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                        March 2007

31.03.2007: Little scientific evidence supporting corn oil health claim [1]
The petition: The FDA received a health claim petition dated April 28, 2006, submitted to the Food and Drug Administration (FDA or the agency) by ACH Food Companies, Inc. pursuant to section 403(r)(4) of the Federal Food, Drug, and Cosmetic Act (21 U.S.C. 343(r)(4)). The petition requested that the agency authorize a qualified health claim characterizing the relationship between the consumption of corn oil and corn oil-containing products and a reduced risk of heart disease. This petition proposed as model qualified health claims:

"Substituting corn oil for solid fats may reduce your risk of heart disease."
"Substituting corn oil for fats high in saturated fat may reduce your risk of heart disease."
"Scientific evidence establishes that including corn oil-containing foods in your diet may reduce your risk of heart disease. To achieve such benefits, include slightly less than 1 tablespoon (12 grams) of corn oil per day in your diet while not increasing calories, saturated fat or cholesterol. One serving of this product contains x grams of corn oil. Although there is scientific evidence supporting the claim, the evidence is not conclusive."

FDA decision: FDA concludes that there is sufficient evidence for a qualified health claim, provided that the claim is appropriately worded so as to not mislead consumers. Thus, FDA intends to consider exercising enforcement discretion for the following qualified health claim:

"Very limited and preliminary scientific evidence suggests that eating about 1 tablespoon (16 grams) of corn oil daily may reduce the risk of heart disease due to the unsaturated fat content in corn oil. FDA concludes that there is little scientific evidence supporting this claim. To achieve this possible benefit, corn oil is to replace a similar amount of saturated fat and not increase the total number of calories you eat in a day. One serving of this product contains (x) grams of corn oil."

The appropriate disclosure statement "See nutrition information for total fat content." must be included on the label and comply with 21 CFR 101.13(h).

[1] CFSAN/Office of Nutritional Products, Labeling, and Dietary Supplements
March 26, 2007: Qualified Health Claims: Letter of Enforcement Discretion - Corn Oil and Corn Oil-Containing Products and a Reduced Risk of Heart Disease (Docket No. 2006P-0243) http://www.cfsan.fda.gov/~dms/qhccorno.html


29.03.2007: Growth hormones and other chemicals in beef may be the link between male fertility and high beef consumption during pregnancy [1]

Shanna H. Swan and colleagues looked at possible long-term risks from anabolic steroids and other xenobiotics in beef. They examined mens' semen quality in relation to their mother's self-reported beef consumption during pregnancy.

The authors in a study published in March 2007, found that sperm concentration was inversely related to mothers' beef meals per week . In sons of "high beef consumers" (>7 beef meals/week), sperm concentration was 24.3% lower than in men whose mothers ate less beef. A history of previous subfertility was also more frequent among sons of "high beef consumers". Sperm concentration was not significantly related to mother's consumption of other meat (pork, veal or lamb), fish, chicken, soy or vegetables, or to the man's consumption of any meat.

The authors conclude that maternal beef consumption, and possibly xenobiotics in beef, may alter a man's testicular development in utero and adversely affect his reproductive capacity.

According to the authors, there were several possible explanations for the findings, including pesticides and other contaminants in cattle feed and lifestyle factors during pregnancy. Therefore they call to be cautious in the interpretation of the data because other factors like pesticides and other contaminants in cattle feed and lifestyle factors during pregnancy could influence results.

The authors say that in the period of 1949 and 1983 numerous chemical additives were used in meat in the US, and it would have been difficult for women to avoid hormone residues.

Dr. Swan call to repeat the study in men born in Europe after 1988 (after the hormone ban in Europe) to determine if prenatal exposure to anabolic steroids is responsible for a change in sperm count.

Anabolic steroids as growth promoters are still used in cattle-breeding in the USA. Six hormones are commonly used in cattle. The use of diethylstilberstrol was banned in 1979 and in 1988 all growth promoters in cattle were banned in the EU.

Comment of the American Meat Institute (AMI) [2]: AMI strongly criticises the methodology and conclusions, saying that the association of the observed effect with chemical compounds in meat is purely speculative, noting that the study did not include any laboratory analysis of compounds suggested to be contained in beef - nor of the actual beef reportedly consumed decades ago. AMI questions that mother can tell what they have eaten 30 to 40 years back.

[1] Swan, S.H.; Liu, F.; Overstreet, J.W.; Brazil, C. and Skakkebaek N.E.: Semen quality of fertile US males in relation to their mothers' beef consumption during pregnancy
Hum. Reprod., Advance Access published on March 28, 2007; doi:10.1093/humrep/dem068

[2] American Meat Institute Urges Consumers to Treat Study on Beef Consumption and Male Fertility With Healthy Dose of Skepticism.  Attribute to AMI Foundation Vice President of Scientific Affairs Dr. Randy Huffman Washington, DC, March 28, 2007
http://www.meatami.com/storylinks/2007/newbeefstudyandsperm.pdf


29.03.2007: Concentrated oat beta-glucan, a soluble fibre lowering serum lipids

Joanne Slavin and colleagues studied soluble fibre such as a concentrated oat beta-glucan on its effects on cardiovascular disease endpoints in human subjects.

Fermentability: In this study the fermentability of concentrated oat beta-glucan with inulin and guar gum in a model intestinal fermentation system was compared. It has been reported that fermentation products like propionate and acetate may suppress cholesterol synthesis and contribute to cholesterol lowering. All three were found to produced similar concentrations of short chain fatty acids and acetate, however, the oat beta-glucan was found to produce the highest concentrations of butyrate at 4, 8, and 12 hours, after which inulin produced the most.

