Groundbreaking opinion on dioxin toxicity

 

Uncertainty2

Curtesy the European Commission

We have previously covered the group of 29 nasty chemicals collectively called dioxins and dioxin-like PCBs because of their similar mode of action.

In brief, they are toxic chemicals that persist in the environment for years and accumulate at low levels in the food chain, usually in the fatty tissues of animals.

However, different interpretations among scientific organisations of their absolute toxicity have led to some confusion.

Harmonisation needed

In an attempt to develop a better understanding of the risks to human and animal health conferred by dioxins and dioxin-like compounds, the European Food Safety Authority initiated a groundbreaking review of the available scientific literature and exposure information. In an exhaustive opinion published in November 2018, EFSA’s Panel on Contaminants in the Food Chain concluded that such environmental pollutants, although only present at low levels in food and feed, pose a considerable health concern.

Accordingly, the Panel set a new tolerable weekly intake (TWI) for dioxins and dioxin-like PCBs in food of 2 picograms per kilogram of body weight, an incredibly low limit reflecting their severe toxicity.

The new TWI is seven-times lower than the previous EU tolerable intake set by the European Commission’s former Scientific Committee on Food in 2001. The change is based on the availability of new epidemiological human and experimental animal data on the toxicity of these substances and more refined modelling techniques for predicting levels in the human body over time.

Current protection not sufficient

eating_meatThe new TWI is protective against effects on semen quality, the most sensitive adverse health effect, as well as a lower sex ratio of sons to daughters, higher levels of thyroid-stimulating hormone in new-borns and developmental enamel defects on teeth.

Worryingly, data from European countries indicate an exceedance of the new tolerable intake level with the main contributors being fatty fish, cheese and livestock meat.

Average and high exposures were, respectively, up to five and 15 times the new TWI in all age groups.

Should you take action?

As there are little or no acute health effects from consuming single foods containing dioxins and dioxin-like PCBs, it’s more a matter of cumulative chronic effects outside the direct control of individual consumers.

Although the presence of these compounds in food and feed has declined in the last 30 years thanks to the efforts of public authorities and industry, a further concerted effort is needed to bring current exposure to safe levels.

Thus, continued vigilance is important, particularly in light of the new proposed TWI. As this is not always the case and testing of food is expensive, some pressure from consumer groups could be beneficial.

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Tea in the News

tea jugTea is the second most consumed beverage on earth after water. The daily cup of tea has many positive associations. Winding down (thought to be due to the relaxing presence of the amino acid L-theanine), or winding up (thanks to caffeine’s influence).

Several health benefits have been attributed to tea, especially green tea consumption. There are claims that green tea has the potential to fight cancer and heart disease, that it can lower cholesterol, burn fat, prevent diabetes and stroke, and stave off dementia. Pretty impressive stuff, but probably far from the real truth. Sure the catechins in tea act as free radical scavengers and might prevent DNA damage. However, it is more likely that the theory that drinking green tea is good for memory is true. Researchers have actually shown that epigallocatechin-3 gallate, a key property of green tea, can affect the generation of brain cells, providing benefits for memory and spatial learning.

So should you drink more tea?

Time to be a little careful as recent research has uncovered a connection of a less pleasant kind – the possibility of pesticides and other carcinogenic chemicals in your tea. Independent lab testing in 2018 by CBC News Canada found that many tea brands contain pesticides over levels permitted in that country.

CBC tested 10 samples of black and green teas including Canada’s most popular brands: Lipton, Red Rose, Tetley and Twinings. Other popular brands tested included No Name, Uncle Lee’s Legends of China, King Cole and Signal. Half of the teas tested contained pesticide residues above the allowable limits in Canada. And eight of the 10 brands tested contained multiple chemicals, with one brand containing residues of 22 different pesticides.

In a way this is nothing new. In 2012, Greenpeace found  that every one of 18 tea samples from nine Chinese tea manufacturers contained a mixture of at least three different kinds of pesticides. In total, as many as 29 different pesticides were detected. Six of the samples contained more than 10 different kinds of pesticides. Pesticides banned in China for use on tea plants and tea leaves were found on 12 samples from eight different tea companies.

