD insufficient (higher or
equal to 29 ng/ml). Serum 25OHD wasa found to inversely related to percent
muscle fat. The relation between 25OHD and muscle adiposity was independent
of body mass or visceral fat. The authors concluded that vitamin D
insufficiency is associated with increased fat infiltration in muscle young
women but stress that more studies are necessary before a supplementation can
be recommended.
In a study of 2009 the group around Kremer found that vitamin D insufficiency
is associated with increased body fat and decreased height but not changes in
peak bone mass. [3543]
[3544]
Lu Wang and colleagues 2008 investigated the associations of intake of dairy
products, calcium, and vitamin D with the incidence of hypertension trend. The
risk of hypertension decreased with high dietary calcium intake, but did not
change with calcium or vitamin D supplements, or with high-fat dairy products
for which the saturated fats in high-fat dairy products may my be responsible
for. High calcium intake facilitates weight loss and enhances insulin
sensitivity, which also contribute to blood pressure reduction.
The study concluded that intakes of low-fat dairy products, calcium, and
vitamin D reduced the risk of hypertension in middle-aged and older women,
suggesting their potential roles in the primary prevention of hypertension and
cardiovascular complications.
The study supports the 2005 Dietary Guideline from the US Department of
Agriculture recommending the intake of milk and milk products to three
servings per day and stresses the importance of low-fat dairy products.
[3545]
According to Cannell and colleagues 2008 the metabolic product of vitamin D is
a potent, pleiotropic,repair and maintenance, secosteroid hormone. Vitamin D
deficiencies are common, standing for a host of diseases other than cancer.
Daily ingestion of 1100 IU of colecalciferol (vitamin D) over a 4-year period
were suggested to reduced the incidence of non-skin cancers. The authors
stress that official recommendations were never designed and are not effective
in preventing or treating vitamin D deficiency.
Diagnosis of vitamin D deficiency
The authors say that assessing serum 25-hydroxy-vitamin D is the only way to
make the diagnosis and to assure that treatment is adequate and safe.
They recommend that the of serum levels of 25-hydroxy-vitamin D should be
raised
40 ng/ml, year around, which is the level found in humans living
naturally in a sun-rich environment. Sunlight, artificial ultraviolet B
radiation or supplementation are being suggested by the authors which say that
benefits of all treatment modalities outweigh potential risks.
Cannell and colleauges suggest a supplementation of
5000 IU (125
microg) of vitamin D/day for obese, aged and/or dark-skinned patients to
maintain adequate levels during the winter at many temperate latitudes
[3546]
Both forms of vitamin D (D
and D
) used in supplementation had been
regarded as equivalent and interchangeable.
However, according to Lisa A Houghton and Reinhold Vieth, ergocalciferol
(Vitamin D
should not be regarded as a nutrient suitable for
supplementation or fortification because it is less efficient in raising serum
25-hydroxyvitamin D, its metabolites have a diminished binding to vitamin D
binding protein in plasma, and a nonphysiologic metabolism and shorter shelf
life compared with cholecalciferol (vitamin D
).
Consumer should look at the ingredient list of fortified foods such as
margarine, cereals and probiotics for good cholecalciferol (vitamin D)
[3546]
[3536]
The 25-(OH)D is the major circulating vitamin D metabolite found in human
serum and is determined by diet and exposure to sun. Several recent studies
advocate a high level of vitamin D to reduce risk of coronary and other
diseases, such as pancreatic cancer. Pancreatic cells express 25-(OH)
D(3)-1alpha-hydroxylase that generates the biologically active
1,25-dihydroxy(OH)(2) D form, and a high vitamin D status may affect the cells
of the pancreas. Stolzenberg-Solomon 2009, however, cites a nested
case-control study conducted in a population of male Finnish smokers which
showed a 3-fold increased risk for pancreatic cancer with high vitamin D
status. This study was conducted in male smokers, limiting therefore its
conclusions to this group. The author writes that there are more studies
necessary to make a final conclusion on the association of vitamin D and
pancreatic cancer.
[3537]
In a nested case-control study in the Prostate, Lung, Colorectal, and Ovarian
Screening Trial cohort of men and women prediagnostic serum 25(OH)D
concentrations study Stolzenberg-Solomon and colleagues found no association
of Vitamin D with pancreatic cancer overall. This study could not support the
strong positive association of 25(OH)D and pancreatic cancer of the foregoing
Finnish study. However, increased risk of pancreatic cancer was found in
persons with low solar exposure, but not in those with moderate to high
annual exposure, which is similar to the Finish study.
[21]
[] [3535] [3539]
Several recent epidemiological studies demonstrate reduced bone density and
increased rates of bone loss in individuals habitually consuming low protein
diets.
In short term studies Women's Health Research at Yale found that a low animal
and plant protein diet caused levels of certain hormones (calcitropic
parathyroid hormone (PTH) ) to rise, which act to stimulate bone breakdown to
compensate for the calcium it was not getting from the diet.
The calcitropic hormones were NcAMP, Midmolecule PTH, Intact PTH and
calcitriol.
Replacing all meat and animal proteins with soy foods, the low soy protein diet
seemed to interfere with intestinal calcium absorption to an even greater
extent than did the low mixed source protein diet. Should this be confirmed in
ongoing studies, inclusion of additional calcium when consuming soy foods
will prove to be necessary.
[3547]
A novel sunscreen-antioxidant was developed by Damiani and colleagues contains
the UVB absorber, 2-ethylhexyl-4-methoxycinnamate (OMC) combined with the
piperidine nitroxide TEMPOL, which has antioxidant properties. This sunscreen
could reduce the risk of melanoma caused by sun exposure.
[3555]
According to DeAnn Lazovic and colleagues 2010 the use of indoor tanning devices
increases the risk of melanoma by 74 percent if tanning beds are used for any
amount of time. Frequent uses of tanning beds increases melanoma risk 2.5 to 3
times compared with persons who never use it. Frequent users of indoor tanning
beds ( 50 plus hours, more than 100 sessions, or for 10-plus years.) are 2.5 to 3
times more likely to develop melanoma than those who never use tanning devices.
The risk was directly related to the time spent tanning. These findings were
independent of the type of tanning device, gender or age, contradicting previous
studies of Cokkinides and the position of the American Cancer Society which
say that indoor tanning before the age of 35 years increases the risk of
melanoma.
The study of Cokkinides and colleagues 2010
refers to the meta analysis which says that indoor tanning use before the age
of 35 years increases the risk of melanoma. These believes leaded to state
legislation restricting minors' access to indoor tanning.
[3556]
The American Cancer Society
says that using a tanning bed before age 35 increases a person's risk of
developing melanoma by 75 percent. Physicians hope that recent actions by the
FTC, along with TMA-supported state legislation placing age restrictions on
minors' use of tanning beds, will spur the tanning industry to operate more
responsibly and stop spreading false information to the public.
[3557]
Public health implication of tanning beds
[3558]
Tanning bed proponents claim that vitamin D supplementation supports indoor
tanning health effect. They support the theory that reduced vitamin D levels
or certain vitamin D receptor polymorphisms may increase melanoma risk.
Woo and Eide 2010 clarify that ultraviolet A is used by most tanning devices.
This light is relatively ineffective in stimulating vitamin D synthesis. Health
benefits from this association is therefore significant. The authors stress,
therefore, the importance of education of the general public and a stricter
indoor tanning legislation to reduce public health risks.
[3559]
The proposed Tanning Bed Cancer Control Act intends to regulate the use of
tanning beds. It proposes a limit on the amount of UV rays emitted by a tanning
bed and how long someone can be exposed to them, along with an age limit of over
18.
[3560]
Incidence rates of skin cancer are rising in Great Britain. Some occupations are
exposed to sunlight, such as farmers, construction workers and some public
service workers. Young 2009 found a clear association between solar radiation and
skin cancer and calls for protective measures to reduce the burden of
occupational skin cancer in Great Britain.
[3531]
According to Dr. Anthony Norman of the University of California, Riverside and
there are evidences that vitamin D, when converted into a hormone, promotes
the normal growth of cells and has anticancer properties rising the interest to
develop the vitamin D hormone or analogues for use in cancer treatment vitamin
D hormone to decrease the proliferation of cells and control malignant cell
growth.
[3561]
According to the paediatrician Dr. Tamer Adham the children over eight years
old in the United Arab Emirates (UAE) need 15-20 minutes of exposure to
sunlight per day because they often have a high level of vitamin D deficiency
due to lack of exposure to sunlight in this region. This may be due to clothing
habit of the region.
Other authors recommend 2000 IU, equal to the so-called upper safe limit,
however, scientists do not recommend taking high doses of the vitamin warning
against increased calcium blood levels and kidney problems.
[3548]
Bo-Ying Bao from the University of Rochester and Taipei Medical University
found evidences that indicate that vitamin D, in the form of the highly active
1 alfa, 25-dihydroxyvitamin D
(1,25-VD) suppresses prostate cancer
progression by inhibition of tumour growth and metastasis. Vitamin D acts
inhibiting the function of protease enzymes that are involved in tumour
invasion.
These findings support the idea that vitamin D-based therapies might be
beneficial in the management of advanced prostate cancer.
Bo-Ying Bao found that 1,25-Vitamin D decreased matric metalloproteinases
(MMP-9) and cathepsins (CPs), while it also increased the activity of their
counterparts, tissue inhibitors of metalloproteinase-1 (TIMP-1) and cathepsin
inhibitors. 1,25-VD did not suppress MMP-9 expression at the transcriptional
level, but reduced its mRNA stability.
[3549]
Elina Hypponen and Chris Power in a British study found significantly higher
concentrations of vitamin D in persons which used vitamin D supplements or
oily fish, but were not significantly higher in participants who consumed
vitamin D-fortified margarine than in those who did not. The authors conclude
that the prevalence of hypovitaminosis D in the general population was
alarmingly high duringthe winter and spring, which warrants action at a
population level rather than at a risk group level.
Julia Knight and colleagues found, in an epidemiological study, that reduced
breast cancer risks were associated withincreasing sun exposure cod liver oil
use and increasing milk consumption for more than 10 glasses per week from
ages 10 to 19 but less in ages 20 to 29, no evidence was found for ages 45
to 54. The authors conclude that vitamin D could help to prevent breath cancer
in early life, particularly during breast development, but found reduced and
even no such effect in higher ages. [3550]
Evidences for a better survival of patients with non-small-cell lung cancer
due to vitamin D were reported by Wei Zhou and colleagues (2007). The
researchers investigated the results of circulating 25-hydroxyvitamin D
(25(OH)D) levels on overall survival (OS) and recurrence-free survival (RFS)
in early-stage non-small-cell lung cancer (NSCLC).
For the joint effects of 25(OH)Dlevel and vitamin D intake, the combined high
25(OH)D levels and high vitamin D intake were associated with better survival
than the combined low 25(OH)D levels and low vitamin D intake.. Similar
effects of 25(OH)D levels and vitamin D intake were observed for RFS. The
authors concluded that vitamin D may be associated with improved survival of
patients with early-stage NSCLC. [3551]
Evaluation of most relations of health and disease that involve vitamin D
leads to the conclusion that a desirable 25(OH)D concentration is
75 nmol/L
(30 nanog/mL). [3552] [3553]
Supplemental intake of 400 IU vitamin D/d has only a modest effect on blood
concentrations of 25(OH)D, raising them by 7-12 nmol/L, depending on the
starting point. To raise 25(OH)D from 50 to 80 nmol/L requires an additional
intake of about 1700 IU vitamin D/d.