In their study the authors found that six grams concentrated oat beta-glucan per day for six weeks significantly reduced total and LDL cholesterol in subjects with elevated cholesterol. No significant changes were observed in HDL cholesterol, glucose, insulin, homocysteine or C-reactive protein (CRP) as a result of the beta-glucan intervention. This oat beta-glucan was fermentable, producing higher amounts of butyrate than other fibers. The authors conclude that a practical dose of oat beta-glucan can significantly lower serum lipids in a high-risk population and may improve colon health. The authors also stress the fact that concentrated oat beta-glucan is suitable as a "stand-alone" supplement for cholesterol reduction, it can also be used as a food ingredient to increase fibre content of food.

[1] Queenan, Katie M.; Stewart, Maria L.; Smith, Kristen N.; Thomas, William; Fulcher, Gary R.; Slavin, Joanne L.: Concentrated oat beta-glucan, a fermentable fiber, lowers serum cholesterol in hypercholesterolemic adults in a randomized controlled trial Nutrition Journal 2007, 6:6 (26 March 2007) doi:10.1186/1475-2891-6-6

http://www.nutritionj.com/content/pdf/1475-2891-6-6.pdf

27.03.2007: Cloning of animals for better foods [2]

The European Commission requested the European Food Safety Authority to advise on food safety, animal health, animal welfare and environment implication of live cloned animals, obtained through somatic cell nucleus transfer (SCNT) technique, their offspring and of the products obtained from those animals. [1]

At present in Europe cloning is not a commercial practice and there is no specific regulation on the authorisation of food products from cloned animals for human consumption in the EU. EFSA's opinion will therefore help inform any future EU measures for cloned animals and their products.

Food safety officials from the 27 member states decided that milk and meat from cloned animals and their offspring should be considered in the same way as any other novel food, such as genetically-modified organisms (GMOs).

To prepare the advice, the EFSA refers to the Opinion Nr. 9 - 28.February 1997 - Ethical aspects of cloning techniques.Opinion requested by the European Commission on 28 February 1997 [2]. This opinion was prepared by European Group on Ethics in Science and New Technologies . [3]

The Group defines cloning as the process of producing "genetically identical" organisms. It may
involve division of a single embryo, in which case both the nuclear genes and the small number of mitochondrial genes would be "identical", or it may involve nuclear transfer, in which case only the nuclear genes would be “identical”.

But genes may be mutated or lost during the development of the individual: the gene set may be identical but it is unlikely that the genes themselves would ever be totally identical. In the present context, we use the term "genetically identical" to mean "sharing the same nuclear gene set".

According to the European Group on Ethics in Science and New Technologies [3] in their Opinion nr. 9 - 28/05/1997 - Ethical aspects of cloning techniques express that these new technologies increase the power of people over nature and thus increase their responsibilities and duties.

The Group cites the potential uses of cloning animals:
- in the field of medicine and medical research, to improve genetic and physiological knowledge, to make models for human diseases, to produce at lower cost proteins like milk proteins to be used for therapeutic aims, to provide source of organs or tissues for xenotransplantation;

- in agriculture and agronomical research, to improve the selection of animals or to reproduce animals having specific qualities (longevity, resistance,...) either innate, or acquired by transgenesis.

From the point of view of animal breeding, the technology could be useful, in particular if it increases the medical and agricultural benefits expected from transgenesis (genetic modification of animals).

By using genetic modification and selection in cultured cell lines, rather than in adult animals, it could become possible to remove genes, such as those provoking allergic reactions, as well as adding genes, for the benefit of human health.

Cloning of animals

The Group gives their opinion concerning cloning of animals:
Research on cloning in laboratory and farm animals is likely to add to our understanding of biological processes, in particular ageing and cell commitment, and hence may contribute to human well-being. It is ethically only acceptable if carried out with strict regard to animal welfare, under the supervision of licensing bodies.

Cloning of farm animals may prove to be of medical and agricultural as well as economic benefit. It is acceptable only when the aims and methods are ethically justified and when it is carried out under ethical conditions.

These ethical conditions include:
- the duty to avoid or minimize animal suffering since unjustified or disproportionate suffering is unacceptable;

- the duty of reducing, replacing and when possible refining the experimentation adopted for the use of animals in research;

- the lack of better alternatives;

- human responsibility for animals, nature and the environment, including biodiversity.

The group stresses the need to preserve genetic diversity in farm animal stocks. Strategies to incorporate cloning into breeding schemes while maintaining diversity should be developed by European institutions.

On regard to human reproductive cloning the Group writes that the European Community should clearly express its condemnation of human reproductive cloning and should take this into account in the relevant texts and regulations.

According to the Group, further efforts must be made to inform the public, to improve public awareness of potential risks and benefits of such technologies, and to foster informed opinion.

Cloned meat in USA
The US Food and Drug Administration (FDA) said it planned to approve cloning for food production in 2007 and to allow the product into the food chain without the need for labelling.

[1]European Commission request to EFSA for advice on the implications of animal cloning on food safety, animal health and welfare and the environment News 9.3.2007
http://www.efsa.europa.eu/en/science/sc\_commitee/requests\_mandates/sc\_wns\_cloning.html

[2]EFSA: Opinion Nr. 9 - 28.February 1997 - Ethical aspects of cloning techniques.Opinion requested by the European Commission on 28 February 1997 Rapporteur : Dr Anne McLaren.
http://ec.europa.eu/european_group\_ethics/docs/opinion9\_en.pdf

[3]European Group on Ethics in Science and New Technologies
http://ec.europa.eu/european\_group\_ethics/index\_en.htm


26.03.2007: Gene expressing saturated fatty acids [1]
John Shanklin and colleagues found that the gene beta-Ketoacyl-acyl carrier protein (ACP) synthase II (KASII) elongates 16:0-ACP to 18:0-ACP in the plastid, where it competes with three other enzymes at the first major branch point in fatty acid biosynthesis.

