The Recipe of the "Gans Bread" by Jedi Simon is as follows.

 

1 cube of brewer's yeast.

Gans water according to needs. Look warm, 35 c° to melt yeast.

Add a spoon of pure cane sugar, dark one, to feed the yeast.

Add flour, 800 grams, possibly natural, the best you can find, and add 100 grams of durum wheat flour.

Add a pinch of salt for every loaf you will make. Normally 4 or five.

Add olive oil, one table spoon per loaf.

Place the mixture in a container above the oven, 80 c° to rest at least one hour to three hours. ( cover it with a lid or cloth ) ( it will double or triple the size, so choose

a big container ).

 

Please, if you are going to use white bleached flour, consider the elements that should not be there and shall interact with it.

We should avoid : list from wikipedia.... these chemicals...

The four most common additives used as bleaching/maturing agents in the US are:

• Potassium bromate , listed as an ingredient, is a maturing agent that strengthens gluten development. It does not bleach.
• Benzoyl peroxide bleaches, but does not act as a maturing agent. It has no effect on gluten.
• Ascorbic acid is listed as an ingredient, either as an indication that the flour was matured using ascorbic acid or that a small amount is added as a dough enhancer. It is a maturing agent that strengthens gluten development, but does not bleach.
• Chlorine gas is used as both a bleaching agent and a maturing agent. It weakens gluten development and oxidizes starches, making it easier for the flour to absorb water and swell, resulting in thicker batters and stiffer doughs. The retarded gluten formation is desirable in cakes, cookies, and biscuits, as it would otherwise make them tougher and bread-like. The modification of starches in the flour allows the use of wetter doughs (making for a moister end product) without destroying the structure necessary for light, fluffy cakes and biscuits.^[10] Chlorinated flour allows cakes and other baked goods to set faster and rise better, and the fat to be distributed more evenly, with less vulnerability to collapse.

Some other chemicals used as flour treatment agents to modify color and baking properties include:

• Chlorine dioxide (unstable to be transported in the U.S.)
• Calcium peroxide
• Azodicarbonamide or azobisformamide (synthetic)
• Atmospheric oxygen causes natural bleaching.

Common preservatives in commercial flour include:

• Calcium propanoate
• Sodium benzoate
• Tricalcium phosphate
• Butylated hydroxyanisole

When the preparation is ready, we shall rise the temperature of the oven to 260 c°

whilst preparing the loafs. Use some more flour to make them, without compressing them too much,

because touch should be a delicate one, and never a strong one.

Place the 5 loafs on the baking tray, and then, with a knife, cut the surface of the loafs, half cm deep, in parallel cuts,

at a distance of 1 cm each, to allow the expansion of the bread in the oven.

Finally, place them in the oven, and wait. If you have a ventilated oven, one hour should be the approximate time.

Minimum 48 minutes to 1hr 10 maximum, according to different models.

 

About Gans Water to be used to make Gans Bread

 

I usually use Radiant Gans Water, that has been exposed to a specific quantity of CO2 gans, for at least one week to 4 months.

The quantity of gans shall be of 100 grams minimum, placed in variable positions and configurations, according to Your needs. I usually use a central one within the water, and external ones, around it.

In case you would like to use a stronger Radiant Gans Water, so, for example, one that will be charged for 30 days, you shall add a small quantity ( a few drops  30 to 90 ) of Silver Colloidal, to keep it pure.

This water, shall be kept in the dark, but before using it, it shall be exposed to direct sun light for some hours.

 

The use of Direct Gans Water, one that has been in contact for some time with the gans, directly and alchemically, shall only be advised to solve those conditions which require particular strengths that are not reachable by Radiant, and,

in this specific case, should be used in very small quantities to be added to the water that you will use to make your loafs.

 

Take care and good appetite. “May the loaf be with you”, shall be the blessing used to offer this bread, and the receiver shall answer, “and with your heart and soul”.

 

Jedi Simon      

 

Concerning additives, then, I developed the study a little more, so that you may avoid them and know what eventually bread could contain, to avoid allergies etc...

This second study, is based on well known information that you may easily find in wikipedia: I data mined this search for you, to allow you to go a little deeper....

 

The Recipe of the Gans Bread is as follows.

 

1 cube of brewer's yeast.

Gans water according to needs. Look warm, 35 c° to melt yeast.

Add a spoon of pure cane sugar, dark one, to feed the yeast.

Add flour, 800 grams, possibly natural, the best you can find, and add 100 grams of durum wheat flour.

Add a pinch of salt for every loaf you will make. Normally 4 or five.

Add olive oil, one table spoon per loaf.