The most advantageous serum concentrations of 25(OH)D begin at 75 nmol/L (30
ng/mL), and the best are between 90 and 100 nmol/L (36-40 ng/mL).
In most persons, these concentrations could not be reached with the current
recommendation of the Institute of Medicine of intakes are 200 IU/d from
birth through age 50 years, 400 IU for those aged 51-70 years, and 600 IU for
those aged
70 years.
Bischoff-Ferrari and colleagues suggest therefore in 2006 that an intake for
all adults of
1000 IU (40 microg) vitamin D (cholecalciferol)/d is needed
to bring vitamin D concentrations in no less than 50% of the population up
to 75 nmol/L. The authors stress that the implications of higher doses for
the entire adult population should be addressed in future studies.
[3552]
Based on these facts Reihold Veight an colleagues call for international
agencies such as the Food and Nutrition Board and the European Commission's
Health and Consumer Protection Directorate-General to reassess as a matter of
high priority their dietary recommendations for vitamin D, because the formal
nationwide advice from health agencies needs to be changed. [3554]
[3562]
A report of the DIPART (Vitamin D Individual Patient Analysis of Randomized
Trials) Group says that Vitamin D
plus calcium, but not vitamin D alone in doses of 10 to 20 μg, reduces the
risk for fractures and hip fractures. The link between vitamin D plus calcium
and a reduced risk for fractures is not affected by age, sex, fracture
history, or hormone replacement therapy. A better undestanding of the effect
od vitamin D is essential because fragility fractures are a significant source
of morbidity and mortality in older persons.
These ingredients give
taste,hide off flavour and permit standardisation of the taste of food.
They increase the value of the food bearing however the danger of excessive
consume.
According to labelling rules of the European Community aromes can be included
in the label without mentioning their origin. Artificial aromes and synthetic
aromes are found under this class.Natural aromes are more valuable as
artificial ones.They are more complex having therefore a better taste.The
composition of synthetic flavours is more simple in their composition as
natural ones. The taste is therefore not so specific.
Natural aromes are extracts of of spices such as vanilla
and orange peeling.
Aroma, identical with natural aromas
are synthetic origin.They have identical chemical structure of natural
aromas.
Artificial aromas are of synthetical origin.They are
not found in nature, for example: ethyl vanillin, methyl cumarine,resorcine
dimethyl ether.
[3563]
Nine smoke flavourings used in food production,were found not safe by the
European Food Safety Authority (EFSA). Safety concerns, and possible risk of
cancer could not be ruled out for one of those smoke flavourings. Only two
were found to be safe.
All these flavourings are currently, or have previously been, on the market
in the EU. They are added to meat, fish, cheeses, soups, sauces, drinks and
confectionery to give them a "smoked" flavour, as an alternative to
traditional smoking.
Of concern were TRADISMOKE A MAX, Scansmoke R909, Scansmoke PB 1110, SmokEz
C‐10, SmokEz Enviro 23, SmokEz Enviro 23, Zesti Smoke Code 10, AM 01, and
Fumokomp which presented insufficient data. Of no concern were Scansmoke
SEF7525 and Smoke Concentrate 809045. See the whole list
[3564] of assessed smoke flavourings and safety concerns
at:
http://www.efsa.europa.eu/en/ceftopics/doc/ceftable.pdf
All smoke flavourings are being assessed according to EU Regulation
2065/2003 to see if they are suitable for human consumption. They will only be
allowed for use in food if they are shown to be safe and are not a risk to health.
The Regulation 2065/2003EC states: " Because smoke flavourings are produced
from smoke which is subjected to fractionation and purification processes, the
use of smoke flavourings is generally considered to be of less health concern
than the traditional smoking process.
Several international regulations cover smoke flavourings because of the
concern about PAHs (Polycyclic Aromatic Hydrocarbons).
Summary of the Regulation EC 2065/2003: [3565] The chemical composition of smoke depends
among other things on the type of wood used, the method used for developing
smoke, the water content of the wood and the temperature and oxygen
concentration during smoke generation. Smoked foods in general give rise to
health concerns, especially with respect to the presence of polycyclic aromatic
hydrocarbons.
The production of smoke flavourings starts with the condensation of smoke. The
condensed smoke is normally separated by physical processes into a water-based
primary smoke condensate, a water-insoluble high-density tar phase and a
water-insoluble oily phase. The water-insoluble oily phase is a by-product and
unsuitable for the production of smoke flavourings.
The primary smoke condensates and fractions of the water-insoluble high density
tar phase, the "primary tar fractions", are purified to remove components of
smoke which are most harmful to human health. They may then be suitable for
use as smoke flavouring.
Smoke is generated from wood which has not been treated with chemical
substances during six month preceding felling. Herbs, spices, wigs of juniper
and twigs, needles and cones of picea may be added if they are free of
residues or chemical treatment. The source material is subjected to controlled
burning, dry distillation or treatment with superheated steam in a controlled
oxygen environment with a maximum temperature of 600
.
The smoke is condensed. Water and/or solvents may be added to achieve phase
separation. Physical processes may be used for isolation, fractionation and/or
purification to obtain the following phases:
It contains mainly
carboxylic acids, carbonylic and phenolic compounds, having a maximum content of:
benzo(a)pyrene 10
g/kg
benz(a)antracene 20
g/kg
This fraction precipitates
during the separation phase and cannot be used as such for the production of
smoke flavourings but only after appropriate physical processing to obtain
fractions from this water-insoluble tar phase which are low in polycyclic
aromatic hydrocarbons, already defined as "primary tar fraction" having a
maximum content of:
benzo(a)pyrene 10
g/kg
benz(a)antracene 20
g/kg
If no phase separation has occurred
during or after the condensation, the smoke condensate obtained must be
regarded as a water-insoluble high-density tar phase, and must be processed by
appropriate physical processing to obtain primary tar fractions which stay
within the specified limits.
Contamination of foods with PAHs can happen by environmental PAHs that are
present in air (by deposition), soil (by transfer) or water (by deposition or
transfer), and during processing and cooking. The major contributors to PAH
intake in the average diet are oils and fats, cereals, fruits and vegetables.
The waxy surface of vegetables and fruits can concentrate low molecular mass
PAH through surface adsorption and particle-bound high-molecular-mass PAH can
contaminate the surface due to atmospheric fallout.
Flavour enhancer intensify flavour of
food.Persons which are sensible to glutaminic acid may experience the "Chinese restaurant syndrome".There were related pressure on
brainsides, headache,stiffness of neck[50].
On rats flavour enhancer cause alterations of reproduction and retarded
learning.
Flavour enhancer potentiate voracity.
Flavour enhancer in human metabolism are transformed in uric acid which is
undesired. Animals like rats do not form uric acid from flavour enhancers
because they metabolise them as alantoine. Toxicological
tests on rats are therefore irrelevant. Glutaminic acid is part of the
proteins of our body. However there is a capital difference between glutaminic
acid bound in a sequence of proteins and glutaminic acid or their salts being
obtained synthetically. Glutaminic acid of the protein sequence is not free.
It is liberated during digestion and reaches the bloodstream slowly. Flavour
enhancer are already free and reach the bloodstream immediately in great
amount and may cause the above mentioned syndrome.[49]
People with the characteristic symptom should ask for food without glutamate.
Industry should reduce glutamate in their formulas and try to avoid completely
its use in dry soups,dry sauces and an infinity of other product which are on
market. Industry should return to natural ingredients avoiding synthetic other
products. In doing so there is also a benefit on marketing because the
products from natural resource have great acceptance by consumers. Please read
the list of ingredients on the label, carefully, especially those of dry
soups and dried sauces because they have a great amount of salts of glutamic
acid.
The INTERMAP study links glutamate to obesity
[51]
Consumption of the
flavour enhancer monosodium glutamate (MSG) may increase the risk of gaining weight, regardless of energy intake according to a study
on humans by Ka He and colleagues 2008.
The authors cite that animal studies indicate that monosodium glutamate (MSG)
can induce hypothalamic lesions and leptin resistance, possibly influencing
energy balance, leading to overweight.
In his study He found that people with an average intake of 0.33 g/day of MSG in
food preparation had an average BMI 23.5 kg per sq. m. and Non-MSG users had an
average BMI of 22.3 kg per sq. m. The authors concluded that prevalence of
overweight was significantly higher in MSG users than in non-users.
[52]
The Glutamate Association questions the study in a statement from 22.08.2008.
The Association says that according to data of the WHO the countries with
high intakes of glutamate do not have high population BMI.
The average person in the United States consumes approximately 11 grams of
glutamate daily from all food sources (primarily dietary protein), while the
body produces about 50 grams of free glutamate daily. Dietary glutamate from
MSG averages less than one half gram/person/day .
Human studies where MSG was added to the diet have failed to show changes in
body weight (Essed et al., Appetite 2007,48:29) [53]
A study on rats suggests that MSG in the diet actually suppresses body weight.
(Kondoh and Torii, PhysiolBehav2008,doi:10.1016/j.physbeh.2008.05.010)
[54]
E620 Glutamic acid
Glutamate has a neurotransmitter function in the physiology of nervous
cells.[55]
The neural function was used to promote selling of Intelligence Drugs to
improve marks at school
Unfortunately there was no such benefit.
E622 Potassium glutamate
E624 Monoammonium glutamate
E626 Guanylic acid
E627 Sodium guanylate
E629 Calcium guanylate
E630 Inosinic acid
E631 Disodium inosinate
E633 Calcium inosinate
E634 Calcium 5'ribonucleotid
E635 Disodium
5'ribonucleotid
E640 Glycine and salts
It is used as flavour enhancer in sweet product mainly together with
artificial sweetener s.It is used in chocolate, cakes and desserts.There is
doubt about ethylmaltol being responsible for talasemia (a rare anaemia).
It is a widely used substance. as medicine against gout and infections of the
urinary tract.It is also a vulcanisation accelerator and is used in the
chemistry of explosives.In food it is a donator of formaldehyd and is used to
to improve the optical appearance of food.At the moment it is used only in some
kind of cheese.
It is an antibiotic used in infections of mouth,foot and genitals.It is
employed in food industry to treat the shell of cheese. Resistance against this
antibiotic will soon be established in bacteria coming in contact with it.His
use should therefore forbidden in food industry
Antioxidants are used to improve the shelf life of food interfering in the
reaction of oxygen with different components of food avoiding their chemical
decomposition. They are used in soups,sauces in powder,chewing gum,dried
products of potatoes margarineoil, icecream.
The methods used to evaluate antioxidant activity of phytochemicals such as
food extracts, dietary supplements, fruits and juices are:
Oxygen radical absorbance capacity (ORAC):
ORAC is a method of quantitating the oxygen-radical absorbing capacity (ORAC) of
antioxidants in serum using a few microliter. The ORAC assay determines the total antioxidant capacity of a
sample which is estimated by taking the oxidation reaction to completion
when all of the nonprotein antioxidants (which include alpha-tocopherol,
vitamin C, beta-carotene, uric acid, and bilirubin) and most of the albumin in
the sample are oxidized by the peroxyl radical. Results are quantified by
measuring the protection produced by antioxidants. [387]
When comparing ORAC data, care must be taken to ensure that the units and food
being compared are similar. Some evaluations will compare ORAC units per grams
dry weight, others will evaluate ORAC units wet weight and still others will
look at ORAC units/serving. [388]
Marketing uses ORAC as a selling argument for concentrated supplements claiming
to be the number one ORAC product. However, there are no published the scientific
literature so are difficult to evaluate on these values. [388]
[389]
According to Bortolotti and colleagues total radical-trapping antioxidant parameter (TRAP)
is being proposed to measure antioxidant property of plasma of diabetes
patients. It may be either directly measured by a fluorescence-based method
(TRAPm) or calculated (TRAPc) by a mathematicalformula, taking into account
the serum levels of protein-bound SH (thiol) groups, uric acid, vitamin E, and vitamin C.