The authors conclude that early embryo development appears sensitive to elevated 16:0, whereas at later stages, up to 53% of 16:0, i.e., a 7-fold increase over wild-type levels, is tolerated. According to the authors, the role of KASII in seed metabolism are herewith explained. They say that the modulation of Arabidopsis KASII levels is sufficient to convert its temperate oilseed composition to that of a palm-like tropical oil.

This knowledge may lead to transform oilseed plants growing in moderate climate to produce palm oil similar fats which do not require hydrogenation and are thus free of trans-fatty acids. This could reduce the pressure on palm oil plantations.

[1] Pidkowich, Mark S.; Tam Nguyen, Huu; Heilmann, Ingo; Ischebeck, Till; and Shanklin, John: Modulating seed beta-ketoacyl-acyl carrier protein synthase II level converts the composition of a temperate seed oil to that of a palm-like tropical oil. Proceedings of the National Academy of Science of the United States of America PNAS March 13, 2007 vol. 104 no. 11 4742-4747
Doi:10.1073/pnas.0611141104
http://www.pnas.org/cgi/content/abstract/104/11/4742

25.03.2007: Trehalose proposed use
The function of trehalose during dehydration
[1]: Job Ubbink and colleagues studied the free volume in trehalose demonstrating that changes in free volume are intimately connected with molecular organization and mobility of water in the crystalline and amorphous states. The study proposes a mechanism for bioprotection for the survival of (micro) organisms under conditions of extreme temperature or dehydration, like baker's yeast which can be successively dehydrated and rehydrated without losing their viability. It is believed that during dehydration, baker's yeast produces high levels of trehalose, a key factor in biopreservation.

According to the authors, organisms, under extreme drought, form an intracellular carbohydrate glass This glass state has high viscosity and hydrogen-bonding interactions and stabilizes and protects the integrity of complex biological structures and molecules.

Trehalose as ingredient for dehydrated fruit products [2]: Drazenka Komes and colleagues found in a study that the best retention of aroma compounds in dehydrated pear purees was noticed in the case when freeze drying and trehalose addition were combined. In dehydrated pear cubes, previously dipped in trehalose solution, the highest aroma retention was also determined. This study showed possible application of trehalose as potentially beneficial food ingredient, with the aim to improve the quality of dehydrated fruit products, especially their aroma, and to produce superior dried fruit products or ingredients, which are widely used in food formulation.

The authors suggest that glass transformation properties of the material change from a crystalline (glass) to a liquid could prevent the loss of small volatile compounds such as esters during drying and storage.volatiles are encapsulated in the amorphous glass and low mobility leading to the increased stability of the material being preserved. Above the glassy state, temperature collapses and sometimes crystallization takes place… and the encapsulated volatiles are released.

[1] Kilburn, Duncan; Townrow, Sam; Meunier, Vincent; Richardson, Robert; Alam, Ashraf and Ubbink, Job: Organization and mobility of water in amorphous and crystalline trehalose Natur Materials, August 2006 pp. 632 - 635 doi:10.1038/nmat1681
http://www.nature.com/nmat/journal/v5/n8/abs/nmat1681.html

[2] Komes, Drazenka; Lovric, Tomislav and Kovacevic Ganic, Karin: Aroma of dehydrated pear products LWT - Food Science & Technology doi: 10.1016/j.lwt.2006.12.011


25.03.2007: Serious concerns regarding the food safety of GM corn MON 863 [1]
The maize for animal and human in many countries, including the EU, Japan, Mexico and the USA.

Signs of liver and kidney disruption: Seralini and colleagues at CRIIGEN (Committee for Independent Research and Genetic Engineering) based at the University of Caen, in a study supported by Greenpeace, found signs of liver and kidney toxicity in rats fed with transgenic maize MON863 which expresses the bt-toxin (Cry3Bb1) protecting against the corn rootworm pest. According to the researchers, It appears that the statistical methods used by Monsanto were not detailed enough to see such disruptions in biochemical parameters.

Difference in weight gain: The authors found significant differences in the weight gains data [2], with differences between male and females, and suggest
that this could be due to endocrine disruption and/or hormonal metabolism differences caused by the GM corn.

Cause of toxicity not known: It is not known whether the signs of toxicity are caused by the Bt protein, or from some changes in the plant's own DNA caused by the genetic engineering event.

The authors cannot conclude that GM corn MON863 is a safe product. Companies should be more rigorous in the studies and ensure that their data stands up to scrutiny, and the regulatory authorities such as the EFSA in Europe [3], have failed to recognise the warning signs, recommending for approval a genetic engineered crop that has potential to cause adverse effects on health.

[1] Seralini, G-E, Cellier, D. & Spiroux de Vendomois, J. 2007. New analysis of a rat feeding study with a genetically modified maize reveals signs of hepatorenal toxicity. Archives of Environmental Contamination and Toxicology
doi: 10.1007/s00244-006-0149-5.

[2] Hammond, B., Lemen, J., Dudek, R., Ward, D., Jiang, C., Nemeth, M. & Burns, J. 2006. Results of a 90-day safety assurance study with rats fed grain from corn rootworm-protected corn. Food and Chemical Toxicology 44: 147-160.