Place the mixture in a container above the oven, 80 c° to rest at least one hour to three hours. ( cover it with a lid or cloth ) ( it will double or triple the size, so choose

a big container ).

 

Please, if you are going to use white bleached flour, consider the elements that should not be there and shall interact with it.

We should avoid : list from wikipedia.... these chemicals...

The four most common additives used as bleaching/maturing agents in the US are:

• Potassium bromate , listed as an ingredient, is a maturing agent that strengthens gluten development. It does not bleach.
• Benzoyl peroxide bleaches, but does not act as a maturing agent. It has no effect on gluten.
• Ascorbic acid is listed as an ingredient, either as an indication that the flour was matured using ascorbic acid or that a small amount is added as a dough enhancer. It is a maturing agent that strengthens gluten development, but does not bleach.
• Chlorine gas is used as both a bleaching agent and a maturing agent. It weakens gluten development and oxidizes starches, making it easier for the flour to absorb water and swell, resulting in thicker batters and stiffer doughs. The retarded gluten formation is desirable in cakes, cookies, and biscuits, as it would otherwise make them tougher and bread-like. The modification of starches in the flour allows the use of wetter doughs (making for a moister end product) without destroying the structure necessary for light, fluffy cakes and biscuits.^[10] Chlorinated flour allows cakes and other baked goods to set faster and rise better, and the fat to be distributed more evenly, with less vulnerability to collapse.

Some other chemicals used as flour treatment agents to modify color and baking properties include:

• Chlorine dioxide (unstable to be transported in the U.S.)
• Calcium peroxide
• Azodicarbonamide or azobisformamide (synthetic)
• Atmospheric oxygen causes natural bleaching.

Common preservatives in commercial flour include:

• Calcium propanoate
• Sodium benzoate
• Tricalcium phosphate
• Butylated hydroxyanisole

When the prepartion is ready, we shall rise the temperature of the oven to 240 c° 260 c°

whilst preparing the loafs. Use some more flour to make them, without compressing them too much,

because touch should be a delicate one, and never a strong one.

Place the 5 loafs on the baking tray, and then, with a knife, cut the surface of the loafs, half cm deep, in parallel cuts,

at a distance of 1 cm each, to allow the expansion of the bread in the oven.

Finally, place them in the oven, and wait. If you have a ventilated oven, one hour should be the approximate time.

Minimum 48 minutes to 1hr 10 maximum, according to different models.

 

About Gans Water to be used to make Gans Bread

 

I usually use Radiant Gans Water, that has been exposed to a specific quantity of CO2 gans, for at least one week to 4 months.

The quantity of gans shall be of 100 grams minimum, placed in variable positions and configurations, according to Your needs. I usually use a central one within the water, and external ones, around it.

In case you would like to use a stronger Radiant Gans Water, so, for example, one that will be charged for 30 days, you shall add a small quantity ( a few drops  30 to 90 ) of Silver Colloidal, to keep it pure.

This water, shall be kept in the dark, but before using it, it shall be exposed to direct sun light for some hours.

 

The use of Direct Gans Water, one that has been in contact for some time with the gans, directly and alchemically, shall only be advised to solve those conditions which require particular strengths that are not reachable by Radiant, and, in this specific case, should be used in very small quantities to be added to the water that you will use to make your loafs.

 

This second recipe, shall be probably described in detail in a Blue Print in the near future. Take care and good appetite.  “May this bread feed your body, heart and soul". ( blessing ).

Addendum: Since there are at least a couple of substances that shall be added by the transmutation itself, that we did not consider in the formula, but appear in the final composition of the bread, We should take great care of them because even in very small quantities, these could create problems. A missing one, present in most of the industrial flour we buy is a dangerous mushroom that is present in silos where the flour is kept, but shall not appear as an ingredient, although it is a toxic one, and in reality, is a consequence of parasitic infestation.

I shall copy here Wikipedia’s shared knowledge for educational purposes.

