Deadly bug in sprouts

SummarySeed sprouting provides an ideal environment with optimal temperature and humidity for bacterial growth. Once the bugs are there they are very difficult to remove from fresh sprouts. A German case study shows the serious impact of sprout contamination with a particularly nasty bug that can cause diarrhoea, kidney disease and death.

On 21 May 2011, Germany reported an outbreak of Shiga-toxin producing Escherichia coli (STEC), serotype O104:H4. At the conclusion of the outbreak at least 4,300 cases of diarrhoeal disease, 773 cases of haemolytic uraemic syndrome (HUS) and 50 deaths across Europe linked to the outbreak in Germany had been reported to the European Centre for Disease Prevention and Control (ECDC). In addition, outside the EU eight cases of STEC and five cases of HUS, including one death had been reported in the USA, Canada and Switzerland through the international health regulations (IHR), all with recent travel history to Germany.

The clinical onset of the last outbreak-related case in Germany was 4 July 2011. The Robert Koch Institute (RKI) in Germany announced the end of the E. coli outbreak on 26 July 2011 after more than two months of intensive investigative activities.

Sprouted seeds

Early case-control studies conducted by the RKI demonstrated that clinical disease was associated with the consumption of fresh salad vegetables. The high proportion of adult women among cases, was consistent with fresh salad vegetables as the source of infection. This led to a false warning about some Spanish grown vegetables causing havoc for some Spanish growers. Later, a detailed cohort study demonstrated an association with sprouted seeds. Epidemiological studies on an associated French outbreak also implicated sprouted seeds as the outbreak vehicle.

A tracing back and tracing forward study showed that most of the clusters could be attributed to consumption of sprouted seeds from one producer in Germany. Investigation of the production site showed no evidence of environmental contamination. This left the seeds used for the sprout production as the prime suspect vehicle of infection. Fenugreek seeds were found to be common to both outbreaks and that a specific consignment of fenugreek seeds imported from Egypt was the most likely link between the outbreaks.

Import ban

A ban on imports into the EU of Egyptian fenugreek seeds and certain other sprouting seeds was imposed in July 2011 after the European Food Safety Authority said this was the most likely cause of the E. coli outbreaks.

The European Commission’s Food and Veterinary Office (FVO) visited Egypt in August 2011 and found that Egypt did not differentiate between seeds for sprouting and seeds for planting. The trace-back exercise found that three implicated lots were produced in upper Egypt by the same farmer in separate farms grown under organic conditions.

The Egyptian investigation found no evidence of STEC O104:H4 presence, although there was plenty of potential for contamination from human populations and animals, and problems with analytical methods. The FVO said Egypt must ensure that seeds produced specifically for sprouting must comply with hygiene rules and microbiological criteria.

Given an exchange of information with the Egyptian authorities and new measures to prevent contamination, the ban on fenugreek imports from Egypt was lifted on 31 March 2012.

Rare strain

The published data for STEC O104:H4 are scarce as this is a very rare serogroup infecting humans in Europe and globally. According to the information reported to ECDC, there were 10 reported cases of STEC O104:H4 infection in the EU Member States and Norway during 2004-2010. Five of the 10 cases between 2004 and 2010 were related to travel to Afghanistan (2008), Egypt (2010), Tunisia (2009, 2010) and Turkey (2009).

In addition to those cases reported to ECDC, a review of the scientific literature revealed that STEC O104:H4 has been isolated twice in Germany in 2001 and once in Korea in 2005. The German isolates differed from the 2011 outbreak strain.

Inherent problems in sprout production

The preparation of fresh sprouted seeds rarely includes a step where bacterial contamination is eliminated. Hence, food preparation of fresh sprouted seeds is based on the understanding that they are sold as ready-to-eat, i.e. safe to eat as is, or following only minimal preparation. For fresh produce, this assumes and relies on a production process which prevents contamination and an ability to detect contamination when it occurs. These conditions have proven not to be satisfied in this case.

Aspartame controversy

SummaryNormal use of the synthetic sweetener aspartame in diet products is considered safe by several national and international authorities, but has been questioned by public groups raising a range of concerns. The European Food Safety Authority, in a re-evaluation of the safety of aspartame to be completed by May 2013, recently requested more information on potential degradation products.

Aspartame is a low-calorie, intense sweetener which is approximately 200 times sweeter than sucrose (table sugar). It is used to sweeten a variety of foods and beverages such as drinks, desserts, sweets, chewing gum, yoghurt, energy-reduced and weight control products and as a table-top sweetener. Aspartame was first approved for use in dry goods in 1981 and for carbonated beverages in 1983 by the U.S. Food and Drug Administration. During the 1980s, aspartame was authorised for use in foods and as a table-top sweetener by several EU Member States. European legislation harmonising its use in food wa introduced in 1994.

Early controversy

Aspartame was discovered by accident in 1965, when James Schlatter, a chemist of the G.D. Searle Company was testing for an anti-ulcer drug and licked his contaminated finger to pick up a piece of paper. He noticed an intense sweet taste. The company set out to benefit from his findings and patented the substance. Early controversy over aspartame safety was due to perceived irregularities in the aspartame approval process during the 1970s and early 1980s, including allegations of conflicts of interest and claims that aspartame producer G.D. Searle had withheld and falsified safety data. Aspartame consumption has since been claimed to cause 92 different health side effects including brain tumors, preterm delivery, birth defects, diabetes, emotional disorders and chronic neurological disruptions including epilepsy/seizures. Most claims are populistic in nature without credible scientific backing, but there are also some published scientific studies providing initial support for the theories. The published reports have been reviewed several times by government authorities in different countries without any clear confirmation of their validity.