[3] EFSA 2004. Opinion of the Scientific Panel on Genetically Modified Organisms on a request from the Commission related to the safety of foods and food ingredients derived from insect-protected genetically modified maize MON 863 and MON 863 x
MON 810, for which a request for placing on the market was submitted under Article 4 of the Novel Food Regulation (EC) No 258/97 by Monsanto (Question No EFSA-Q-2003-121).Opinion adopted on 2 April 2004. The EFSA Journal 50: 1-25


24.03.2007 Citrus canker: USDA APHIS study not supported by scientifically sound evidence.
The USDA APHIS evaluation of asymptomatic citrus fruit, (Citrus spp.) as a pathway for the introduction of citrus canker disease (Xanthomonas axonopodis pv. citri) concludes that it is highly unlikely that citrus canker could be introduced on asymptomatic, commercially produced citrus fruit that has been treated with disinfectant dips and subject to other mitigations. Even if infected fruit were to enter a canker-free area with susceptible hosts, the establishment of citrus canker via this pathway appears to be unlikely.[1]

The new Plant Health (PLH) Panel of the European Food Safety Authority (EFSA) evaluated a recent study on citrus canker disease published by the US Agriculture Department’s Animal and Plant Health Inspection Services (APHIS) with special attention to its conclusion that citrus canker is not likely to spread by means of citrus fruit that show no signs of the disease. The PLH Panel concluded that key arguments in the study, and its conclusions, were not supported by scientifically sound evidence. [2]

Citrus canker is an economically significant plant disease caused by the bacterium Xanthomonas axonopodis pv. citri (Xac) affecting most of the citrus growing areas in the world, including Florida. Once established, various control methods including spraying of copper compounds must be combined to reduce the damage by Xac. [3]

Rigorous phytosanitary measures have insured that some areas, including Europe, are still free of the disease. These include the use of systems approaches. The current systems approach for the trade of citrus fruit requires that fruit are coming from disease-free area surrounded by a non-export buffer zone. The APHIS document proposes to modify the systems approach so that asymptomatic fruit coming from infected/contaminated areas are eligible for trade. [3]

The APHIS proposal to allow fruit from contaminated groves to be traded is a major deviation from existing phytosanitary measures. The APHIS document analyses the five events that must occur for successful introduction and proposes a new systems approach to prevent entry and establishment. However, no new or additional studies are presented and the analysis of the evidence provided in the document does not justify a change in the regulations. None of the preventative measures in the systems approach proposed by APHIS are shown to give effective control of Xac. Therefore, it can be concluded that, where an initial inoculum load exists, the transmission of Xac in the scheme proposed by APHIS is more likely than with the current systems approach. [3]

This demonstrates the necessity to ensure that work like the affirmations of APHIS is peer reviewed before it is disseminated. (see 24.03.2007 Universal Ethical Code for Scientists ).

[1] Federal Register: April 6, 2006 (Volume 71, Number 66)Page 17434-17435 Docket No. APHIS-2006-0045: Availability of an Evaluation of Asymptomatic Citrus Fruit as a Pathway for the Introduction of Citrus Canker Disease.
http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-5015.htm

[2] EFSA: Plant Health Panel evaluates study on citrus canker disease.
http://www.efsa.europa.eu/en/press_room/press_release/pr_plh_citrus_canker.html

[3] Opinion of the Scientific Panel on Plant Health on a request from the Commission on an evaluation of asymptomatic citrus fruit as a pathway for the introduction of citrus canker disease (Xanthomonas axonopodis pv. citri) made by the US Animal and Plant Health Inspection Service, The EFSA Journal (2006) 439, 1-41
http://www.efsa.europa.eu/en/science/plh/plh_opinions/plh_ej349_aphis.html


24 03.2007: Universal Ethical Code for Scientists [1] [2]
The UK Government Chief Scientific Advisor, Sir David King, on the 13.03.07,  gave a presentation
on the Universal Ethical Code for Scientists- Rigour, Respect and Responsibility.

The code has three key aims:

  • Foster ethical research
  • Encourage active reflection among scientists on the implication and impacts of their work.
  • Support communication between scientists and the public on complex and challenging issues

It covers the natural sciences and also the wider disciplines of social, medical and veterinary sciences and mathematics. Some comments include not committing plagiarism or condoning acts of plagiarism by others; ensuring that work is peer reviewed before it is disseminated; reviewing the work of others fairly; ensuring that primary data that may be needed to allow others to audit, repeat or build on work, are secured and stored.

[1] DTI: Rigour, respect and responsibility: A universal ethical code for scientists http://www.dti.gov.uk/science/science-and-society/public_engagement/code/page28030.html

[2] To access the code, go to:
http://www.dti.gov.uk/science/science-and-society/public_engagement/code/page28029.html

23.07.2007: Peanut, vaccination and atopic allergic disease revision
The UK Department of Health advice issued by the Committee on Toxicity in Chemicals in Food, Consumer Products and the Environment (COT) issued in 1998 a precautionary advice that pregnant or breast-feeding women with a family history of atopy, may wish to avoid eating peanuts during pregnancy and lactation as this could increase the chances of peanut sensitisation in children.

Atopy or atopic syndrome is an allergic hypersensitivity affecting parts of the body not in direct contact with the allergen. There appears to be a strong hereditary component linked to genes such as 5q31-33 with a cluster of cytokine genes. The individual components, such as asthma, eczema or hay fever, are all caused at least in part by type I I hypersensitivity reactions. [1] [2]

Consumption of peanut during pregnacy: Dr. Tara Dean and Dr. Carina Venter assessed the compliance with this recommendation and its impact upon peanut sensitization.

In this study children sensitized to peanuts were found, but their mothers had not consumed peanuts during pregnacy. The scientists conclude therefore that maternal consumption of peanuts during pregnancy was not associated with peanut sensitization in the infant.