The three substances are:

Benzopyrene, ( that shall appear every time you heat up food, burning it, and use fire to cook, not balancing it with the right quantity of water…. )

Benzo[a]pyrene is a polycyclic aromatic hydrocarbon and the result of incomplete combustion of organic matter at temperatures between 300 °C (572 °F) and 600 °C (1,112 °F). The ubiquitous compound can be found in coal tar, tobacco smoke and many foods, especially grilled meats. The substance with the formula C₂₀H₁₂ is one of the benzopyrenes, formed by a benzene ring fused to pyrene. Its diol epoxide metabolites (more commonly known as BPDE) react and bind to DNA, resulting in mutations and eventually cancer. It is listed as a Group 1 carcinogen by the IARC. In the 18th century a scrotal cancer of chimney sweepers, the chimney sweeps' carcinoma, was already known to be connected to soot. Benzo[a]pyrene (BaP) is a polycyclic aromatic hydrocarbon found in coal tar with the formula C₂₀H₁₂. The compound is one of the benzopyrenes, formed by a benzene ring fused to pyrene, and is the result of incomplete combustion at temperatures between 300 °C (572 °F) and 600 °C (1,112 °F). The main source of atmospheric BaP is residential wood burning.^[4] It is also found in coal tar, in automobile exhaust fumes (especially from diesel engines), in all smoke resulting from the combustion of organic material (including cigarette smoke), and in charbroiled food. A 2001 National Cancer Institute study found levels of BaP to be significantly higher in foods that were cooked well-done on the barbecue, particularly steaks, chicken with skin, and hamburgers: Cooked meat products have been shown to contain up to 4 ng/g of BaP,^[5] and up to 5.5 ng/g in fried chicken^[6] and 62.6 ng/g in overcooked charcoal barbecued beef.

Toxicity

Nervous system

Prenatal exposure of BaP to rats is known to affect learning and memory in rodent models. Pregnant rats eating BaP were shown to negatively effect the brain function in the late life of their offspring; at a time when synapses are first formed and adjusted in strength by activity BaP diminished NMDA receptor-dependent nerve cell activity measured as mRNA expression of the NMDA NR2B receptor subunit.^[10]

Immune system

BaP has an effect on the number of white blood cells, inhibiting some of them from differentiating into macrophages, the body’s first line of defense to fight infections. In 2016, the molecular mechanism was uncovered as damage to the macrophage membrane's lipid raft integrity by decreasing membrane cholesterol at 25%. This means less immunoreceptors CD32 (a member of the Fc family of immunoreceptors) could bind to IgG and turn the white blood cell into a macrophage. Therefore, macrophage membranes become susceptibile to bacterial infections.^[11]

Reproductive system

In experiments with male rats, sub-chronic exposure to inhaled BaP has been shown to generally reduce the function of testicles and epididymis with lower sex steroid/ testosterone production and sperm production.^[12]

Carcinogenicity

BaP's metabolites are mutagenic and highly carcinogenic, and it is listed as a Group 1 carcinogen by the IARC. Chemical agents and related occupations, Volume 10, A review of Human Carcinogens, IARC Monographs, Lyon France 2009 ^[13]

In June 2016, BaP was added as benzo[def]chrysene to the REACH Candidate List of Substances of very high concern for Authorisation.^[14]

Numerous studies since the 1970s have documented links between BaP and cancers.^[15] It has been more difficult to link cancers to specific BaP sources, especially in humans, and difficult to quantify risks posed by various methods of exposure (inhalation or ingestion).^{[citation needed]} A link between vitamin A deficiency and emphysema in smokers was described in 2005 to be due to BaP, which induces vitamin A deficiency in rats.^[16]

A 1996 study provided molecular evidence linking components in tobacco smoke to lung cancer. BaP was shown to cause genetic damage in lung cells that was identical to the damage observed in the DNA of most malignant lung tumours.^[17]

Regular consumption of cooked meats has been epidemiologically associated with increased levels of colon cancer^[18] (although this in itself does not prove carcinogenicity),^[19] A 2005 NCI study found an increased risk of colorectal adenomas was associated with BaP intake, and more strongly with BaP intake from all foods.^[20] However, the foods themselves are not necessarily carcinogenic, even if they contain trace amounts of carcinogens, because the gastrointestinal tract protects itself against carcinomas by shedding its outer layer continuously.^{[citation needed]} Furthermore, detoxification enzymes, such as cytochromes P450 have increased activities in the gut for protection from food-borne toxins. Thus, in most cases, small amounts of BaP are metabolized prior to being passed into the blood.^{[citation needed]} The lungs are not protected in either of these manners.^{[citation needed]}

The detoxification enzymes cytochrome P450 1A1 (CYP1A1) and cytochrome P450 1B1 (CYP1B1) are both protective and necessary for benzo[a]pyrene toxicity. Experiments with strains of mice engineered to remove (knockout) CYP1A1 and CYP1B1 reveal that CYP1A1 primarily acts to protect mammals from low doses of BaP, and that removing this protection accumulates large concentrations of BaP. Unless CYP1B1 is also knocked out, toxicity results from the bioactivation of BaP to benzo[a]pyrene -7,8-dihydrodiol-9,10-epoxide, the ultimate toxic compound,.^{[21][better source needed]}

Interaction with DNA

Metabolism of benzo[a]pyrene yielding the carcinogenic benzo[a]pyren-7,8-dihydrodiol-9,10-epoxide.