Indian tea didn’t fare much better. About 94 per cent of 49 Indian tea brands tested by Greenpeace in 2014 contained pesticide residues, and 59 per cent contained at least one pesticide above the Maximum Residue Level (MRL) set by the EU. Similar to the Chinese teas, 68 per cent of the pesticides discovered in the teas weren’t registered for use in tea cultivation.

Recent European Union pesticide report

Tea plantsFew samples were used for the ad hoc testing above, which could have biased the results. A more comprehensive report from the 2016 testing of pesticide residues in food in the European Union was published in 2018 by the European Food Safety Authority. Although pesticide levels exceeding the MRL amounted to only 3.9 per cent in total, for some products, including tea, the levels were much higher. Of 1016 tea samples tested, 36 per cent contained no detectable pesticides at all, while 24 per cent contained pesticide residue levels exceeding the European Union MRL.

Anthraquinone was one of the substances detected in the European testing. In recent years, issues have emerged with regard to the MRL of anthraquinone, which is set at the analytical detection limit of 0.02mg/kg for food, including tea leaves. In many cases, anthraquinone has not even been used as a pesticide on tea plants. The tea becomes contaminated during drying or packaging, or by smoke caused by tea drying.

Should you be worried about pesticides in tea?

The simple answer is not necessarily, but to understand the issue we need to delve a bit deeper into the setting of MRLs.

The MRL is the highest amount of an agricultural or veterinary chemical residue that is legally allowed in a food product. Levels are set based on how much of the chemical is needed to control pests and/or diseases. The product’s chemistry, metabolism, analytical methodology and residue trial data are also assessed.

Limits are set using internationally recognised methods and national scientific data and are well below the level that could pose health and safety risks to consumers. MRLs help enforcement agencies monitor whether an agvet chemical has been used as directed to control pests and diseases in food production.

Unfortunately, allowable maximum residue levels, that fuzzy line of safe use defined by governments, varies greatly from country to country.

Thus, pesticide residues in tea has been a major non-tariff trade barrier affecting tea trade globally as pointed out by the Food and Agriculture Organisation of the United Nations (FAO). The problem was due mostly to certain default MRLs set at analytical detection limits, like for anthraquinone, and not according to agricultural practice or human toxicity.

As a matter of fact the European Union use a default MRL set at the detection limit for at least 6 other pesticides used on tea in some countries.

FAO pointed out that the only way to tackle this problem would be to help fix realistic MRLs which would be acceptable to all stakeholders in order to ensure food safety as well as smooth tea trade globally.

Not sure yet?

Organic tea 2You might question if we really want any toxins in our tea? Well, like any agricultural food product, tea leaves can be contaminated with agri-chemicals that are used to control pests and diseases. This is an irrefutable fact.

The solution? If you’re health conscious and a big tea drinker, paying a bit more for certified organic loose-leaf teas, and infusing it in an old-fashioned pot or stainless steel infuser, would probably be your best bet.

For the rest of us we can be assured that using only 2g of tea leaves for a cup of tea will pose no major health hazard.

Still it would be good if the tea producing countries could get their act together and sharpen their agricultural practices.

 

Ignoring responsibility at your peril

oil_(Illuminati Owl)

Oils aren’t always what they say (Photo: Illuminati Owl)

The agri-food industry is no innocent bystander. Maximising sales and profit is more important than looking after their customers. They cleverly invent crops tolerant to their own herbicides through genetic engineering so they can sell both seeds and encourage the spread of questionable poisons. They add sugar to many of their products for children so that people will crave sweet foods throughout life. They cheat on extra virgin oil because they can and reap the profit. They replace beef in processed beef products with cheaper horse meat to gain an upper hand. The lists goes on and on.

And rightly the public is upset. This is reflected by the many news items published by the popular press condemning the latest cheat by industry.

But what about consumer responsibility?

Acrylamide is a good example as it is formed during heating of food as we have previously pointed out. Evidence from animal studies have shown that acrylamide and its metabolite glycidamide are genotoxic and carcinogenic: they damage DNA and cause cancer. While evidence from human studies on the impact of acrylamide in the diet is inconclusive, scientists agree that acrylamide in food has the potential to cause cancer in humans as well and it would be prudent to reduce exposure.

toaster_(Donovan_Govan)

Go easy with the toaster (Photo: DonoVan Govan)

Thus, in early 2017, the UK Food Standards Agency issued consumer recommendations on how to minimise the formation of acrylamide during home cooking by avoiding singeing their toast or leaving roast potatoes to char in the oven.