The majority of mothers avoided peanut consumption during pregnancy. The authors found that either the government advice is misunderstood by mothers, or that those who communicate the advice have not fully explained who it is targeted at, and stress the necessity of a review of the 1998 COT document.

The authors call for clear, consistent factual advice and information about the real risks associated with peanut consumption during pregnancy/lactation and peanut allergy in the developing child, and specifically to whom these risks apply. [3]

Atopy and vaccination: Analysing prevalences of allergic sensitization and atopic disease in relation to vaccination coverage. Grüber and colleagues (2003) found that children with a higher vaccination coverage seemed to be transiently better protected against development of atopy in the first years of life. [4]

Grüber reassured in 2005 that common childhood vaccines are unlikely to promote atopic disease. He wrote that possible future development of atopic symptoms is most likely not causally related to vaccination but a coincidence. However, according to Grüber, vaccines specifically designed to down-regulate Th-2 type immunity have to be further elucidated if they are safe and effective in preventing the development of atopic disease. He concludes that effective protection against potentially life threatening or disabling infectious diseases should be offered to every child-atopic or not. [5]

According to Nakajima and colleagues in 2007 all few effects, which were seen in their study concerning vaccination and atopic disease, were small and age-dependent. The study supports numerous previous studies of no effect of vaccines on asthma. The authors conclude that the fear of their child developing atopic disease should not deter parents from immunising their children, especially when weighed against the benefits.[6]

[1] Wikipedia, the free enzyclopedia: Atopy.
http://en.wikipedia.org/wiki/Atopy

[2] Johansson SGO et al. A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force. Allergy 2001; 56: 813-824

doi:10.1034/j.1398-9995.2001.t01-1-00001.x

[3] Dean, T.; Venter, C.; Pereira, B.; Grundy, J.; Clayton, C. B.; Higgins, B.; (2007): Government advice on peanut avoidance during pregnancy – is it followed correctly and what is the impact on sensitization? Journal of Human Nutrition and Dietetics 20 (2), 95–99. doi:10.1111/j.1365-277X.2007.00751.x
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1365-277X.2007.00751.x

[4] Grüber, Christoph. Illi, Sabina; Lau, Susanne; Nickel Renate; Forster Johannes; Kamin, Wolfgang; Bauer, Carl-Peter; Wahn,Volker; Wahn, Ulrich; MAS-90 Study Group: Transient suppression of atopy in early childhood is associated with high vaccination coverage. Pediatrics Vol. 111 No. 3 March 2003, pp. e282-e288
http://pediatrics.aappublications.org/cgi/content/full/111/3/e282

[5] Grüber, Christoph: Childhood immunisations and the development of atopic disease. Archives of Disease in Childhood 2005;90:553-555
http://adc.bmj.com/cgi/content/full/90/6/553

[6] Nakajima, K.; Dharmage, S. C.; Carlin, J.B.; Wharton, C.L.; Jenkins, M.A.; Giles, G.G.; Abramson, M.J.; Haydn Walters, E. and Hopper J.L.: Is childhood immunisation associated with atopic disease from age 7 to 32 years? Thorax, March 1, 2007; 62(3): 270 - 275.

http://thorax.bmj.com/cgi/content/abstract/62/3/270


22.03.2007: BASF and Monsanto are united in plant biotechnology.The two giants wich dominate agricultural products joined at March 21, 2007.

The cooperation will focus on the development of crops with higher yields and crops
that lead to consistent yields under adverse environmental conditions, such as drought.

The most promising candidate genes of both companies will be advanced for
accelerated joint development and for commercialization by Monsanto.

The two companies expect to generate a greater number of viable research projects
than they could have done on their own, accelerate the development of new products,
and bring a greater number of traits to the market at a faster speed.

Monsanto will receive 60 percent of net profits and BASF will receive 40 percent of
net pr
ofits.[1]

[1]BASF and Monsanto Announce R&D and Commercialization Collaboration Agreement
in Plant Biot
echnology
http://monsanto.mediaroom.com/index.php?s=43&item=470

21.03.07: Studies reveal hypovitaminosis of vitamin D and call to increase vitamin D intake.
Elina Hyppönen 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 during the winter and spring, which warrants action at a population level rather than at a risk group level. [1]

Julia Knight and colleagues found, in an epidemiological study, that reduced breast cancer risks were associated with increasing 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, and 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.[2]

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)D level 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. [3]

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).  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. [4] [5]

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 colleauges 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. [6]

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. [7]


[1] Hyppönen, Elina and Power, Chris: Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors Am J Clin Nutr 2007 85: 860-868.
http://www.ajcn.org/cgi/content/abstract/85/3/860

[2]Knight, Julia A.; Lesosky, Maia; Barnett, Heidi; Raboud, Janet M. and Vieth, Reinhold: Vitamin D and Reduced Risk of Breast Cancer: A Population-Based Case-Control Study Cancer Epidemiology Biomarkers & Prevention 2007 16: 422-429 doi: 10.1158/1055-9965.EPI-06-0865

[3] Zhou, Wei; Heist, Rebecca S.; Liu, Geoffrey; Asomaning, Kofi; Neuberg, Donna S.; Hollis, Bruce W.; Wain, John C.; Lynch, Thomas J.; Giovannucci, Edward; Su, Li ; Christiani, David C.: Circulating 25-Hydroxyvitamin D Levels Predict Survival in Early-Stage Non-Small-Cell Lung Cancer Patients J. Clin. Oncol., February 10, 2007; 25(5): 479 - 485.
http://jnci.oxfordjournals.org/cgi/reprint/98/7/428