A DNA adduct (at center) of benzo[a]pyrene, the major mutagen in tobacco smoke.^[22] Properly speaking, BaP is a procarcinogen, meaning that its mechanism of carcinogenesis depends on its enzymatic metabolism to BaP diol epoxide. It intercalates in DNA, covalently bonding to the nucleophilic guanine bases. X-ray crystallographic and nuclear magnetic resonance structure studies have shown how this binding distorts the DNA^[23] by confusing the double-helical DNA structure. This disrupts the normal process of copying DNA and causes mutations, which explains the occurrence of cancer after exposure. This mechanism of action is similar to that of aflatoxin which binds to the N7 position of guanine.^[24]

There are indications that benzo[a]pyrene diol epoxide specifically targets the protective p53 gene.^[25] This gene is a transcription factor that regulates the cell cycle and hence functions as a tumor suppressor. By inducing G (guanine) to T (thymidine) transversions in transversion hotspots within p53, there is a probability that benzo[a]pyrene diol epoxide inactivates the tumor suppression ability in certain cells, leading to cancer.

Benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide is the carcinogenic product of three enzymatic reactions:^[26]

1.       Benzo[a]pyrene is first oxidized by cytochrome P450 1A1 to form a variety of products, including (+)benzo[a]pyrene-7,8-epoxide.^[27]

2.       This product is metabolized by epoxide hydrolase, opening up the epoxide ring to yield (-)benzo[a]pyrene-7,8-dihydrodiol.

3.       The ultimate carcinogen is formed after another reaction with cytochrome P450 1A1 to yield the (+)benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide. It is this diol epoxide that covalently binds to DNA.

BaP induces cytochrome P4501A1 (CYP1A1) by binding to the AHR (aryl hydrocarbon receptor) in the cytosol.^[28] Upon binding the transformed receptor translocates to the nucleus where it dimerises with ARNT (aryl hydrocarbon receptor nuclear translocator) and then binds xenobiotic response elements (XREs) in DNA located upstream of certain genes. This process increases transcription of certain genes, notably CYP1A1, followed by increased CYP1A1 protein production.^[28] This process is similar to induction of CYP1A1 by certain polychlorinated biphenyls and dioxins. Seemingly, CYP1A1 activity in the intestinal mucosa prevents major amounts of ingested benzo(a)pyrene to enter portal blood and systemic circulation.^[29] Intestinal, but not hepatic, expression of CYP1A1 depends on TOLL-like receptor 2 (TLR2),^[30] which is a eucaryotic receptor for bacterial surface structures such as lipoteichoic acid. Moreover, BaP has been found to activate a transposon, LINE1, in humans

Acrilammide: the second substance that will form in the oven, as soon as we heat up food.

Acrylamide (or acrylic amide) is a chemical compound with the chemical formula C₃H₅NO. Its IUPAC name is prop-2-enamide. It is a white odorless crystalline solid, soluble in water, ethanol, ether, and chloroform. Acrylamide decomposes in the presence of acids, bases, oxidizing agents, iron, and iron salts. It decomposes non-thermally to form ammonia, and thermal decomposition produces carbon monoxide, carbon dioxide, and oxides of nitrogen.

Acrylamide can be prepared by the hydrolysis of acrylonitrile by nitrile hydratase. In industry, most acrylamide is used to synthesize polyacrylamides, which find many uses as water-soluble thickeners. These include use in wastewater treatment, gel electrophoresis (SDS-PAGE), papermaking, ore processing, tertiary oil recovery, and the manufacture of permanent press fabrics. Some acrylamide is used in the manufacture of dyes and the manufacture of other monomers.

The discovery of acrylamide in some cooked starchy foods in 2002 prompted concerns about its toxic effects in humans. According to the EFSA, the main toxicity risks of acrylamide are "Neurotoxicity, adverse effects on male reproduction, developmental toxicity and carcinogenicity".^[5][6] However, according to their research, there is no concern on non-neoplastic effects. Furthermore, while the relation between consumption of acrylamide and cancer in rats and mice has been shown, it is still not clear whether acrylamide consumption has an effect on the risk of developing cancer in humans, and existing epidemological studies in humans are very limited and don't show any relation between acrylamide and cancer in humans.^[5][7]

Acrylamide is classified as an extremely hazardous substance in the United States as defined in Section 302 of the U.S. Emergency Planning and Community Right-to-Know Act (42 U.S.C. 11002), and is subject to strict reporting requirements by facilities which produce, store, or use it in significant quantities.^[8]

Molecular biology laboratories

Polyacrylamide was first used in a laboratory setting in the early 1950s. In 1959, the groups of Davis and Ornstein^[9] and of Raymond and Weintraub^[10] independently published on the use of polyacrylamide gel electrophoresis to separate charged molecules.^[10] The technique is widely accepted today, and remains a common protocol in molecular biology labs.