The authors found decreased TRAP levels in patients suggesting that antioxidant
defenses in diabetes are lower than normal. They conclude that TRAP is more
reliable than the measurement of each known antioxidants. In their research the
authors found a correlation between TRAPc and TRAPc values, and suggest TRAPc,
for routine assessment of oxidative stress in diabetic patients.
Trolox equivalent antioxidant capacity (TEAC)
[390]
The TEAC assay is based on the suppression of the absorbance of radical
cations of 2,2'-azinobis(3-ethylbenzothiazoline 6-sulfonate) (ABTS) by
antioxidants in the test sample when ABTS incubates with a peroxidase
(metmyoglobin) and H
O
. If the inhibition time is fixed at 3 min.
There is lack of correlation between TEAC and other assays. This may result
from underestimation of overall antioxidant capacity. Underestimation may be
related to the effects of dilution and to premature measurement of inhibition
percentage at a fixed time of 3 minutes.
Wang and colleagues conclude that the length of the inhibition time for the TEAC
assay must be taken into account when determining the total antioxidant capacity
of plasma, and that 30 min of inhibition is required for complete suppression of
ABTS radical formation in the TEAC assay. The results from the TEAC assay at 30
min were similar and correlated with the results obtained by the ORAC assay over
70 min.
Total oxyradical scavenging capacity (TOSC)
[391]
The total oxyradical scavenging capacity (TOSC) is based on the oxidation of
alfa-keto-y-methiolbutyric acid (KMBA) by 2,2'-azobis-amidinopropane (ABAP)
with the evolution of ethylene as the quantifiable end product.
MacLean and colleagues modified the development of the assay of Winston et al.
(Free Radical Biol. Med. 24 (1998) 480) and incorporated a standard curve
resulting in a simple but reliable method to quantify the total water-soluble
antioxidant capacity (TAC) of plant tissues such as apple fruit.
Peroxyl radical scavenging capacity (PSC)
[392]
Rui Hai Liu and colleagues developed an assay for assessing peroxyl radical
scavenging capacity (PSC) of both hydrophilic and lipophilic antioxidant
compounds and food extracts. It is based on the inhibition of
dichlorofluorescin oxidation by antioxidants that scavenge peroxyl radicals,
generated from thermal degradation of 2,2'-azobis(amidinopropane).
According to the authors the PSC assay is used to analyse or screen both
hydrophilic and lipophilic antioxidants or food extracts and will be a valuable
alternative biomarker for future epidemiological studies of chronic diseases.
Ferric reducing/antioxidant power (FRAP)
[393]
The ferric reducing antioxidant power (FRAP) assay determines directly the
reducing capacity of a compound. Firuzi and colleagues used FRAP to study the
antioxidant activities of 18 structurally different flavonoids. In this study
it was found that the o-dihydroxy structure in the B ring and the 3-hydroxy
group and 2,3-double bond in the C ring give the highest contribution to
the antioxidant activity. [393]
Woodrow and colleagues used the FRAP assay, standardized against plant
flavonoids and ascorbic aci, to quantify total antioxidant power in fruit
samples, such as currants (Ribes nigrum), gooseberries (Ribes grossularia),
raspberries and blackberries (Rubus spp.). Black currant demonstrated the
highest antioxidant activities followed by raspberries and gooseberries.
Furthermore, the authors found that some wild Rubus species exhibited activities
significantly higher than the cultivars. [394]
DPPH free radical method
[395]
Zheng DeYong and An XinNan presented a method for determining
1,1-diphenyl-2-picryl-hydrazyl (DPPH) free radical scavenging activity of natural
antioxidants. The DPPH free radical scavenging activity of 21 species of
cluster-bamboo's leaf were determined.
New cellular antioxidant activity (CAA) assay
[396]
Kelly Wolf
and colleague developed the cellular antioxidant activity (CAA) assay using
the bioactivity inside human hepatocarcinoma HEPG2 cells, which relies on
cellular biological activity rather than chemicalreactions which may not
mirror reactions inside a living cell.
Dichlorofluorescin trapped within HEPG2 cells is subjected to oxidation by
2,2'-azobis(2-amidinopropane) dihydrochloride (ABAP)-generated peroxyl
radicals. During the oxidation fluorescent dichlorofluorescein (DCF) and
cellular fluorescence is produced. The difference between the fluorescence of
control cells and those which with added solution of the foods on test
indicates the antioxidant capacity of the compounds. Results of CAA assay are
expressed in micromoles of quercetin equivalents per 100 micromol of
phytochemical or micromoles of quercetin equivalents per 100 g of fresh fruit.
The CAA values from phytochemicals decreased from quercentin, kaempferol,
epigallocatechin gallate (EGCG myricetin, luteolin, gallic acid, ascorbic
acid, caffeic acid, to catechin.
The CAA values decreased from Blueberries, craberry, apples, red grapes to green
grapes. The authors conclude that the CAA assay is more biologically relevant
than known chemical reaction because it considers uptake, metabolism,
distribution and location of antioxidant compounds within cells.
There are two main antioxidants classes:
- Enzymatic Antioxidants:The most important enzymatic
antioxidants are superoxide dismutase, glutathione peroxidase, and catalase.
which are inherent to cell biochemistry and cannot be supplied by intake of
food and supplements.
- Non-Enzymatic Antioxidants: Vitamins E and C, and b -carotene
are supplied by intake of food and supplements.
Vitamins as dietary supplements:
There are many dietary supplements being sold at
supermarkets.The prices differ enormously.The amount of vitamins are almost the same and cannot
justify the difference of price between the products.
Some products have minerals and other trace elements varying from product to product.Their
benefit should be analysed considering the local nutritional habits.
It is is very difficult to establish general rules concerning the amount of
daily supplements to be taken because of different nutritional habits. To
explain these problems the case of selenium, potassium, magnesium and vitamin
A is here cited:
- Selenium is an essential part in the building of
glutathione peroxidase. An undersupply of
selenium causes diseases. An oversupply of selenium causes on his turn serious
harm. Fish and meat bears much selenium and vegetables very little of it.
Therefore a well balanced nutrition is important, and vegetarians should
consider to take selenium as dietary supplement.[397]
[398]
Christine D Thomson and colleagues 2008 assessed the bioavailability of
selenium from Brazil nut, compared with seleniumethionine used to fortify
foods and in dietary supplements. They found that the consumption of 2 Brazil
nuts daily is as effective for increasing selenium status and enhancing GPx
activity as 100
g Se as selenomethionine. The
authors suggest to include Brazil nut in the diet to avoid to fortify foods or
use supplementation of selenium in New Zealand.
This would also benefit residents in Europe where the recommended daily
intake (RDI) is 65 micrograms. The selenium intake in UK is estimated to have
fallen from 60 to 34 micrograms. on account of reduced import of selenium
rich wheat from U.S.
[399]
However, an unhampered consume of Brazil nuts should consider the high
radiactivity of the nut. According the UK DEFRA, among other foodstuffs,
Brazil nuts contain some of the highest levels of natural radioactivity, in
particular radium-226 and radium-228. The consumption of a 100g bag (about
30-40 nuts) per week (about 5 nuts a day) throughout the year would give rise
to an annual dose of 0.2 mSv.
Ingestion and inhalation of long-lived natural radionuclides are estimated to
give rise to an average annual dose of 0.27 mSv.
Potassium and magnesium stabilises
heart rhythmic disturbaces. Both minerals should be supplemented up to 50% from the
normal daily intake of 2-3 grams for potassium and 200-350 milligramme
for magnesium. People with this kind of disorder need therefore
supplementation of these minerals. Normal people can supply the minerals out
of a balanced nutrition.[400]
Vitamin A is important for the north and the south of the globe because
of having less sun incidence. People living near the equator don't have to
bother supplementing with vitamin A. Because of high incidence of sunlight
boosting biological synthesis of vitamin A of the body in these countries one
fears an hypervitaminosis of vitamin A. Therefore regulations in these
countries forbid adding vitamin A to food.
[401]
[402]
EFSA's AFC Panel has issued an unfavourable opinion on vanadium
containing compounds which may be added for nutritional purposes in foods for particularly
uses and foods (including food supplements) intended for the general
population. The assessed compounds were vanadium citrate, bismaltolato oxo
vanadium and bisglycinato oxo vanadiumand vanadyl sulphate, vanadium pentoxide
and ammonium vanadate. The non-vanadium constituents of these sources of
vanadium are of no safety concern at the levels considered in this opinion.
However, according to the FSA NDA Panel vanadium itself present various toxic
effects, and a tolerable upper intake level could not be established in lack
of appropriate data.
The bioavailability of vanadium from five of these six compounds is higher
than that of vanadium absorbed from the normal diet. Consequently consumers
could be exposed to higher levels of vanadium through products containing
these five compounds than from a normal diet.
The Panel concluded that the safe use of the six sources for vanadium added to
foods intended for the general population, including food supplements, and foods
for particular nutritional uses, could not be established.
[403]
These sources for vanadium are not included in the list of vitamin and
mineral substances which may be used in certain foods including food
supplements. However they have been allowed to remain in use in Member States
of the European Union.
Vanadium forms are typically used as a dye and colour-fixer in foods and
supplements. Vanadyl sulfate, has been used to increase insulin sensitivity in
supplements and has therefore been targeted at diabetes sufferers and the
body-building market.
Occurrence of vanadium in food, food supplements:
According to the UK Food Standards AgencyBeverages, fats,
oils, fresh fruits and vegetables contain the lowest levels of vanadium, whereas whole grains, seafood, meats
and dairy products contain more (0.005 - 0.03 mg/kg). A few foods, including
spinach, parsley, mushrooms and oysters, contain relatively high amounts of
vanadium (
0.10 mg/kg).
Vanadium is present in a number of multi-vitamin/mineral dietary supplements at
levels of approximately 0.025 mg per day. There are no licensed medicines
containing vanadium.
Exposure to vanadium
by inhalation may occur occupationally. In the production of vanadium pentoxide,
dust concentrations of the pentoxide can range from 0.1 to 30 mg/m
, and
concentrations of 0.5-5 mg/m
are not uncommon in the production of
vanadium metal and vanadium catalysts.
Vanadium
has not yet been proven to be an essential trace element for mammals. There is no
evidence to suggest that the vanadium we get from food is harmful. It is unlikely
that we need vanadium for good health and too much could be harmful.
No specific function has been identified for
vanadium in higher animals. In vitro and animal studies suggest that vanadium may
function as an oxidation-reduction catalyst, and may regulate the sodium,
potassiumadenosine triphosphatase enzyme, however, this has not been proven.
In humans, the reported signs of deficiency
are questionable, although it has been suggested that low intakes may be
associated with cardiovascular disease.
Although no
specific data have been identified, it is possible that vanadium may interfere
with the storage and metabolism of iron, because absorbed vanadium is bound to
transferrin.
Intestinal absorption of vanadium is
low, less than 5%. The mechanism of absorption has not been defined.
Absorbed vanadium is mainly transported in the
plasma, associated with transferrin. Concentrations reported in human blood
vary widely, with levels in whole blood and serum in the range of 0.01 - 0.4 mg/L.
The concentrations in all tissues are low, but are higher in the liver, kidney
and lung. Vanadium is also present in breast milk and saliva and passes through
the blood brain barrier. Small amounts have been identified in the placenta.