[4]Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr 2006;84:18–28.
http://www.ajcn.org/cgi/ijlink?linkType=ABST&journalCode=ajcn&resid=84/1/18

[5]Visser M, Deeg DJ, Puts MT, Seidell JC, Lips P. Low serum concentrations of 25-hydroxyvitamin D in older persons and the risk of nursing home admission. Am J Clin Nutr 2006;84:616-22. http://www.ajcn.org/cgi/ijlink?linkType=ABST&journalCode=ajcn&resid=84/3/616

[6]Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr 2006;84:18–28.
http://www.ajcn.org/cgi/ijlink?linkType=ABST&journalCode=ajcn&resid=84/1/18

[7] Reinhold Vieth, Heike Bischoff-Ferrari, Barbara J Boucher, Bess Dawson-Hughes, Cedric F Garland, Robert P Heaney, Michael F Holick, Bruce W Hollis, Christel Lamberg-Allardt, John J McGrath, Anthony W Norman, Robert Scragg, Susan J Whiting, Walter C Willett, and Armin Zittermann: The urgent need to recommend an intake of vitamin D that is effective AJCN 2007 85: 649-650. http://www.ajcn.org/cgi/content/full/85/3/649


19.03.2007: Improved absorption of omega-3 fatty acids by pre-emulsification.

Plummer and colleagues ( January 2007) studying the absorption of omega-3 fatty acid, found that pre-emulsifying a blend of a standardized oil increases significantly the postprandial plasma triacylglycerol (TAG) and the C18:3 (n-6), C18:3(n-3), C20:5(n-3) and C22:6 (n-3) polyunsaturated fatty acid (PUFA) levels. C16:0 and C18:0 saturated fatty acids, the C18:1 (n-9) monounsaturated fatty acid and the C18:2 PUFA were not significantly changed..compared with a non-emulsified oil group.

The authors conclude that the emulsification of an oil mixture prior to ingestion increases the absorption of longer chain more highly unsaturated fatty acids (especially eicosapentaenoic acid and docosahexaenoic acid) but does not affect absorption of shorter chain less saturated fatty acids,and suggest that pre-emulsification of fish oils may be a useful means of boosting absorption of these beneficial fatty acids. This study may lead to improved fish oil supplementation

[1] Garaiova, Iveta; Guschina, Irina A.; Plummer, Sue F.; Tang, James; Wang, Duolao and Plummer, Nigel T.: A randomised cross-over trial in healthy adults indicating improved absorption of omega-3 fatty acids by pre-emulsification. Nutrition Journal 2007, 6:4 doi:10.1186/1475-2891-6-4 http://www.nutritionj.com/content/6/1/4/abstract


18.03.02007New discussion connecting high fructose syrup with obesity
High fructose corn syrup (HFCS) was introduced in the 1970s. Food industry, particularly the soft drink industry, uses fructose syrup in excess. Removing fructose from soft beverages could help to reduce obesity, as a possible mechanism is suggested which may explain the link between rising obesity and sweetened beverages.

Three important studies report that high fructose corn syrup is an important factor in the rising obesity epidemic:
According to Hella S. Jürgens and colleagues (2005), from the Department of Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, exposure to fructose water increased adiposity, whereas increased fat mass after consumption of soft drinks or diet soft drinks did not reach statistical significance. Total intake of energy was unaltered, because mice proportionally reduced their caloric intake from chow. The researchers found that  fructose also produced a hepatic lipid accumulation with a characteristic pericentral pattern.
The authors conclude that that a high intake of fructose selectively enhances adipogenesis, possibly through a shift of substrate use to lipogenesis. [1]

Swiss researcher Kim-Anne Lê and colleagues report in December 2006 that moderate fructose supplementation over 4 weeks increases plasma triacylglycerol and glucose concentrations without causing ectopic lipid deposition or insulin resistance in healthy humans. [2]

In a recent article from February 27, 2007 Juan Carlos Laguna and colleagues note that liquid fructose changes the metabolism of fat in the liver by impacting a specific nuclear receptor called PPAR-alpha, leading to a reduction in the liver's ability to degrade the sugar. According to the authors, this would partly explain the link between increased consumption of fructose and widening epidemics of obesity and metabolic syndrome. In their article the authors conclude that hypertriglyceridemia and the retention of fat in liver induced by fructose ingestion result from a reduction in the hepatic catabolism of fatty acids driven by a state of leptin resistance.
According to this research, the fructose increased fat synthesis in the liver and also acted on the PPAR-alpha receptor( which controls the oxidation of fatty acids) to reduce the degradation of the fructose, and reduces the activity of the hormone leptin which is engaged in the metabolism of faty acids in liver.[3]

The Corn Refiners Association CRA position
The Corn Refiners Association (CRA), claims in a release from April 6, 2006, that that HFCS is not the unique factor responsible for obesity.  http://www.hfcsfacts.com/
High fructose corn syrup (HFCS), according to Kathleen J Melanson is similar to sugar in the production of leptin, insulin and ghrelin and regulation of the body’s calorie control mechanisms. (Experimental Biology conference on April 1-5, 2006, San Francisco.) [4]

Martine Perrigue et al compared the level of fullness (satiety) after consuming HFCS-, sucrose- and aspartame-sweetened beverages with milk and a no-beverage control. The study found that all four caloric beverages suppressed hunger ratings and increased satiety ratings relative to the no beverage control. However, there were no significant differences in satiety profiles among the sucrose- and HFCS-sweetened beverages, diet cola, and 1% milk.  [5]