Acrylamide has many other uses in molecular biology laboratories, including the use of linear polyacrylamide (LPA) as a carrier, which aids in the precipitation of small amounts of DNA. Many laboratory supply companies sell LPA for this use.^[11]

Other uses

The majority of acrylamide is used to manufacture various polymers.^[12][13] In the 1970s and 1980s, the proportionately largest use of these polymers was in water treatment.^[14] Additional uses include as binding, thickening or flocculating agents in grout, cement, sewage/wastewater treatment, pesticide formulations, cosmetics, sugar manufacturing, soil erosion prevention, ore processing, food packaging, plastic products, and paper production.^[12][15] Polyacrylamide is also used in some potting soil.^[12] Another use of polyacrylamide is as a chemical intermediate in the production of N-methylol acrylamide and N-butoxyacrylamide.^[15]

US demand for acrylamide was 253,000,000 pounds (115,000,000 kg) as of 2007, increased from 245,000,000 pounds (111,000,000 kg) in 2006.^[15]

Toxicity and carcinogenicity

Acrylamide is considered a potential occupational carcinogen by U.S. government agencies and classified as a Group 2A carcinogen by the IARC.^[15] The Occupational Safety and Health Administration and the National Institute for Occupational Safety and Health have set dermal occupational exposure limits at 0.03 mg/m³ over an eight-hour workday.^[4] In animal models, exposure to acrylamide causes tumors in the adrenal glands, thyroid, lungs, and testes.^[1] Acrylamide is easily absorbed by the skin and distributed throughout the organism; the highest levels of acrylamide post-exposure are found in the blood, non-exposed skin, kidneys, liver, testes, and spleen. Acrylamide can be metabolically-activated by cytochrome P450 to a genotoxic metabolite, glycidamide, which is considered to be a critical mode of action to the carcinogenesis of acrylamide. On the other hand, acrylamide and glycidamide can be detoxified via conjugation with glutathione to form acrylamide- and isomeric glycidamide-glutathione conjugates,^[16] subsequently metabolized to mercapturic acids and excreted in urine. Acrylamide has also been found to have neurotoxic effects in humans who have been exposed. Animal studies show neurotoxic effects as well as mutations in sperm.^[15]

As of 2018 it is still not clear whether dietary acrylamide consumption affects people's risk of developing cancer. Experimental results that are based on feeding acrylamide to animals might not be applicable to humans.^[17] Food industry workers exposed to twice the average level of acrylamide do not exhibit higher cancer rates.^[5]

Acrylamide is also a skin irritant and may be a tumor initiator in the skin, potentially increasing risk for skin cancer. Symptoms of acrylamide exposure include dermatitis in the exposed area, and peripheral neuropathy.^[15]

Laboratory research has found that some phytochemicals may have the potential to be developed into drugs which could alleviate the toxicity of acrylamide.^[18]

Occurrence in food and associated health risks

Discovery of acrylamide in foods

Hot french fries

Acrylamide was discovered in foods in April 2002 by Eritrean scientist Eden Tareke in Sweden when she found the chemical in starchy foods, such as potato chips (potato crisps), French fries (chips), and bread that had been heated higher than 120 °C (248 °F) (production of acrylamide in the heating process was shown to be temperature-dependent).^[19] It was not found in food that had been boiled^[19][20] or in foods that were not heated.^[19]

Acrylamide has been found in roasted barley tea, called mugicha in Japanese. The barley is roasted so it is dark brown prior to being steeped in hot water. The roasting process revealed 200–600 micrograms/kg of acrylamide in mugicha.^[21] This is less than the >1000 micrograms/kg found in potato crisps and other fried whole potato snack foods cited in the same study and it is unclear how much of this is ingested after the drink is prepared. Rice cracker and sweet potato levels were lower than in potatoes. Potatoes cooked whole were found to have significantly lower acrylamide levels than the others, suggesting a link between food preparation method and acrylamide levels.