Based on animal studies, bones and teeth retain the highest concentrations of
vanadium.
Ingested vanadium is predominantly eliminated unabsorbed
via the faeces. Absorbed vanadium is mainly excreted via the urine.
The toxicity of vanadium compounds increases as
valency increases, V5+ being the most toxic. In humans, exposure by inhalation
causes diverse toxic effects on the respiratory, digestive, and central nervous
systems, the kidney and skin. There are very few reported cases of vanadium
toxicity in humans, when it is taken by mouth.
Supplementation of human volunteers with
vanadyl compounds at oral doses of 50-125 mg/day caused cramps, loosened stools
and "green tongue" in all patients, and fatigue and lethargy in a minority.
Orally administered vanadium has low overt toxicity, but
is reported to have adverse effects on reproduction and development in both males
and females. There is some evidence of increased pre and post-implantation foetal
loss and significant accumulation of vanadium in the foetus. Skeletal anomalies
and reduced ossification in the offspring, as well as an increased incidence of
cleft palate have been reported.
Lifetime studies in animals
indicate that vanadium is not carcinogenic. Positive results have been obtained
in some in vitro mutagenicity tests.
Food Mean: 0.013 mg/day (1980 UK TDS)
Supplements up to 0.025 mg/day (Annex 4)
Drinking Water 0.01 mg/day (estimated from 0.005 mg/L, WHO 1988)
Estimated maximum daily intake 0.013 + 0.025 + 0.01 = 0.05 mg/day
The table below gives some information about the usual products on the
German market:
| Ingredients |
Centrum |
Multibionta |
Multivitamin
Krüger |
Hermes Multivit |
| Vitamin A |
800 g |
- |
- |
- |
| Provitamin A |
- |
- |
- |
2 mg |
| Vitamin E |
10 mg |
12 mg |
10 mg |
12 mg |
| Vitamin C |
60 mg |
300 mg |
60 mg |
75 mg |
| Vitamin K1 |
30 g |
- |
- |
- |
| Vitamin B1 |
1,4 mg |
1,3 mg |
1,4 mg |
1,6 mg |
| Vitamin B2 |
1,6 mg |
1,7 mg |
1,6 mg |
1,8 mg |
| Vitamin B6 |
2,0 mg |
1,8 mg |
2,0 mg |
2,1 mg |
| Vitamin B12 |
1 g |
3 g |
1 |
3 g |
| Vitamin D |
5 g |
- |
- |
- |
| Biotin |
150 g |
30 g |
0,15 mg |
30 g |
| Folic acid |
200 g |
150 g |
200 g |
160 g |
| Nicotinamid |
- |
18 mg |
18 mg |
- |
| Niacin |
18 mg |
- |
- |
20 mg |
| Pantothenate |
6 mg |
8 mg |
6,0 mg |
6,5 mg |
| Calcium |
162 mg |
- |
- |
100 mg |
| Phosphate |
125 mg |
- |
- |
- |
| Iron |
4 mg |
- |
- |
- |
| Magnesium |
100 mg |
- |
- |
- |
| Iodine |
100 g |
- |
- |
- |
| Potassium |
40 mg |
- |
- |
- |
| Chloride |
36,3 mg |
- |
- |
- |
| Copper |
1 mg |
- |
- |
- |
| Manganese |
1 mg |
- |
- |
- |
| Chromium |
25 g |
- |
- |
- |
| Molybdenum |
25 g |
- |
- |
- |
| Selenium |
25 g |
- |
- |
10 g |
| Silicium |
2 g |
- |
- |
- |
| Zinc |
- |
- |
- |
2 mg |
| |
|
|
|
|
Food supplements should have a ratio of half as much magnesium as calcium. A
daily intake of 1.200 mg calcium needs 600 mg of magnesium[405].
Provitamin A can be modified by the body to vitamin A.This happens only to the
extent of need. Therefore one says provitamin A to be a safe source of
vitamin A bearing no danger of overfeeding.
Hipervitaminosis of vitamin B1 may lead to nervousness and headache.
There is no maximum limit for vitamin B2.Even in high dose there are no
undesired reactions.
Accentuated hipervitaminosis of vitamin B6 causes alterations of the
mobility,numbness and psychical alterations.Alterations similar to
contergan in neonates were also observed.
The UK Committee on Toxicity of Chemicals in Food recommend not to exceed 10
mg per day.
A sufficient supply of vitamin B6 is guaranteed with consumption of
meat,fish,eggs, and some vegetables. Some food supplements contain up to 100
mg.The Committee tries to organise a voluntary producer limit of vitamin B6 in
food supplements and include more informations on label.The commission is
concerned about possible damage of the nervous system in case of high dose.
There are no major problems noted by excessive consumption of vitamin B12. A
predisposition to thrombosis is possible.
Niacin is a global denomination of nicotinic acid and her
acid amid denominated as nicotinamide, also called
niacinamide.Both vitamins have same properties.
Nicotinamide is important to the transport of electrons in cells and is
engaged in the following reactions:
- Anaerobic glicolysis
- In the cycle of cancer (oxidative phosphorilation)
- In the synthesis of fatty acids.
Nicotinic acid and nicotinamide can be assimilated directly or are created
by hydrolysis of coenzyme. Adenine is transformed in NAD(P) in the liver.
NAD(P) stands for Nicotinamide-AdenineDinucleotide-Phosphate.
To synthesises NAD in human cells 60 mg of tryptophane corresponding to 1 mg
equivalents of nicotinamide are necessary.For this reason the unit " niacin equivalent " was created.
1 niacin equivalent = 1 mg niacin = 60 mg tryptophane
Niacin is not deposited. Poisonings resulting from
excessive addition of niacin to food are documented.Symptoms are
ictericia, failures of liver, icteric skin with burning flushes. Toxic reactions
were not noted after daily intake of 3 to 6 grams of nicotinic acid trying to
inhibit the production of hepatic VLDL causing parallel dilatation of the
peripheric vascular system producing the red flush which disappears after some
days.
Nicotinamide does not produce flush and does not reduce cholesterol.
It is therefore that nicotinamide is being used in treatment of insufficiency
of niacin, using dose between 50 to 250 mg/day.
Niacin is present mainly in animal food (meat)as coenzymes.
Absorption of Niacin from meat is near 100%.The amount of niacin in plants is
very low.
In cereals niacin is being found in the aleurone coat (external coat of the
grain). Niacin is lost during polishing of grains to obtain white flour.
In cereal niacin is bound as a complex in macromolecules
niacitine, therefore only 30% of vegetable niacin can be assimilated.
Triptophane is sometimes much higher as free niacin, therefore the equivalent
of niacin is being used. In vivo conversion of triptophane in niacin depends
on coexistence of vitamin B6.
| Food |
mg niacin in 100 g |
| Meat |
5 to 11 |
| Fish |
3 to 4 |
| Sardine |
9,7 |
| Tuna |
8,5 |
| Mackerel |
7,5 |
| Milk |
0,09 |
| Butter |
0,03 |
| Cheese |
1,2 |
| Black bread |
3,3 |
| White bread |
0,9 |
| Lentil |
2 |
| Soya meal |
2,2 |
| Sunflower seed |
4 |
| Yeast, dry |
45 |
| Yeast, fresh |
17 |
| Fruits |
0,65 |
| Vegetables 0,6 to 2,0 |
|
| Coffee, ground |
13,7 |
| Group |
babies |
children |
men |
women |
| Under 4 month |
5 |
|
|
|
| From 4 to 12 month |
6 |
|
|
|
| From 1 to 4 years |
|
9 |
|
|
| Over 4 and under 7 years |
|
12 |
|
|
| From 7 to under 10 years |
|
13 |
|
|
| From 10 to 13 years |
|
|
15 |
14 |
| From 13 to under 15 years |
|
|
20 |
16 |
| From 15 to under 19 years |
|
|
20 |
16 |
| From 19 years and up |
|
|
18 |
15 |
| Pregnant |
|
|
|
17 |
| During lactation |
|
|
|
20 |
[826]
Transglutaminase is an enzyme which polymerizes
proteins with the result of a network like structures. This effect is used in
the production of meat, sausages, cheese, yogurt and related products, ice
creams and production of gelatin improving consistency and cream character of
the products.
[827]
Ice-structuring proteins (ISPs) in edible plants and fish that need to protect
themselves against freeze damage. ISPs have potential applications in a number
of areas including cryopreservation and frozen foods manufacture.
ISP type III HPLC 12 being of particular interest. No evidence of a genotoxic
potential or notable subchronic toxicity were found by T. Hall-Manning during a
safety evaluation of ice-structuring protein (ISP) type III HPLC
12.[828]
Anti-freeze protein, also called "ice structuring proteins" (ISPs) found in
Ocean Pout (Marcrozoarces americanus) has been approved for use as ice
structuring proteins in ice cream improving flavour and texture of the product
using less sugar and fat. It is obtained from the fermentation of a
genetically modified food grade yeast (Saccharomyces cerevisiae). This affects
a huge market of dairy ice cream, milk ice, water ice, fruit ice, sorbets,
frozen deserts and any similar products.
Professor Malcolm Hooper from Sunderland University, Professor Joe Cummins from
the University of Western Ontario in Canada, and Dr Mae-Wan Ho, director of the
Institute of Science in Society are against EU approval of ISP alleging that it
could cause serious allergies. They say Unilever tests with people allergic to
cod, not to ocean pout were insignificant.
AFP claims that their antifreeze proteins type III are all purified from their
natural sources cold ocean teleost fish.
[829]
Ice structuring proteins (ISPs) are naturally produced by a variety of living
organisms - including certain fish, plants and vegetables - to help them cope
with very cold environments by lowering the temperature at which ice crystals
form.
A joint opinion on the EFSA found these proteins to be safe for use in
foods. They will be added to ice cream in order to control the formation of
ice crystals during manufacture permitting a creamy consistency with lower fat
content. The technique involves production of the isolated proteins using a
genetically modified strain of baker's yeast. The protein produced does not
contain any residual modified yeast cells or detectable recombinant DNA.
EFSA's NDA and GMO Panels concluded that the proposed use of ISPs - in ice
cream at no more than 0.01% of weight - is safe subject to the specification
and production practices described by the applicant. The Panels found no
evidence of genotoxic activity in a variety of trials. Based on a range of
test results, the risk of an allergic reaction in fish-allergic people or the
population at large is considered very unlikely, as is the possibility that
allergic reactions to yeast allergens could occur due to eating the
ISP-containing products.
Ice structuring proteins are in common foods such as oats, rye, wheat, barley,
carrot, potato and cold water fish. No safety issues have been reported either
from consuming natural dietary sources or through the addition of ISPs to foods,
which is authorized in countries including the United States, Australia and New
Zealand.
The baker's yeast Saccharomyces cerevisiae. Strain CENPK338 has been used
since
2003 for commercial production of the ISP for use in non European ice cream
production. No gene encoding antibiotic resistance and no bacterial DNA were
introduced. From 2003 to 2007 more than 470 million ISP-containing edible ice
products have been sold in the USA and 47 thousand litres of ISP containing
ice cream has been sold in Australia/New Zealand. There have been no reported
safety issues.
With regards to the potential of adverse allergic reactions against yeast
allergens, the Panel considers it is unlikely that such reactions would occur
after ingestion of the ISP-containing products. The Panel concludes that the use
of the ISP type III HPLC 12 preparation at a maximum level equivalent to 0.01%
ISP type III HPLC 12 in edible ices is safe.