[1] Jürgens, Hella; Haass, Wiltrud; Castaneda, Tamara R.; Schürmann, Annette; Koebnick, Corinna; Dombrowski, Frank; Otto, Bärbel; Nawrocki, Andrea R.; Scherer, Philipp E.; Spranger, Jochen; Ristow, Michael; Joost, Hans-Georg; Havel, Peter J. and Tschöp Matthias H.: Consuming Fructose-sweetened Beverages Increases Body Adiposity in Mice Obes. Res. 2005 13: 1146-1156. http://www.obesityresearch.org/cgi/content/abstract/13/7/1146?maxtoshow=&HITS=10&hits=10&
RESULTFORMAT=&searchid=1&FIRSTINDEX=0&sortspec=relevance&volume=13&firstpage=1146&
resourcetype=HWCIT

[2] Lê, Kim-Anne; Faeh, David; Stettler, Rodrigue; Ith, Michael; Kreis, Roland; Vermathen, Peter; Boesch, Chris; Ravussin, Eric and Tappy, Luc: A 4-week high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans. Am. J. Clinical Nutrition, December 1, 2006; 84(6): 1374 - 1379.
http://www.ajcn.org/cgi/content/abstract/84/6/1374

[3] Roglans, Núria; Vilà, Laia; Farré, Mireia; Alegret, Marta; Sánchez, Rosa María; Vázquez-Carrera, Manuel; Laguna, Juan Carlos: Impairment of hepatic Stat-3 activation and reduction of PPARalfa activity in fructose-fed rats . Hepatology (p 778-788) online 26 Feb 2007 Doi: 10.1002/hep.21499

[4] Kathleen J Melanson (2006): Program Abstract # 391.2,
http://www.prnewswire.com/cgi-bin/stories.pl?ACCT=104&STORY=/www/story/
04-06-2006/0004335873&EDATE=

[5] Martine Perrigue (2006): New Obesity Research Shows High Fructose Corn Syrup Similar to Sugar. Prnewswire April 6,2006
http://www.prnewswire.com/cgi-bin/stories.pl?ACCT=104&STORY=/www/story/
04-06-2006/0004335873&EDATE=


08.03.2007: UK Traffic Light and food
Front-of-pack nutrition labelling: Food Traffic Light for a better food choice in UK
[1]


The red, amber and green colour coding used in the traffic light system provides easy-to-understand advice on foods that have high, medium and low amounts of saturated fats, sugars and salt.

Another system currently being used by some manufacturers and retailers is based on percentages of Guideline Daily Amounts (GDA) of fat, sugar and salt (for example a portion contains 35% of your GDA of salt).According to FSA chair Deirdre Hutton the FSA traffic light system and the GDA system may be compliment each other. Here are some examples [2]:


IGD published guidelines for voluntary nutrition labelling including the use of GDAs (Guideline Daily Amounts) for men and women, for calories, fat and saturated fats in 1998. They were developed following collaboration between government, consumer organisations and the food industry. However following industry and consumer research in 2003 IGD established a GDA Technical Working Group to revise the current values and to extend the guidelines to include GDAs for carbohydrates, total sugars, protein, fibre, salt and sodium for men, women and children. [3]

The GDA system tells consumers the percentage of the adult male Guideline Daily Amount of the four key nutrients that each product contains.

GDAs publications are free to download [3]
  • GDAs - Best Practice Guidance (2006)
  • GDAs - Technical Working Group Report (2005)
  • GDAs - Consumer Research Report (2005/6)
  • Voluntary Nutrition Labelling Guidelines (1998)

[1] Food Standard Agency:Agency's new traffic light TV ad launched
http://www.food.gov.uk/news/newsarchive/2007/mar/tvadsignpost
[2] Food Standard Agency: Traffic light labelling http://www.eatwell.gov.uk/foodlabels/trafficlights/
[3] IGD: Best Practice Guides http://www.igd.com/CIR.asp?menuid=36&cirid=1887


06.03.2007: GM rice with human genes
In 2004 the company, Ventria Bioscience, Californis, started to cultivate rice engineered to produce lactiva and lysomin. These proteins are found in breast milk and should improve recovery from diarrhoea. [1]

The company has now received approval from the US Department of Agriculture to cultivate this rice in the state of Kansas.

According to Robert Wittler, from Kansas University School of Medicine at Wichita the outcomes of a clinical trial using the new rice suggests that children suffering from diarrhoea may recover sooner compared with traditional traditional medication. [2]

GeneWatch UK and Friends of the Earth, point out the danger of a broad contamination of staple foods with pharmaceutical producing genes. The genes, cultivated and copied in a laboratory to produce a synthetic version, are carried into embryonic rice plants inside bacteria.[3]

[1]Oryza: Biotech Company Cultivates New Field January 27, 04
http://www.oryza.com/global/genetic/index.shtml
[2] Zavaleta, N; Figueroa, D; Rivera, J; Sanchez, J; Alfaro, S: Lonnerdal, B: Efficacy of rice-based oral rehydration solution containing recombinant human lactoferrin and lysozyme in Peruvian children with acute diarrhea. Journal of Pediatric Gastroenterology and Nutrition February 2007, Volume 44, Number 2, Pages 258-264
http://www.jpgn.org/pt/re/jpgn/currenttoc.htm;jsessionid=
FtYTdRM1VdrgSTyfrvwn0XTyxKvTW4hPhPLMFjJThT62hWYTyxnh!428374954!-949856145!8091!-1

[3] Daily Mail: The rice with human genes By Sean Poulter, 06.03.2007 http://www.dailymail.co.uk/pages/live/articles/news/news.html?in_article_id=440302&in_page_id=1770





05.03.2007: Bovine TB: Pre-movement testing for all cattle over 42 days old in UK. [1] [2]
Defra wants to reduce the risk of the spread of bovine tuberculosis by TB pre-movement tests as well as routine surveillance tests. The tests were extended beginning with the age of 42 days as it was noted that infection is also being picked up earlier in high-risk herds. With this policy the Defra hopes to prevent 610 new incidents a year. Pre-movement testing was introduced in March 2006 in England and May 2006 in Wales. 
To avoid  human tuberculosis adquired from infectuous milk pasteurized (heat treatment developed by Louis Pasteur).
According to FDA [3] more than 300 people in the United States got sick from drinking raw milk or eating cheese made from raw milk in 2001, and nearly 200 became ill from these products in 2002, according to the Centers for Disease Control and Prevention.  Some of the diseases that pasteurization can prevent are tuberculosis, diphtheria, polio, salmonellosis, strep throat, scarlet fever, and typhoid fever.