It has been shown that even at very high doses of aspartame (over 200 mg/kg), no aspartame as such is found circulating in the body due to its rapid breakdown. Hypotheses of adverse health effects have thus focused on the three metabolites aspartic acid, methanol and phenylalanine, which are formed through hydrolysis of aspartame in the small intestine. However, aspartame is far from a unique source of the three metabolites. Aspartic acid (aspartate) is one of the most common amino acids in the typical diet and in a fairly high consumer of aspartame, it still provides only between 1-2 % of the daily intake of aspartic acid. Equally, the amount of methanol formed from aspartame is less than that found in fruit juices and citrus fruits, and there are other dietary sources for methanol such as fermented beverages. Phenylalanine is one of the essential amino acids and is required for normal growth and maintenance of life. Common foods such as milk, meat, and fruit provide far greater amounts of this metabolite than aspartame.

Adverse health effects

There has been some speculation that aspartic acid, in conjunction with other amino acids like glutamate, may lead to excitotoxicity, inflicting damage on brain and nerve cells. However, clinical studies have shown no signs of neurotoxic effects, and studies of metabolism suggests it is not possible to ingest enough aspartic acid and glutamate through food and drink to levels that would be expected to be toxic.

On the other hand, there is clear proof that people with the rare genetic disorder called phenylketonuria (that is tested for in many countries at birth) should keep phenylalanine levels in the diet low. In affected persons, usual levels of phenylalanine in the diet can cause problems with brain development, leading to progressive mental retardation, brain damage, and seizures.  Other concerns about the safety of phenylalanine from aspartame largely centers around hypothetical changes in neurotransmitter levels as well as ratios of neurotransmitters to each other in the blood and brain that could lead to neurological symptoms. Reviews of the literature have found no consistent findings to support such concerns, and while high doses of aspartame consumption may have some biochemical effects, these effects are not seen in toxicity studies to suggest aspartame can adversely affect neuronal function.

The methanol produced by the metabolism of aspartame is absorbed and quickly converted into formaldehyde and then completely converted to formic acid, which, due to its long half life, is considered the primary mechanism of toxicity in methanol poisoning. With regards to formaldehyde, it is rapidly converted in the body, and the amounts of formaldehyde from the metabolism of aspartame is trivial when compared to the amounts produced routinely by the human body and from other foods and drugs. At the highest expected human doses of consumption of aspartame, there is no increased blood levels of methanol or formic acid, and ingesting aspartame at the 90th percentile of intake would produce 25 times less methanol than would be considered toxic.

Cancer

Concern about possible carcinogenic properties of aspartame was originally raised and popularised in the mainstream media in the 1970s and again in 1996 by suggesting that aspartame may be related to brain tumours. Independent agencies reanalysing multiple studies based on such claims could not confirm any credible association between aspartame and brain cancer.

Later the European Ramazzini Foundation of Oncology and Environmental Sciences (ERF) released  study results in 2007 and 2010 which claimed that aspartame could increase some malignancies in rats, concluding that aspartame is a potential carcinogen at normal dietary doses. These conclusions were contradicted by other carcinogenicity studies which found no significant danger. After reviewing the foundation’s claims, independent experts have discounted the study results. Reported flaws were numerous and included comparing cancer rates of older aspartame-consuming rats to younger control rats; a diet leading to possible nutritional deficiencies; lack of animal randomisation; overcrowding and a high incidence of possibly carcinogenic infections; and misdiagnosing of hyperplasias as malignancies.

Reviews of numerous carcinogenicity studies in animals, epidemiologic studies in humans, as well as in vitro genotoxicity studies have found no significant evidence that aspartame causes cancer in animals, damages the genome, or causes cancer in humans at doses currently used.

Neurological and psychiatric symptoms

Numerous allegations have been made in popular media purporting neurotoxic effects of aspartame leading to neurological or psychiatric symptoms such as seizures, headaches, and mood changes. Reviews of the biochemistry of aspartame have found no evidence that the doses consumed would plausibly lead to neurotoxic effects. Comprehensive reviews have not found any evidence for aspartame as a cause for these symptoms, although one review did provide a theoretical biochemical background of neurotoxicity and suggested further testing.

A review of the pediatric literature did not show any significant findings for safety concerns with regards to neuropsychiatric conditions such as panic attacks, mood changes, hallucinations or with ADHD or seizures.

Headaches are the most common symptom reported by consumers as associated with aspartame consumption. While there are some indications that aspartame might be one of many dietary triggers of migraines, in a list that includes “cheese, chocolate, citrus fruits, hot dogs, monosodium glutamate, aspartame, fatty foods, ice cream, caffeine withdrawal, and alcoholic drinks, especially red wine and beer”, other studies have failed to prove such links.

The current state of play

Although aspartame and its metabolites have been studied in a wide range of populations including infants, children, adolescents, and healthy adults, even at very high doses, without identifying any safety concerns in healthy adults and children there are still some lingering doubts. However, equally to the proof of safety needed for authorisation of an additive for use in food, to withdraw such an approval requires some verified safety concerns. That is not yet the case for aspartame.

The good thing is that concerned consumers can identify food containing aspartame by looking at the ingredients lists on product labels. Like all food additives, aspartame has been assigned an “E-number” following authorisation. Its presence in foods can be indicated either by name (i.e. “aspartame”) or by its number E 951.