[830]
Enzymes play an increasingly important role in food production, and can be used
as alternatives to chemicals in improving the texture, appearance, nutritional
value and flavour of food, as well as helping in certain food production
processes (e.g. helping bread to rise). Currently food enzymes used as
processing aids are not covered by EU legislation. Member States' legislation
on food enzymes differs significantly, which can lead to problems for the
internal market and an unclear situation for the EU consumer.
Historically, food enzymes were considered to be non-toxic. However, the food
enzyme industry is continually striving to develop improved technology
resulting in the development of food enzymes which became through the years
more complex and sophisticated. There could be some potential hazards arising
from their chemical nature and source such as allergenicity, activity-related
toxicity, residual microbiological activity, and chemical toxicity. Therefore
safety evaluation of all food enzymes, including those produced by genetically
modified micro-organisms (GMOs), is essential in order to ensure consumer
safety.
Directive 95/2/EC on food additives other than colours and sweeteners allows
for the use of two enzymes as food additives: E1103 Invertase and E1105
Lysozyme.In addition, Council Directive 2001/112/EC relating to fruit juices
and certain similar products intended for human consumption, Council Directive
83/417/EEC relating to certain lactoproteins (caseins and caseinates) intended
for human consumption and Council Regulation (EC) No 1493/1999 on the common
organisation of the market in wine, regulate the use of certain food enzymes in
these specific foods.
Under the new proposed legislation, harmonised EU rules would be laid down for
the evaluation, approval and control of enzymes used in food. The draft
Regulation foresees the way to draw up an initial positive list of enzymes.
The proposal also includes requirements for the labelling of food enzymes other
than those used as processing aids. Food enzymes with a technological function
in the final food will have to be labelled as ingredients with their function
(e.g. stabiliser) and name.
[830]
In most cases food enzymes will be used as processing aids i.e. will be present
in food in the form of a residue, if at all and will have no technological
effect on the finished product. Taking into account that all food enzymes will
be assessed for their safety, it is proposed that food enzymes which are used
as processing aids are exempted from labelling.
Food enzymes used to exert a technological function in the final food, will be
labelled with their function (e.g. stabiliser etc) and specific name.
[831]
The Enzyme Commission number (EC number) is a
numerical classification scheme for enzymes, based on the chemical reactions
they catalyze. As a system of enzyme nomenclature, every EC number is
associated with a recommended name for the respective enzyme.
Every enzyme code consists of the letters "EC" followed by four numbers
separated by periods. Those numbers represent a progressively finer
classification of the enzyme. For example, the enzyme tripeptide aminopeptidase
has the code "EC 3.4.11.4", whose components indicate the following groups of
enzymes: EC 3 enzymes are hydrolases (enzymes that use water to break up some
other molecule), EC 3.4 are hydrolases that act on peptide bonds, EC 3.4.11
enzymes are only those hydrolases that cleave off the amino-terminal amino acid
from a polypeptide, and EC 3.4.11.4 are those that cleave off the
amino-terminal end from a tripeptide.
Strictly speaking, EC numbers do not specify enzymes, but enzyme-catalyzed
reactions. If different enzymes (for instance from different organisms)
catalyze the same reaction, then they receive the same EC number.
| Group |
Reaction
catalyzed |
Typical |
Trivial |
| |
|
reactions |
names |
| EC 1 |
To catalyse oxidation/reduction |
AH + B -A+ |
Dehydrogenase, |
| Oxyreductases |
reactions; transfer of H and O atoms |
BH (reduced) |
oxidase |
| |
or electrons from one substance |
A + O - AO |
|
| |
to another |
(oxidized) |
|
| EC 2 |
Transfer of a functional group from one |
AB + C - A
+ |
Transaminase, |
| Transferases |
substance to another. The group may |
BC |
Kinase |
| |
be methyl-, acyl-, amino- or phospate |
|
|
| |
group. |
|
|
| EC 3 |
Formation of two products from a |
AB + H O - |
Lipase,
amylase, |
| Hydrolases |
substrate by hydrolyses |
AOH + BH |
peptidase |
| EC 4 |
Non-hydrolytic addition or removal of |
RCOCOOH - |
|
| Lyases |
groups from subnstrates. C-C, C-N, C-O |
RCOH + CO |
|
| |
or C-S bonds may be cleaved |
|
|
| EC 5 |
Intramolecule rearrangement, i.e. |
AB - BA |
Isomerase, |
| Isomerases |
isomerization changes within a single |
|
mutase |
| |
molecule |
|
|
| EC 6 |
Join together two molecules by |
X + Y + ATP -> |
Synthetase |
| Ligases |
sythesis of new C-O, C-S, C-N or C-C |
XY + ADP + Pi |
|
| |
bonds withg simultaneous breakdown of |
|
|
| |
ATP |
|
|
[832]
UniProt is the universal protein database, a central repository of protein data
created by combining Swiss-Prot, TrEMBL and PIR. This makes it the world's most
comprehensive resource on protein information. The UniProt Consortium is
comprised of the European Bioinformatics Institute (EBI), the Swiss Institute
of Bioinformatics (SIB), and the Protein Information Resource (PIR). UniProt
identifiers uniquely specify a protein by its amino acid sequence.
EBI, located at the Wellcome Trust Genome Campus in Hinxton, UK, hosts a large
resource of bioinformatics databases and services.
SIB, located in Geneva, Switzerland, maintains the ExPASy (Exprt Protein
Analysis System) servers that are a central resource for proteomics tools and
databases.
PIR, hosted by the National Biomedical Researche Foundation (NBRF) at the
Georgetown University Medical Center in Washington, DC, USA, is the
oldest protein sequence database, Margaret Dayhoff's Atlas of Protein Sequence
and Structure.
In 2002, EBI, SIB, and PIR joined forces as the UniProt Consortium.
Combination of food additives and interference with development of
nervous cells:
The effects of food colouring brilliant blue (E133) combined with monosodium
glutamate (MSG; E621) and colouring quinoline yellow (E951) combined with the
sweetener aspartame (E951) were tested at the University of Liverpool. This
combination presented neurotoxic effects.
The combination of brilliant blue and MSG could inhibit cell growth up to four
times more than the additives on their own, while for quinoline yellow and
aspartame the figure rises to seven. The research has been supported by Organix
Brands.
Inhibition of neurite outgrowth was found at concentrations of additives
theoretically achievable in plasma by ingestion of processed foods like sweets
and snacks they are typically present in combinations and are foods which are
consumed by children whose nervous system is still developing.
[833]
In response to the study, UK regulatory body Food Standards Agency said that
the safety of all additives is kept under review. The European Food Safety
Authority (EFSA) had been asked to review food additives currently permitted
within the EU in order to determine whether full re-evaluation is required.
[864]
The authors of the Liverpool study call upon the European Food Safety
Authority (EFSA) to look upon the combined effects of the mentioned
substances. Some researches concerning mixtures of substances are already being
undertaken by FSA funding research on the effects of two groups of colour
additives on the behaviour children is expected to report in 2007.
[869]
Monosodium glutamate (MSG) is a flavour enhancer for foods such as soups, fish
and meat dishes, and ready meals in produces of Nestle, Unilever and others.
Glutamate was linked to headache, known as the China restaurant syndrome and other problems.
Ajinomoto Foods Europe, the only MSG producer in the EU, complainted of Chinese
firms dumping sodium glutamate on the EU market undercutting Ajinomoto's price by
up to 24 per cent. Following the complaint, the European Commission imposed in
2008 anti-dumping tariffs of 39,7 per cent on monosodium glutamate (MSG)
imported to the EU from China.
[870]
Ohguro Hirishi and colleagues
2002 found a significant accumulation of glutamate in vitreous was observed in rats on high sodium glutamate. Thickness
of retinal neuronal layers was remarkably thinner in rats fed on sodium
glutamate diets than in those on a regular diet.
The authors concluded that a diet high in sodium glutamate over a period of
several years may increase glutamate concentrations in vitreous and may cause
retinal cell destruction.
[871]
Jinab and Hajeb 2010 of the University Putra Malaysia reviewed application,
benefits of monosodium glutamate as flavor enhancer. The authors say that
glutamate adds a fifth basic taste to the four basic ones, whicch are saltiness,
sourness, sweetness and bitterness. It is also an energy source, acts as a
substrate for glutathione synthesis and enhances food intake in older
individuals. Glutamate may partially replace salt in food preparation. The Joint
Expert Committee on Food Additives of the United Nations Food and Agriculture
Organization and World Health Organization classified glutamate as safe. The
authors stress that there are no consistent clinical data to support believes
that glutamate causes asthma, migraine headache, Chinese Restaurant Syndrome, and
there are no evidences indicating that individuals may be uniquely sensitive to
glutamate.
[872]
The Food Standards Australia New Zealand in a technical report of 2003 found that
some studies reported a complex of symptoms which came to be known as the Chinese
restaurant syndrome (CRS) because they typically followed ingestion of a Chinese
meal. Two outstanding studies were Kwok, R. (1968) [873]
and Schaumburg HH(1969) [7]
suggesting monosodium glutamate as the causative agent in CRS embracing symptoms
such as headache, numbness/tingling, flushing, muscle tightness, and generalised
weakness. MSG symptom complex is now being used instead of CRS. A possible
association between MSG and bronchospasm in asthmatic individuals were also
suggested.
The FSA study found no convincing evidence that MSG
is a significant factor in causing systemic reactions resulting in severe
illness or mortality, and studies have failed to demonstrate a causal
association with MSG. Some reactions were noted by administrating large doses
of 3g or more MSG without food were not serious and are likely to be
attenuated when MSG is consumed with food. Bronchospasm in asthmatic
individuals is, according to actual data, not significantly triggered by MSG.
Patricia Tagliaferro in an article of 1995 [875],
stressed inconsistent data of studies on the possible effect ofMSG. The study of
Jinab and Hajeb 2010 confirms that glutamate is not related to asthma, migraine
headache and Chinese Restaurant Syndrome.
[876]
According to the UK Food Standards Agency,
parents of children showing signs of hyperactivity are being advised that
cutting certain artificial colours from their diets might have some beneficial
effects.
The colours found to give adverse reactions were: Sunset yellow (E110),
Quinoline yellow (E104), Carmoisine (E122), Allura red (E129), Tartrazine
(E102) Ponceau 4R (E124), and Sodium benzonate (E211)
Hyperactivity is the occurrence of the following behaviours at the
same time: over-activity, inattention and impulsivity. Attention Deficit
Hyperactivity Disorder (or Hyperkinetic Disorder) (ADHD) is an extreme form of
hyperactivity that is clinically diagnosed when specific patterns of behaviour
occur together to a strong degree. This comprises a behavioural disorder which
adversely affects children's function at home and in school.
The Committee on Toxicity of Chemicals in Food (COT) reviewed a research,
carried out by Southampton University, suggesting that eating or drinking
certain mixes of these artificial food colours together with the preservative
sodium benzoate could be linked to a negative effect on children's behaviour.
The findings of the research were presented to the European Food Safety
Authority (EFSA), which is conducting a review of the safety of all food colours.
Following the COT statement, the FSA holds on the following advice:
FSA advice to consumers: if a child shows signs of hyperactivity or Attention
Deficit Hyperactivity Disorder (ADHD) then eliminating the colours used in the
Southampton study from their diet might have some beneficial effects.
However, the FSA also reminds that there are many factors associated with
hyperactive behaviour in children. These are thought to include genetic
factors, being born prematurely, or environment and upbringing.
[877]
[878]
The study tested two combinations of colours and a preservative most likely to be
found in foods popular with children such as soft drinks, confectionery, and
ice cream.