Acrylamide is a natural by-product of heating and has been present in our food since fire started to be used for food preparation. It is formed by a reaction between amino acids and sugars when foods are heated at high temperatures (over 120°C) during frying, roasting or baking. It can thus be found in a wide range of foods including roasted potatoes and root vegetables, chips, crisps, toast, cakes, biscuits, cereals and coffee.

The formation of acrylamide can be reduced by some simple measures as pointed out by the Food Standards Agency. Aim for a golden yellow colour or lighter when frying, baking, toasting or roasting starchy foods like potatoes, root vegetables and bread. Carefully follow cooking instructions on the pack when frying or oven-cooking packaged food products such as chips, roast potatoes and parsnips. Don’t store raw potatoes in the fridge as it may lead to the formation of more free sugars in the potatoes that can increase overall acrylamide levels.

Parts of the popular press objected

All sensible and practical recommendations. You would have thought that the popular press would support such a consumer initiative. But you would be wrong. Rather, parts of the press attacked the Food Standards Agency for being alarmist. Critics of the advice were quick to point out that animal studies linking acrylamide to cancer have used doses far above the average daily consumption in humans so that extrapolating the results is questionable – even assuming the effect is comparable across species.

DNA

Acrylamide is a genotoxic carcinogen.

But genotoxic carcinogens don’t follow the minimum threshold concentration rule below which they are not dangerous at all. With chemicals that damage DNA it’s a linear dose response, so even the smallest dose contributes to the risk. There is no threshold dose for the effect. And to add to the problem it is almost impossible to prove in epidemiological studies that acrylamide is a human carcinogen as its presence is too common to find a group that is not exposed at all.

Therefore, the united verdict of organisations like the International Agency for Research on Cancer, the World Health Organisation, the European Food Safety Authority (EFSA) and UK scientific advisory committees is that acrylamide has the potential to cause human cancer by interacting with the genetic material in cells. In 2015, EFSA published their risk assessment of acrylamide in food confirming that acrylamide levels found in food potentially increases the risk of cancer for all age groups. This means that acrylamide might contribute to our lifetime risk of developing cancer; although it is not possible to estimate how big this contribution may be.

Time for action

With that united front I suggest that you better follow the recommendations issued by the UK Food Standards Agency. I know that you feel safer when driving your own car compared to flying, although the probability of an accident is much higher on the road. I know that it is so much easier to blame the food industry for all ills, rather than take some responsibility for your own food handling.

Maybe it’s time for some action!

Smoke might not be so hot

fire2

The good news about smoke and fire

We have previously mentioned the potential harmful effects of smoke-induced compounds formed during barbecuing or smoking of food. Now new findings point to a developmental edge for humans.

A genetic mutation may have helped modern humans adapt to smoke exposure from fires. This might have produced an evolutionary advantage over competitors like Neanderthals as modern humans are the only primates that carry this genetic mutation.

No fire without smoke

There is evidence that both humans and Neanderthals used fire. Our ancestors were likely using fire at least a million years ago, and maybe even two million years ago. Fire would have played an important role for cooking, protection and heating. Cooking with fire allowed our ancestors to incorporate a broader range of foods in the diets by softening roots and tubers and help increase the digestibility of other foods. Fire also provided warmth, and has long been used for landscape burning and as part of hunting and gathering.

But no fire without smoke (or is it the opposite?). And smoke-derived toxins like dioxins and polycyclic aromatic hydrocarbons can lead to respiratory infections and, for expectant mothers, exposure to these toxins can increase the chance of low birth weight and infant mortality. Even worse, they can increase the risk of cancer and lead to cell death at high concentrations.

Increased tolerance to smoke-induced toxins

Human_Evolution

Exclusive mutation that protects humans (Illustration: MagneticHyena)

The mutation may have offered ancient humans a potentially increased tolerance to toxic materials produced by fires. Although you want your body to be able to detoxify the compounds, doing it too rapidly might overload the system and cause cell death. It is all about differences in the aryl hydrocarbon receptor that regulates the body’s response to smoke-derived toxins. The mutation in the receptor is located in the middle of the ligand-binding domain and is found in all present-day humans. Ligands are small molecules that attach to receptor proteins in certain areas in much the same way that keys fit into locks.