Acrylamide levels appear to rise as food is heated for longer periods of time. Although researchers are still unsure of the precise mechanisms by which acrylamide forms in foods,^[22] many believe it is a byproduct of the Maillard reaction. In fried or baked goods, acrylamide may be produced by the reaction between asparagine and reducing sugars (fructose, glucose, etc.) or reactive carbonyls at temperatures above 120 °C (248 °F).^[23][24]

Later studies have found acrylamide in black olives,^[25] dried prunes,^[26][27] dried pears,^[26] coffee.,^[28][29] and peanuts^[27]

The FDA has analyzed a variety of U.S. food products for levels of acrylamide since 2002.^[30]

Acceptable limits

Although acrylamide has known toxic effects on the nervous system and on fertility, a June 2002 report by the Food and Agriculture Organization of the United Nations and the World Health Organization attempting to establish basic toxicology (threshold limit value, no-observed-adverse-effect levels, tolerable daily intake, etc.) concluded the intake level required to observe neuropathy (0.5 mg/kg body weight/day) was 500 times higher than the average dietary intake of acrylamide (1 μg/kg body weight/day). For effects on fertility, the level is 2,000 times higher than the average intake.^[31] From this, they concluded acrylamide levels in food were safe in terms of neuropathy, but raised concerns over human carcinogenicity based on known carcinogenicity in laboratory animals.^[31]

Opinions of health organizations

According to the American Cancer Society it is not clear, as of 2016, whether acrylamide consumption increases people's risk of developing cancer.^[32]

The World Health Organization (WHO) has set up a clearinghouse for information about acrylamide that includes a database of researchers and data providers; references for research published elsewhere; information updates about the current status of research efforts; and updates on information relevant to the health risk of acrylamide in food.^[33]

In February 2009, Health Canada announced that they were assessing whether acrylamide, which occurs naturally during the cooking of french fries, potato chips, and other processed foods, is a hazard to human health and whether any regulatory action needs to be taken. As of 2017, they are working with food producers and other governments to reduce the amount of acrylamide in processed foods.^[34] In December 2009, after a positive reception from the food industry, Health Canada invited comment from the public on this proposal.^[35] The European Chemical Agency added acrylamide to the list of substances of very high concern in March 2010.^[36]

Heat-generated food toxicants (HEATOX) study

The Heat-generated Food Toxicants (HEATOX) Project was a European Commission-funded multidisciplinary research project running from late 2003 to early 2007. Its objectives were to "estimate health risks that may be associated with hazardous compounds in heat-treated food [, and to] find cooking/processing methods that minimize the amounts of these compounds, thereby providing safe, nutritious, and high-quality food-stuffs."^[37][38] It found that "the evidence of acrylamide posing a cancer risk for humans has been strengthened,"^[39] and that "compared with many regulated food carcinogens, the exposure to acrylamide poses a higher estimated risk to European consumers."^[37] HEATOX sought also to provide consumers with advice on how to lower their intake of acrylamide, specifically pointing out that home-cooked food tends to contribute far less to overall acrylamide levels than food that was industrially prepared, and that avoiding overcooking is one of the best ways to minimize exposure at home.^[37]

Public awareness

On April 24, 2002, the Swedish National Food Administration announced that acrylamide can be found in baked and fried starchy foods, such as potato chips, breads, and cookies. Concern was raised mainly because of the probable carcinogenic effects of acrylamide. This was followed by a strong, but short-lived, interest from the press. On August 26, 2005, California attorney general Bill Lockyer filed a lawsuit against four makers of french fries and potato chips – H.J. Heinz Co., Frito-Lay, Kettle Foods Inc., and Lance Inc. – to reduce the risk to consumers from consuming acrylamide.^[40] The lawsuit was settled on August 1, 2008, with the food producers agreeing to cut acrylamide levels to 275 parts per billion in three years, to avoid a Proposition 65 warning label.^[41] The companies avoided trial by agreeing to pay a combined $3 million in fines as a settlement with the California attorney general's office.^[42]

In 2016 the UK Food Standards Agency launched a campaign called "Go for Gold" warning of the possible cancer risk associated with cooking potatoes and other starchy foods at high temperatures.^[5][43]

In 2018, a judge in California ruled that the coffee industry had not provided sufficient evidence that acrylamide contents in coffee were at safe enough levels to not require a Proposition 65 warning.^[44]

Occurrence in other products

Cigarettes

Cigarette smoking is a major acrylamide source.^[45][46] It has been shown in one study to cause an increase in blood acrylamide levels three-fold greater than any dietary factor.