According to Professor Jim Stevenson from Southampton University, and author
of the report, the consumption of certain mixtures of artificial food colours
and sodium benzoate preservative are associated with increases in hyperactive
behaviour in children.
[879]
According to Professor Ieuan Hughes, Chair
of the COT, said that the study provides supporting evidence for a link
between the colours used in the study and increased hyperactivity in children.
He stresses that the available evidence does not identify whether this
association would be restricted to certain food additives or combinations of them.
The POC study concludes that the findings are consistent with, and add weight
to, previous published reports of behavioural changes occurring in children
following consumption of particular food additives.
[880]
A trial by Southampton University, commissioned by the British Food Standards
Agency (FSA), examines a possible association between the intake of specific
food additives (the food colourings E102, E104, E110, E122, E124, E129 and the
preservative sodium benzoate E211) and the occurrence of Attention Deficit
Hyperactivity Disorder (ADHD) in children. The trial found that artificial
colours or a sodium benzoate preservative (or both) in the diet result in
increased hyperactivity in 3-year-old and 8/9-year-old children in the general
population. [881]
[882]
The UK Committee on Toxicity of Chemicals in Food, Consumer Products and the
Environment (COT) considers the results of the trial by Southampton University
as additional indications of a possible association between the intake of
certain mixes of artificial colouring agents containing the preservative
sodium benzoate and increased hyperactivity in children.
To the extent that there is a causal association, this could be of importance
for individual children particularly for those who are in any case clearly
hyperactive. However, COT stresses that the mean levels of observed
hyperactivity are low compared to normal inter-individual variation and that
behavioural changes did not occur in all children in one group, did not occur
uniformly across all age groups and not in an even manner for the intake of
all additive groups. Hence it is not possible to draw any more extensive
conclusions. Nor is it possible to extrapolate the results to other additives.
After short-term examination of the publication by McCann et al. (2007)
[881] BfR agrees with the conclusions in
the COT opinion. As food additives must be included in the list of
ingredients, consumers wishing to avoid any intake of the examined substances
for precautionary reasons are able to refrain from consuming the corresponding
foods and drinks.
The Southampton study, together with the review of COT, should encourage food
producers to reformulate their products to reduce as much as possible the use
of additives.
[883]
The European Food Safety Authority's (EFSA) AFC Panel assessed the study of
McCann and al 2007 on hyperactivity. The report was released on
14.03.08 concluding that the McCann study (2007) provided limited
evidence that the mixtures of additives tested had a small effect on the
activity and attention of some children. However, the effects observed were
not consistent for the two age groups and for the two mixtures used in the
study.
Considering the overall weight of evidence and in view of the considerable
uncertainties the Panel concluded that the findings of the McCann et al study
could not be used as a basis for altering the ADI of the respective food colours
or sodium benzoate.
Although the findings from the study could be relevant for specific individuals
showing sensitivity to food additives in general or to food colours in
particular, it is not possible at present to assess how widespread such
sensitivity may be in the general population.
The Panel noted that the majority of the previous studies used children described
as hyperactive and these were therefore not representative of the general
population.
[884]
The researcher of the Southampton study on hyperactivity caused by certain
colourings and preservative, leaded by Jim Stevenson, Donna McCann, Edmund
Sonuga-Barke and John Warner, responded to the EFSA evaluation of their study.
They say that despite EFSA saying there is no justification from this
research to change the limits on these additives, that does not mean there are
no grounds for action at all.
The team stresses that since the colours being tested in this study are of no
nutritional value, even the small overall benefit of removing them from
children's diets would come at no cost or risk to the child, and a benefit,
even a small one, would be worthwhile achieving.
According to the authors added weight is given to this conclusion because other
important influences on hyperactivity in children, such as genetic factors, are
difficult to address while the risk arising from exposure to food colours can be
regulated.
[885]
The Southampton study found that a mix of food colours such as sunset yellow
(E110), tartrazine (E102), carmoisine (E122), ponceau 4R (E124) quinoline yellow
(E104), allura red (E129) and sodium benzoate (E210). exacerbate hyperactive
behaviour in children at least up to middle childhood.
The European Food Safety Authority (EFSA) conducted a review of the Southampton
study, as well as other studies and meta-analyses on additives and hyperactivity.
EFSA also concluded that the Southampton study gave no basis for changing
acceptable daily intakes (ADI) of food additives. EFSA stresses that
hyperactivity results from a variety of social and biological causes, focusing on
dietary strategy eliminating food additives alone may detract from the provision
of adequate treatment.
At present, there are three main approaches to tackling ADHD: drugs,
behavioural therapy, and dietary management.
Despite all controversies Professor Andrew Kemp writes that behavioural therapy
is still considered necessary for adequate treatment even though there is less
evidence for its efficacy than there is for eliminating food additives. He calls
not to neglect the dietary factors. Cutting out colours and preservatives from
the diets of hyperactive children should be standard part of the treatment of
ADHD.
[886]
Aldi Australia said it will no longer wait for the food regulator to act. The
supermarket chain has voluntary banned six food colourings from its products
following the results of a research published by The Lancet in 2007. The
artificial colours sunset yellow (E110), tartrazine (E102), carmoisine (E122),
ponceau 4R (E124), quinoline yellow (E104), and allura red (E129) have been
linked to behavioural problems in children such as ADHD.
[878]
The British Southampton study published in the "Lancet" in 2007 found a link
between hyperactivity in children who consumed drinks that contained these additives.
The study tested two combinations of colours and a preservative most likely to be
found in foods popular with children such as soft drinks, confectionery, and
ice cream.
According to Professor Jim Stevenson from Southampton University, and author
of the report, the consumption of certain mixtures of artificial food colours
and sodium benzoate preservative are associated with increases in hyperactive
behaviour in children.
[887]
A list of food additives which should be avoided is given by Food Intolerance
Network. Please see:
http://www.fedupwithfoodadditives.info/information/nastyadditivecard.pdf
[888]
The European Parliament voted in July 2008 for products containing the colours
to be labelled "may have an adverse effect on activity and attention in children".
The European Food Safety Authority (EFSA) reviewing the methodology and
results of the Southampton study stated it found no scientific evidence for
altering intake recommendations of any of the additives, but will look again
at the safety data on all food additives, including the Southampton colours.
[889]
Aldi Australia demonstrated a high level of quality and responsibility for the
health of its customers. Aldi Europe and Lidl Europe still sell products with
the Southampton colours. The marketing department should be aware of the
possible image damage selling products which might harm children. Changing the
six questioned artificial colours to other innocuous ones clears the situation
and demonstrates a precautious way to handle health issues.
[890]
Paprika as food colour is increasingly being used by the food industry.
Safety tests on rats found paprika food colour as safe. The toxicity and
carcinogenicity studies of paprika colour were performed by Inoue and
colleagues 2008.
Treatment with paprika colour caused a significant increase in incidence of
hepatocellular vacuolation, in 5% males, however, no toxicological effects or
other abnormal effects such as tumors were noted.
The authors concluded that, based on slight histopathological changes, noted
as hepatocellular vacuolation, the no-observed-effect level (NOEL) was
estimated to be 2.5% in the diet (1253 mg/kg bw/day) and the the
no-observed-effect level (NOEL) was 2.5 per cent in the diet, or 1253 mg per
kg of bodyweight per day, for the male rats. The NOEL for the female rats was
determine to be five per cent, or 2826 mg per kg of bodyweight per day.
Paprika colour is therefore not carcinogenic nor toxic under present conditions.
[891]
Lien et al 2006 found a relationship between soft drink consumption and mental
distress, conduct problems, and total mentalhealth difficulties score. The
higher the consumption of soft drinks, the more extreme symptoms of
hyperactivity were observed. The highest adverse reaction observed for
conduct problems were found among boys and girls who consumed 4 or more
glasses of sugar-containing soft drinks per day.
The authors concluded that high consumption levels of sugar-containing soft
drinks were associated with mental health problems among adolescents.
[892]
David Benton, in a response to the study of Lien et al 2006, reviewed studies
on sucrose consumption found that food intolerance to sucrose is less frequent
than many other foods.
Low blood glucose levels, but higher than those that can be described
clinically as hypoglycemic, is associated with irritability and violence.
However, sucrose is not the predominant cause of swings in blood glucose levels.
Micro-nutrient decreased anti-social behaviour. Micro-nutrient intake is more
closely associated with the total energy rather than sucrose intake; typically
the amount of sucrose in the diet does not lead to micro-nutrient deficiency.
Benton concluded that studies that have examined the impact of sucrose on the
behaviour of children produced no evidence that it has an adverse influence,
such as attention deficit hyperactivity disorder.
However, sugar fat and salt-reduction should go on in face of the obesity and
cardiovascular risks. Physical activity not also reduces risk of obesity, but
also may improve mental health in adolescents.
[893]
Five to seven weekly hours of physical activity at age 15-16 years was weakly
associated with mental health. The authors called for further studies about
physical activity as a possible protective factor in relation to mental health
problems in adolescence.
Benzene is listed as a poisonous chemical shown to increase the risk of
leukaemia and other cancers. Drinking water limits range from 10 parts per
billion (World Health Organisation), 5ppb in the US and one part per billion in
the EU. Some soft drinks contain up to five times this limit of benzene. The
FDA assured benzene did not present an immediate health risk at the levels
found to date in drinks.
[894]
Mike Redman the National Soft Drink Association (NSDA) in a meeting of the FDA
in 1990 suggests that benzene formation occurs as an interaction among
ingredients in the product for example, sodium Benzoate, ascorbic acid and
FD&C yellow Nr. 5 under certain conditions might produce benzene.
Other chemicals such as erythorbic acid, EDTA, oxygen and sweeteners like high
fructose corn syrup influence benzene formation in the presence of benzoic
acid.
Sweeteners are thought to inhibit the reaction, as the problem seems most
noticeable in diet drinks. EDTA appears to inhibit the reaction also, possibly
by complexing metal ions that could act as catalysts.
Companies added Calcium disodium ethylene diamine tetra-acetate (" EDTA") in
the US to reduce benzene formation. The FDA, however noted that calcium
disodium EDTA is not an approved food additive for non-carbonated soft drinks.
[865]
Erythorbic acid may lead to benzene formation in much the same fashion as
ascorbic acid.
- Removal of oxygen by CO2 or N2 may inhibit benzene formation.
- Solutions containing sodium benzoate and citric acid also form benzene
although perhaps not as readily as those with ascorbic acid.
- Benzene does not form in mineral acid pH adjusted sodium benzoate solutions subjected to heat and light.
- Benzene has also been observed to form after exposure to light for 24 hrs
in ascorbic acid solutions of benzoic acid anhydride, acetophenone, and
benzaldehyde.
- There is some data to suggest that benzene may form from a contaminate in sodium benzoate.
Sodium benzoate and ascorbic acid (vitamin C) are still used together in a wide
range of soft drinks and flavoured waters across the world. They can react
together to cause benzene formation.
Ascorbic acid initially reacts with metals, such as iron or copper, found in
the water to create free radical. These hydroxyl radicals break down Sodium
benzoate into benzoic acid and benzene.
Reactivity of Ascorbic acid in presence of ions of copper and iron has been
studied by Hans Steinhart et col. in 1993. [866]
The State of Florida Laboratories found traces of benzene in Koala Springs
flavoured mineral water. There is speculation that the benzene traces
originated from the sodium benzoate by way of photolytic degradation.
[894]
The combination of sodium or potassium benzoate with ascorbic acid was shown to
produce low levels (ng/g) of benzene in fruit-flavoured soft drinks. The
presence of benzene was also reported in butter, eggs, meat, and certain
fruits; levels of these findings ranged from 0.5 ng/g in butter to 500-1900
ng/g in eggs.