[1] More: Defra, UK: Bovine TB: pre-movement testing extended to younger animals.
http://www.defra.gov.uk/news/latest/2007/animal-0301a.htm
[2] See also: Defra: Bovine TB pages   
http://www.defra.gov.uk/animalh/tb/premovement/index.htm

[3] US FDA: Got Milk? Make Sure It's Pasteurized. FDA Consumer Magazine; September-October 2004.  http://www.fda.gov/fdac/features/2004/504_milk.html


04.03.2007:  Rice genetically modified with high flavonoid content
Researchers from the from Hamburg University and the University of Hyderabad (India) found GM rice with high antiooxidant activity. The rice contains the anthocyanidin synthase (ANS) enzyme. ANS enzyme is involved in the biosynthesis of flavonoids, transforming leucoanthocyanidins into coloured anthiocyanidins. The transgenic rice 10TC is a mutant strain of the rice called Nootripathh.


The authors compared the favonoid content of the transgenic Rice  with that of normal non GM rice:


 Flavonoids Produced in  10TC Rice
micrograms per milligram
 Normal nonGM  Rice
micrograms per milligram
 Anthocyanins
                  2.52
                  0.12
 Flavonol quercetin                  1.37
                  0.55
 Proanthocyanidins                  0.09
                  0.40

The content of flavonoids had 22% higher antioxidant activity than untransformed rice.

The authors claim that their method can be used to enhance the nutritional value and resistance against biotic and abiotic stresses of different food crops. This would strongly support genetic modification of staple foods.

Source:   Reddy, Ambavaram M; Reddy, Vaka S; Scheffler, Brian E; Wienand, Udo and Reddy, Arjula R: Novel transgenic rice overexpressing anthocyanidin synthase accumulates a mixture of flavonoids leading to an increased antioxidant potential, Metabolic Engineering Volume 9, Pages 95-111 http://www.sciencedirect.com/science/journal/10967176


03.03.07: Defra final decision on BASF GM potato trial postponed [1] [2]
The UK's department for the environment, food and rural affairs (Defra), which originally gave approval in December for BASF to undertake research trials of a GM potato at two sites in England, one in Cambridgeshire and the other in Derbyshire, said that it would now consider BASF's proposal as a new application in accordance with the Genetically Modified Organisms (Deliberate Release) Regulations 2002. Similar trials are already underway in in Sweden, Germany and the Netherlands. But before reaching a definitive decision, Defra said that it would consider any representations that people may wish to make about the risk of environmental damage posed by the GM trial.

The deadline for representations is 20 April 2007.

Defra announced in its News Release from 01.12.06 the approval of an application of BASF to undertake trials of a late potato blight disease GM potato on two sites in England, starting in 2007.Evaluation of the application by the Advisory Committee of Releases to the Environment (ACRE ). found that the trials will not result in any adverse effect on human health or the environment.[3]

Clare Oxborrow Friends of the Earth says that the trials pose a significant contamination threat to future potato crops, claiming that there is no need for GM potatoes and no consumer demand for them. This was backed by Lord Peter Melchett from the Soil Association warning that other crops risk contamination by GM.[4]

Professor Philip Dale of the plant-breeding John Innes Centre argued that the Soil Association is opposing this project because the Association see these kinds of advances in general agriculture to be a threat to the profitability of organic farming. [4]

[1] Defra News Release; Defra invites views on proposed new site for GM potato trials, 27.02.2007

 http://www.defra.gov.uk/news/2007/070227b.htm

[2] Defra UK-Environment: Consents Granted to Release Genetically Modified Organisms

http://www.defra.gov.uk/environment/gm/regulation/consents/index.htm


[3] Defra: Defra approves GM potato research trials
http://www.defra.gov.uk/news/latest/2006/farm-1201.htm

[4] BBC 1.12.06: GM potato trials given go-ahead  http://news.bbc.co.uk/1/hi/sci/tech/6197768.stm


01.03.2007: Requirement to house birds in restricted zones lifted in UK

Defra announced on 01.03.2007 changes to the disease control measures put in place to tackle the H5N1 outbreak in Suffolk. This comprisis the removal of the specific Protection Zone (PZ) restrictions which   became part of the wider Surveillance Zone (SZ).
In addition, the requirement to house birds within all of the zones, including the Restricted Zone, were lifted.

Defra had carried out enhanced surveillance of 148 premises of live poultry (including testing ducks and geese) and tested approximately 64 dead wild birds within the zones and tested faecal samples from the environment around the infected premises. This has not revealed the presence of disease outside the affected premises.

  1. Further information on the restrictions that still apply can be found here: www.defra.gov.uk/animalh/diseases/notifiable/disease/ai/latest-situation/zones.htm
  2. Further information on avian influenza can be found on the Defra website at: www.defra.gov.uk/animalh/diseases/notifiable/disease/ai/index.htm