Aflatoxin

Aflatoxins are poisonous carcinogens that are produced by certain molds (Aspergillus flavus and Aspergillus parasiticus) which grow in soil, decaying vegetation, hay, and grains. They are regularly found in improperly stored staple commodities such as cassava, chili peppers, corn, cotton seed, millet, peanuts, rice, sesame seeds, sorghum, sunflower seeds, tree nuts, wheat, and a variety of spices. When contaminated food is processed, aflatoxins enter the general food supply where they have been found in both pet and human foods, as well as in feedstocks for agricultural animals. Animals fed contaminated food can pass aflatoxin transformation products into eggs, milk products, and meat.^[1] For example, contaminated poultry feed is suspected in the findings of high percentages of samples of aflatoxin-contaminated chicken meat and eggs in Pakistan.^[2]

Children are particularly affected by aflatoxin exposure, which is associated with stunted growth,^[3] delayed development,^[4] liver damage, and liver cancer. An association between childhood stunting and aflatoxin exposure^[5] has been reported in some studies^[6][7] but could not be detected in all.^[8][9] Furthermore, a causal relationship between childhood stunting and aflatoxin exposure has yet to be conclusively shown by epidemiological studies, though such investigations are under way.^[10][11] Adults have a higher tolerance to exposure, but are also at risk. No animal species is immune. Aflatoxins are among the most carcinogenic substances known.^[12] After entering the body, aflatoxins may be metabolized by the liver to a reactive epoxide intermediate or hydroxylated to become the less harmful aflatoxin M₁.

Aflatoxins are most commonly ingested. However the most toxic type of aflatoxin, B₁, can permeate through the skin.^[13]

The United States Food and Drug Administration (FDA) action levels for aflatoxin present in food or feed is 20 to 300 ppb.^[14] The FDA has had occasion to declare both human and pet food recalls as a precautionary measure to prevent exposure.

The term "aflatoxin" is derived from the name of one of the molds that produce it, Aspergillus flavus. It was coined around 1960 after its discovery as the source of "Turkey X disease".^[15] Aflatoxins form one of the major groupings of mycotoxins.

Major types and their metabolites

At least 14 different aflatoxins are produced in nature.^[16] Aflatoxin B₁ is considered the most toxic and is produced by both Aspergillus flavus and Aspergillus parasiticus. Aflatoxin M₁ is present in the fermentation broth of Aspergillus parasiticus, but it and aflatoxin M₂ are also produced when an infected liver metabolizes aflatoxin B₁ and B₂.

• Aflatoxin B₁ and B₂, produced by Aspergillus flavus and A. parasiticus
• Aflatoxin G₁ and G₂, produced by some Group II A. flavus and Aspergillus parasiticus^[17]
• Aflatoxin M₁, metabolite of aflatoxin B₁ in humans and animals (exposure in ng levels may come from a mother's milk)
• Aflatoxin M₂, metabolite of aflatoxin B₂ in milk of cattle fed on contaminated foods^[18]
• Aflatoxicol
• Aflatoxin Q₁ (AFQ₁), major metabolite of AFB₁ in in vitro liver preparations of other higher vertebrates^[19]

Contamination conditions

Aflatoxins are produced by both Aspergillus flavus and Aspergillus parasiticus, which are common forms of 'weedy' molds widespread in nature. The presence of those molds does not always indicate that harmful levels of aflatoxin are present, but does indicate a significant risk. The molds can colonize and contaminate food before harvest or during storage, especially following prolonged exposure to a high-humidity environment, or to stressful conditions such as drought.

The native habitat of Aspergillus is in soil, decaying vegetation, hay, and grains undergoing microbiological deterioration, but it invades all types of organic substrates whenever conditions are favorable for its growth. Favorable conditions include high moisture content (at least 7%) and high temperature. Aflatoxins have been isolated from all major cereal crops, and from sources as diverse as peanut butter and cannabis. The staple commodities regularly contaminated with aflatoxins include cassava, chilies, corn, cotton seed, millet, peanuts, rice, sorghum, sunflower seeds, tree nuts, wheat, and a variety of spices intended for human or animal consumption. Aflatoxin transformation products are sometimes found in eggs, milk products, and meat when animals are fed contaminated grains.^[1]

A study conducted in Kenya and Mali found that the predominant practices for drying and storage of maize were inadequate in minimizing exposure to aflatoxins.^[20]

Organic crops, which are not treated with fungicides, may be more susceptible to contamination with aflatoxins.^[21]

Pathology

No animal species is immune to the acute toxic effects of aflatoxins. Adult humans have a high tolerance for aflatoxin exposure and rarely succumb to acute aflatoxicosis,^[22] but children are particularly affected, and their exposure can lead to stunted growth and delayed development, in addition to all the symptoms mentioned below.^[4]