Slightly higher levels were present in some foods and beverages containing both
ascorbic acid and sodium benzoate. [895]
Soft drinks, juices, beers, and waters from processed vegetables were analysed
for trihalomethanes (THMs), benzene, and toluene. The THMs, which include
chloroform, bromodichloromethane, dibromochloromethane, and bromoform, are
reaction by-products of water disinfection by chlorination.
In this study benzene residues were found typically
5 ng/g, except for 7 and
9 ng/g in 2 foods, compared to other contaminants: Toluene residues were
typically
3 ng/g except for 23, 29, and 75 ng/g in 3 canned foods and
chloroform was none detected to 94 ng/g in the 44 foods analysed.
[867]
Industry tests on soft drinks found that temperatures of 30
and exposure
to UV light for several hours were enough to more than triple benzene residues
in some drinks.
America's soft drinks industry association said hot warehouses and cars parked
in direct sunlight are examples of when soft drinks would be exposed to even
higher temperatures as that.
Benzene formation may also occur in dietary supplements, such as liquid aloe
vera and vitamin formulations, and other acidic liquid food products, such as
lemon juice where sodium benzoate and ascorbic acid are present.
Producers should use predictive testing to simulate storage under UV and heat
up to 50
to survey their products for benzene.
The consumer should carefully read the list of ingredients. When sodium
benzoate is listed in soft drinks and other acidified foods do not buy it.
Food regulations worldwide should demand sodium benzoate to be taken out of
juices, soft drink and other acidified food formulas. Technology does not need
sodium benzoate in drinks as modern heat sterilization and aseptic filling
techniques make the use of this preservative unnecessary.
[868]
Christof Van Poucke and colleagues 2008 analysed 134 Belgian soft drinks.
The authors found that ten samples were above the European limit for benzene
in drinking water of 1
g L, and one sample had a concentration of 10.98
g /L, thereby exceeding the action limit for benzene in soft drinks of 10
g/ L. The authors stress that benzene can be formed when benzoic acid, a food
preservative, is combined with ascorbic acid acidity regulators and
interaction with packaging materials in foods like soft drinks.
Benzene oxidises in the body to produce an epoxide, benzene oxide, which is
not excreted readily and can interact with DNA to produce harmful mutations.
The use of preservatives like benzoic acid and benzoates can be avoided by
sanitising filling lines and adopting sound hygienic strategies. Soft drinks and
other beverages are very easy to handle in an sterile environment. Chemical
preservatives are not needed in modern food technology.
[896]
VOCs are a group of low molecular weight aliphatic and aromatic compounds with
low boiling points. Sources of VOCs include solvents, dry cleaning compounds,
degreasers, paints, chemical intermediates, and assorted industrial products.
They are also products of combustion and the chlorination of drinking water.
Additionally, VOCs can come from the process of microwaving foods. Some VOCs
are even allowed as indirect food additives from components of commercial
packaging.
FDA study, published in 2003 a study of Fleming-Jones and Robert E. Smith.
Volatile organic compounds (VOCs), such as benzene, were found in at least one
sample of all foods tested, although no single compound was found in each of
the foods. Benzene levels ranged from 1 to 190 ppb,
Benzene is a human carcinogen and neurotoxin. Other VOCs reported to be human
neurotoxins include 1,1,1- trichloroethane, styrene, toluene,
trichloroethylene, and xylene. However, the doses needed to cause neurotoxicity
are far greater than those detected in foods in the study of Fleming-Jones.
[897] [898]
[899]
The amounts needed to cause these toxicities are much higher than those found
in foods in this study. For all toxicities except carcinogenesis, a threshold
approach is often used, which sets acceptable daily intake levels.
However, it is sometimes stated that a nonthreshold approach is used for
potential carcinogens and that a single molecular adduct can initiate the
multistep process of carcinogenesis. [900]
FDA concluded from data derived from the FDA's Total Diet Study that the
American food supply is comparatively safe. Although there is some oral
exposure to VOCs, they are usually inhaled at much higher doses through
cigarette smoke, gasoline fumes, and industrial pollution.
[901]
Peter Piper proposes a Saccharomyces cerevisiae petri dish test, using yeast
superoxide dismutase mutants to distinguish a compound that enhances the
detrimental effects of endogenous reactive oxygen species production by the
mitochondrial respiratory chain from another chemical that generates oxidative
stress by redox cycling.
Using this test system, Piper found that weak organic acid food preservatives
exert strong pro-oxidant action on aerobic yeast cells, and are mutagenic
toward the yeast mitochondrial genome.
The author concluded that sodium benzoate may generate oxidative stress within
the epithelia of the gastrointestinal tract.
[902]
The International Council of Beverages Associations (ICBA) is a
non-governmental organization representing the interests of the worldwide
beverage industry.
Today, as the beverage industry continues to grow and expand, the International
Council of Beverages Associations (ICBA) is renewing its commitment to provide
guidance on preventing/minimizing benzene formation. This guidance will be made
available to all beverage companies worldwide.
http://www.britishsoftdrinks.com/htm/sv/PDFs/IBCA%20final%20220606.pdf#search=%22ICBA%20Benzene%20Guidance%22
[903]
The Federal Institute for Risk Assessment has issued an expert opinion on
whether benzene may be formed in beverages from the food additive benzoic acid
in the presence of ascorbic acid.
It is advisable to minimise and/or avoid the intake of benzene as far as
possible. This is the standard practice for substances which are to be
considered as carcinogens and germ cell mutagens.
However, further chemical-analytical data are needed in order to assess the
possible risk from simultaneous use of benzoic acid and ascorbic acid in foods.
If it turned out that the simultaneous use of benzoic acid and ascorbic acid in
foods makes a significant contribution to total benzene intake, it may be
necessary to check whether the authorisation framework for a simultaneous use
of benzoic acid and ascorbic acid in foods would have to be changed.
Brilliant blue:
Its name is
brilliant blue E133 and is currently banned in the majority of EU countries.
However , it is used in the UK in sweets, confectionery, dessert, ices, in some
soft drinks, baked goods and tinned processed peas.
FD&C Blue No. 1 may be safely used for
colouring foods (including dietary supplements) generally in amounts
consistent with good manufacturing practice except.
[834]
Quinoleine Yellow:
Quinoline
Yellow is absorbed from the gastro-intestinal tract to only a small extent in
rats and dogs, and most of an orally administered dose is excreted unchanged.
No adverse effects of treatment were seen in the two-generation long-term
study in mice. In particular there was no observed effect on thyroid function
or histopathology and no evidence of carcinogenicity.
Quinoline yellow is banned in foods in Australia, the US and Norway. In UK
it is used in sweets, smoked haddock, confectionery and pickles.
Level causing no toxicological effects: Mouse: 1% of the diet, equal to 1.500
mg/kg/
Estimate of an acceptable daily intake for man: 0-10 mg/kg bw.
The committee noted that there are two quinoline yellows, one of which is about
30% methylated and the other non-methylated, and considered that data from
both compounds could be used for toxicological evaluation of either of the
quinoline yellows for food additive use.[835]
Monosodium glutamate is banned in baby food in
the UK, but is used in a variety of crisps and snacks which are consumed by
children. Parents should watch the ingredient list carefully in order to
avoid to give products with these ingredients to children under 5 years.
[836]
They are used in cured meats such as ham and
bacon, hot dogs and deli meats. Both nitrates and nitrites combine with other
nitrogen-containing substances in the stomach to form N-nitroso compounds
that are known to cause stomach cancer.
Commonly preserved
food by salting, smoking or pickling often contain large amounts of nitrites and
nitrates. Countries where consumption of salted meat and fish and pickled
vegetables is high, such as Japan and Korea tend to have correspondingly high
rates of stomach cancer. Eating a diet high in red meat, especially when the
meat is barbecued or well-done, also has been linked to stomach cancer.
Traditional curing methods using nitrite or nitrate are being substituted by
new products for the sake of a natural label. There are consumers which try to
avoid nitrite cured meat because of health concerns.
[856]
In food preparation, curing refers to various preservation and flavouring
processes, especially of meat and fish by the addition of a combination of
salt, sugar and either nitrate or nitrite. Many curing processes also involve
smoking.
Nitrite curing retards rancidity, stabilises flavour, and establishes the
characteristic pink colour of cured meat.
Salt inhibits the growth of microorganism which cause spoilage by drawing water
out of microbial cells through osmosis. As the unwanted bacterial population
decreases, other beneficial bacteria, primarily of the Lactobacillus genus,
come to the fore and generate an acidic environment (around 4.5 pH).
The sugar included in the cure is used as food by the lactobacilli; generally
dextrose is preferred over sucrose, or table sugar, because it seems to be more
thoroughly consumed by the bacteria. This process is in fact a form of
fermentation and, in addition to reducing further the ability of the spoilage
bacteria to grow, accounts for the tangy flavour of some cured products.
Concentrations of salt up to 20% are required to kill most species of
bacteria.
Smoking adds chemicals to the surface of an item which affect the ability of
bacteria to grow, inhibit oxidation (and thus rancidity), and improve flavour.
Nitrates and nitrites not only help kill bacteria, but also produce a
characteristic flavour, and give meat an appealing pink or red color. Nitrate
(NO
), in the form of either sodium nitrate or potassium nitrate is used
as a source for nitrite (NO
). The nitrite further breaks down in the meat
into nitric oxide (NO), which then binds to the iron atom in the center of
mioglobin's heme group, preventing oxidation.
Commercially Curing salt containing small amounts of sodium nitrite or sodium
nitrate is used in the preserving and curing of meats, and in sausage making.
The nitrate component inhibits the growth of bacteria, specifically botulism,
and helps preserve the color of cured meat.
The presence of nitrates and nitrites in food is controversial due to the
development of nitrosamines when the food, primarily bacon, is cooked at high
temperatures. The nitrate and nitrite compounds themselves are not harmful,
however, and are among the antioxidants found in fresh vegetables.
[857]
The usage of either compound is carefully regulated in the production of cured
products; in the United States, their concentration in finished products is
limited to 200 ppm, and is usually found to be below. Finally, they are
irreplaceable in the prevention of botulinum poisoning from consumption of
dry-cured sausages.
[858]
Chr. Hansen has developed a new natural cure for manufacturers as a nitrite
replacement for cured meats. No synthetic nitrates or nitrites are added,
labelling of nitrite or nitrate can be avoided. The product can be labelled as
'uncured' in accordance with USDA 9CFR317.17 labelling regulations
[836]. Naturally occurring nitrates are converted by the culture
to nitrite which then accounts for the curing of the meat.
According to papers of Chr. Hansen various strains are used. Lactobacillus
sakei BJ-33 was approved by the Danish authorities for bioprotective use. The
bacteria multiplies at chill temperatures as low as 2
/35
F and
suppresses the spoilage flora of indigenous lactic acid bacteria and
Brochothrix thermosphacta. The inhibitory effect possessed by the strain is
due to competition since the ability to produce bacteriocins has not been
detected. It is used in combination with a strain of Staphylococcus xylosus.
Other strains used by Chr Hansen are Leuconostoc carnosum 4010 (formerly named
Lc-1043). Another strain used is B-LC-20 which is an adjunct culture that is
added on top of the existing starter culture without changing the sausage
recipe or the sausage processing procedure for the reduction of Listeria in
fermented dried sausage.