High-level aflatoxin exposure produces an acute hepatic necrosis, resulting later in cirrhosis or carcinoma of the liver. Acute liver failure is made manifest by bleeding, edema, alteration in digestion, changes to the absorption and/or metabolism of nutrients, and mental changes and/or coma.^{[citation needed]}

Chronic exposure increases the risk of developing liver and gallbladder ^[23] cancer, as aflatoxin metabolites may intercalate into DNA and alkylate the bases through epoxide moiety. This is thought to cause mutations in the p53 gene, an important gene in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis (programmed cell death). These mutations seem to affect some base pair locations more than others, for example, the third base of codon 249 of the p53 gene appears to be more susceptible to aflatoxin-mediated mutations than nearby bases.^[24]

Chronic, subclinical exposure does not lead to symptoms so dramatic as acute aflatoxicosis.

The expression of aflatoxin-related diseases is influenced by factors such as species, age, nutrition, sex, and the possibility of concurrent exposure to other toxins. The main target organ in mammals is the liver, so aflatoxicosis primarily is a hepatic disease. Conditions increasing the likelihood of aflatoxicosis in humans include limited availability of food, environmental conditions that favour mould growth on foodstuffs, and lack of regulatory systems for aflatoxin monitoring and control.^[25]

A regular diet including apiaceous vegetables, such as carrots, parsnips, celery, and parsley may reduce the carcinogenic effects of aflatoxin.^[26]

Aflatoxin B₁ can cause immune suppression, and exposure to it is associated with an increased viral load in HIV positive individuals.^[27][28]

There is no specific antidote for aflatoxicosis. Symptomatic and supportive care tailored to the severity of the liver disease may include intravenous fluids with dextrose, active vitamin K, B vitamins, and a restricted, but high-quality protein diet with adequate carbohydrate content.

Detection in humans

There are two principal techniques that have been used most often to detect levels of aflatoxin in humans.

The first method is measuring the AFB₁-guanine adduct in the urine of subjects. The presence of this breakdown product indicates exposure to aflatoxin B₁ during the past 24 hours. This technique measures only recent exposure, however. Due to the half-life of this metabolite, the level of AFB₁-guanine measured may vary from day to day, based on diet, it is not ideal for assessing long-term exposure.

Another technique that has been used is a measurement of the AFB₁-albumin adduct level in the blood serum. This approach provides a more integrated measure of exposure over several weeks or months.

Animals

In dogs, aflatoxin has potential to lead to liver disease. Low levels of aflatoxin exposure require continuous consumption for several weeks to months in order for signs of liver dysfunction to appear.^[29] Some articles have suggested the toxic level in dog food is 100–300 ppb and requires continuous exposure or consumption for a few weeks to months to develop aflatoxicosis.^[30] No information is available to suggest that recovered dogs will later succumb to an aflatoxin-induced disease.

Turkeys are extremely susceptible to aflatoxicosis. Recent studies have revealed that this is due to the efficient cytochrome P450 mediated metabolism of aflatoxin B₁ in the liver of turkeys and deficient glutathione-S-transferase mediated detoxification.^[31][32]

Some studies on pregnant hamsters showed a significant relationship between exposure of aflatoxin B₁ (4 mg/kg, single dose) and the appearance of developmental anomalies in their offspring.^[33]

In 2005, Diamond Pet Foods discovered aflatoxin in a product manufactured at their facility in Gaston, South Carolina.^[34][35] In 23 states, Diamond voluntarily recalled 19 products formulated with corn and manufactured in the Gaston facility. Testing of more than 2,700 finished product samples conducted by laboratories confirmed that only two date codes of two adult dog formulas with the "Best By" dates of April 3, April 4, April 5, and April 11 had the potential to be toxic.^[36]

List of outbreaks

International sources of commercial peanut butter, cooking oils (e.g. olive, peanut and sesame oil), and cosmetics have been identified as contaminated with aflatoxin.^[37][38][39] In some instances, liquid chromatography-tandem mass spectrometry (LC-MS/MS), and other analytical methods, revealed a range from 48% to 80% of selected product samples as containing detectable quantities of aflatoxin. In many of these contaminated food products, the aflatoxin exceeded the safe limits of the U.S. Food and Drug Administration (FDA), or other regulatory agency.^[38][39][40]

• 2003 Kenya: acute poisoning, 120 confirmed deaths.^[41][42]
• February–March 2013: Romania, Serbia, Croatia imported into western Europe - 2013 aflatoxin contamination.
• February 2013: Iowa contamination.^[43]
• 2014 (ongoing): Nepal and Bangladesh, neonatal exposures, found in umbilical cord blood

 

Jedi Simon