[859]
Micha, Wallace and Mozaffarian 2010 found that Consumption of processed
meats, but not red meats, is associated with higher incidence of CHD and
diabetes mellitus. It takes only 50 g (one hot Dog) of processed meat per day
to increase heart disease by 42% and type 2 diabetes by 19%. No link between
eating unprocessed red meat like beef or pork and risk of heart disease and
diabetes was found by the authors. High levels of salt and nitrate
preservatives in sausages, bacon and deli meats, rather than fats, might
explain the higher risk of heart disease and diabetes seen with processed
meats, but not with unprocessed red meats.
The authors call for studies looking at processed and unprocessed meats
separately and focus on salt and nitrate preservatives.
[860]
A controversy concerns nitrites in cured meats. Some say it increases the risk
of stomach cancer, or lung diseases [837], while
other researchers found no proof of such affirmations. Cardiologists found
that nitric oxide from bacterial breakdown of nitrite reduces blood pressure
and avoids damages during an heart attack. [838]
[839]
Ribeiro and colleagues 2006 presents a summary of studies concerning
anti-mutagenic and anti-carcinogenic potential of annatto, mushrooms and
propolis in Brazilian natural diets. Their data shown a clear role for these
compounds in preventing mutation and specific preneoplastic lesions. The
authors stress that these agents may become a promising alternative for
cancer prevention strategies. [861]
Petersson, 2008 suggests that nitrites may protect the stomach from ulcers.
The author says that mouth bacteria reduce nitrate to nitrite. Nitrous oxide
NO produced in the gastric lumen after nitrate ingestion increased gastric
mucosal blood flow and the thickness of the firmly adherent mucus layer in the
stomach. The blood flow and mucus layer are essential defence mechanisms that
protect the mucosa from luminal acid and noxious agents.
[862]
Zarringhalami, Sahari and Hamidi-Esfehani 2008, researchers from Iran,
presented a study claiming that annatto (Bixa orellana L.) powder may replace
up to 60 per cent of nitrite as ingredient of sausage. This might reduce
excessive consumption of nitrite. According to the authors colour, flavour,
aroma, and microbial contamination did not differ significantly compared with
samples with 100 percent nitrite. [860]
Annatto is not allowed in the European Union as ingredient of sausages and other
meat products. Annex IV of the European directive 94/36/EC on colours for use in
foodstuffs cites annatto in a positive list of colours permitted for certain uses
only, meat products are allowed there. [2548]
[836]
With respect to sections 1(n) (7), (9), and (12) of the Act and Sec. 317.2,
any substance mixed with another substance to cure a product must be
identified in the ingredients statement on the label of such product. For
example, curing mixtures composed of such ingredients as water, salt, sugar,
sodium phosphate, sodium nitrate, and sodium nitrite or other permitted
substances which are added to any product, must be identified on the label of
the product by listing each such ingredient in accordance with the provisions
of Sec. 317.2.
(b) Any product, such as bacon and pepperoni, which is required to be labeled
by a common or usual name or descriptive name in accordance with Sec.
317.2(c)(1) and to which nitrate or nitrite is permitted or required to be
added may be prepared without nitrate or nitrite and labeled with such common
or usual name or descriptive name when immediately preceded with the term
"Uncured" as part of the product name in the same size and style of
lettering as the product name, provided that the product is found by the
Administrator to be similar in size, flavour, consistency, and general
appearance to such product as commonly prepared with nitrate or nitrite, or
both.
(c)(1) Products described in paragraph (b) of this section or Sec. 319.2 of
this subchapter, which contain no nitrate or nitrite shall bear the statement
"No Nitrate or Nitrite Added." This statement shall be adjacent to the
product name in lettering of easily readable style and at least one-half the
size of the product name.
(2) Products described in paragraph (b) of this section and Sec. 319.2 of this
subchapter shall bear, adjacent to the product name in lettering of easily
readable style and at least one-half the size of the product name, the
statement "Not Preserved-Keep Refrigerated Below 40 deg.F. At All Times"
unless they have been thermally processed to Fo 3 or more; they have been
fermented or pickled to pH of 4.6 or less; or they have been dried to a water
activity of 0.92 or less.
(3) Products described in paragraph (b) of this section and Sec. 319.2 of this
subchapter shall not be subject to the labeling requirements of paragraphs (b)
and (c) of this section if they contain an amount of salt sufficient to
achieve a brine concentration of 10 percent or more.
Sodium nitrite E250 produces the pink colour of
cured meat. It also retards rancidity and stabilises the flavour.
The third National Health and Nutritional Examination Survey (NHANES) on 7,352
subjects over the age of 45, have suggested that increased consumption of
nitrites from cured meat could increase the risk of lung disease.
[837]
Other studies found nitrite and nitrate to be related to the incidence of
cancer due to the formation of nitrosamines.
But recent research has found no convincing evidence that nitrite and nitrate
pose a cancer risk. In reality they seem to protect heart cells from death
after an heart attack.
The study published in the Proceedings of the
National Academy of Sciences found that nitrites reduce heart cell death in
mice by 48 per cent after an heart attack.
Nathan S. Bryan and colleagues report that mice supplemented with 50 mg
nitrite per litre of drinking water for seven days had a survival rate of 77
per cent compared to 58 per cent for the mice without supplementation.
The researchers say that eating nitrite and nitrate rich foods such as fruits
and vegetables and some meats in moderation can drastically improve outcome
following a heart attack, They suggest to sty the effects of supplementation
of nitrite/nitrate in the diet can decrease the incidence and severity of
heart attack and stroke in patients with known cardiovascular risk factors.
Bryan suggests the formation of nitric oxide (NO) from nitrites to be the
mechanism of the heart protecting effect of nitrates. Nitric oxide causes the
cells of the blood vessels to signal the surrounding muscles to relax. This
results in a reduction in blood pressure, reduction of blood clotting and and
protection against myocardial infarction and strokes. A betaine
in chemistry is any neutral chemical compound with a positively charged
cationic functional group such as ammonium ion or phosphonium ion and with a
negatively charged functional group such as a carboxyl group. Historically the
term was reserved for trimethylglycine only. [840]
Betaine is found in high concentrations in sugar beet, improving consistency
of pig and poultry performance improving the structure of the animals
intestine, increasing gut tensile strength and the absorptive area for
nutrients, which helps to maintain growth, feed conversion and profitability in
the absence of antibiotic growth promoters.
Betaine (trimethylglycine) functions very closely with choline, folic acid,
vitamin B12 and methionine. Betaine is necessary in the biochemistry of
carnitine and serves to protect the kidneys from damage.
[841]
Barak proposed in 1983 that betaine may serve as an important methylating
agent when normal methylating pathways are impaired by ethanol ingestion, drugs
or nutritional imbalances. Furthermore, betaine may prove to have therapeutic
application in cases of altered folate, vitamin B12 or methionine metabolism.
[842]
Glycine betaine (betaine hydrochloride) used as feeding attractant was found
to have a positive effect on the growth and feed conversion of juveniles of
Macrobrachium rosenbergii (deMan). Weight gain, feed intake and food conversion
ratio (FCR) were higher in prawn fed glycine betaine-added diets compared with
the control feed in a study made by Dr Nathan Felix. [843]
Betaine is used in animal feeds as a source of essential methyl groups and as
an osmoregulant. Its osmotic function is useful in maintaining gut wall
integrity. Feeding betaine could compensate the removal of antibiotic growth
promoters. Reduced control of Clostridium perfringens in birds could be
countert with betaine which improves the hydration and integrity of the gut
wall. [844]
Betaine decays in the liver forming methionine. Dietary methionine is spared.
saving feeding costs Feeding betaine saves methionine and choline costs Betaine
also functions as osmoregulator. Betaine in feed or water can help reduce
dehydration by facilitating water retention in the body in case of heat stress.
[845]
Advances in genetics and feed ingredients such as betaine from sugar beets and
enzymes have reduce feed costs and generate a higher percentage of lean meat.
[846]
Amrita Ahluwalia and colleagues 2008 studied the benefits of high nitrate
content of vegetables like beetroot. The authors suggest that the nitrate
content of the vegetables is responsible for a reduction of blood pressure ,
and not by the antioxidant vitamin content as assumed in foregoing studies.
The authors say that drinking 500 ml beetroot juice a day reduces blood
pressure significantly three hours after the consumprtion. The authors explain
that the high nitrate content of the juice increases nitrate content of the
saliva, where it is converted to nitrite by bacteria living on the tong. When
swallowed the nitrite is transformed in nitric oxide NO in the stomach and
can the reenter the blood circulation as nitrite.
The authors reported further that dietary nitrate load also prevented
endothelial dysfunction induced by an acute ischemic insult in the human
forearm and significantly attenuated ex vivo platelet aggregation in response
to collagen and ADP.
Some studies suggest that nitrite (NO(2)(-)), is a physiological signaling
molecule with potential roles in intravascular endocrine nitric oxide (NO)
transport, hypoxic vasodilation, signaling, and cytoprotection after
ischemia-reperfusion. There is evidence that nitrite mediates many of the
systemic therapeutic effects of NO gas inhalation, including peripheral
vasodilation and prevention of ischemia-reperfusion-mediated tissue infarction.
[847] [848]
Michael P. Frenneaux and colleagues 2008 found nitrite to be a potent
venodilator in normoxia and hypoxia. The authors highlight the importance of
nitrite as a selective arterial vasodilator in ischemic territories and as a
potent venodilator in heart failure. [849]
Other studies say that nitrate and nitrite are linked to stomach cancer and
give advice to avoid food with high content of both substances. The Mayo
Clinic names some factors which are believed to increase stomach cancer:
[850]
Thickening agents from Algae
[851]
Carrageenans extracted from red algae and alginates from brown algae are
already being used as stabilisers and thickening agents.
Albert Mihranyan and colleagues from Uppsala University in Sweden studied the
properties of alpha - cellulose of the green algae Cladophora
sp. They found that Cladophora
cellulose powder could be a useful alternative to commercially available
dispersible cellulose grades when very low quantities of stabilizing agents are
required.
[852]
A study by Choi and Curhan suggests that dietary fructose intake is a possible
risk factors for gout increasing serum urate and is associated with
hyperuraemia. Obesity, alcohol, and diet with the aree also associated with
the onset of gout.
Hyon K. Choi and Gary Curhan, authors of the 12 years follow-up study found a
strong association between sugar sweetened soft drinks and gout. They wrote
that two servings a day of a sugar sweetened soft drink, high in fructose,
increased the risk of developing gout by 85% compared with consumption of less
than one serving of sugar sweetened soft drinks a month. Fructose rich fruits
and fruit juices may also increase the risk. Diet soft drinks were not
associated with the risk of gout. [855]
Other foods high in fructose are fruit-yoghurt, candies, backery where corn syrup
is added.
[853]
Sugar-sweetened carbonated beverages and juices have a high glycemic load
relative to other foods and beverages. Mark Pereira and colleagues 2010 write two
or more soft drinks per week, but not juices, may increase the level of insulin
in the body double the pancreatic cancer risk compared with persons which do not
drink soft drinks. However limitations of this study are seen in the fact that
soft drink consumption is often associated with overweight increase, smoking, red
meat intake and reduced exercise and may not be sufficiently considered in this
study.
Interestingly South Chinese population differ from European and Western
population regarding the effect of nutrition health related issues. Increased BMI
is a robust risk factor for type 2 diabetes. This, however is not valid for South
Asians which have relatively low BMIs despite a high prevalence of type 2
diabetes. Odegaard and colleagues 2009 found that Singaporean Chinese with lean
or normal BMI have an increased risk of type 2 diabetes.
[854]

OurFood (c) 1998 - 2010 by Karl Heinz Wilm - Imprint (Impressum)