By inhaling smoke and eating charcoal-broiled meat Neanderthals were exposed to large amounts of smoke-derived toxins they metabolised too quickly, while humans would exhibit decreased toxicity because they metabolised these compounds more slowly. Thus, our tolerance allowed us to pick up other bad habits like smoking cigarettes.

But remember that the mutation is not giving us a free-out-of-jail card. Although we are at a great advantage compared to Neanderthals, having the mutation made a hundred-fold to as much as a thousand-fold difference, there is still quite a considerable risk remaining. So go easy with the barbecuing and don’t adopt the bad smoking habit.

Lead – up to no good

car-exhaust

Lead in petrol an earlier culprit in lead poisoning.

Lead has been used for thousands of years because it is widespread, easy to extract, and easy to work with. It is highly malleable and easily meltable. Equally, lead poisoning has been documented since ancient Rome, ancient Greece and ancient China. It is thus clear that, ingested or inhaled, lead is poisonous to animals and humans. Still we were foolish enough to add it to petrol starting in the 1920s and use lead pigments particularly in white but also in yellow, orange, and red paint to spread its occurrence even further.

We have lived with the consequences ever since. Lead poisoning typically results from ingestion of food or water contaminated with lead, but may also occur after accidental ingestion of contaminated soil, dust, or lead-based paint. It is a neurotoxin that accumulates both in soft tissues and the bones, damaging the nervous system and causing brain disorders. Lead has been shown many times to permanently reduce the cognitive capacity of children at extremely low levels of exposure. Lead exposure in early childhood has also been linked to violent crime.

But there is more

As if that was not enough, new research has shown that early life exposure can alter the composition of the gut microbiota (remember one of my favourite topics), increasing the chances for obesity in adulthood. So far at least in mice. Lead was added to the drinking water of female mice prior to breeding through nursing their young. The lead levels used  were designed to be within past and present human population exposure levels. Thus the lowest dose used of 5 µg/dL is the same as the current US blood lead action level, while the higher dose mirrored exposure levels during the 1960s and 1970s to be able to evaluate both current and historically relevant lead levels.

Once weaned, the offspring were raised to adulthood without additional exposure, and then tested for lead effects acquired from their mothers. The guts of both males and females exposed to lead had all of the similar complexity in microbiota as those not exposed. The differences were in the balance of the different groups of microorganisms. Due to differences in their gut microbiota, adult male mice exposed to lead during gestation and lactation were 11 percent heavier than those not exposed. But not females, although the researchers speculate that females might have shown effects on obesity if they had followed them longer.

Although improving, it is not over yet

fatmouse

Lead exposure linked to obesity in mice.

So now we have obesity added to the long list of potential harm caused by lead contamination. Fortunately, by the mid-1980s, a significant shift in lead end-use patterns had taken place with lead use phased out from petrol in many countries and banned from paint, but still remaining in some grades of aviation fuel, and in some developing countries.

Although the situation has improved, it is not over yet. Lead may be introduced to foods from the use of lead containing pottery or lead crystalware. Another source is water from lead containing pipes. And wild game that has been shot with lead pellets. Not to forget some odd Chinese herbs found to contain high lead levels.

So vigilance is still needed.

Iron – friend or foe?

red blood cells

Iron is necessary for the red blood cell supply.

Well the answer to the question is both, but that might be a surprise to you since iron has a clearly positive reputation among the general public. Iron is a mineral and a friend in that it plays a key role in the making of red blood cells. Too little iron may lead to anaemia, a low level of red blood cells. Anaemia can cause fatigue and other symptoms. Too little iron can also have disastrous effects on memory, growth, and overall physical health. It is often said that the more iron, the better. But that is actually not true since excess iron can be a foe. Let me explain in more detail.

Too much iron

Large amounts of ingested iron can cause excessive levels of iron in the blood.  There is also the issue of haemochromatosis, a genetic disorder where affected people absorb too much iron from a perfectly normal diet. Excess iron is stored in the body. Over time this leads to iron overload.

The problem is that although we have mechanisms in place for regulating iron absorption, men of any age and post-menopausal women have no mechanisms that can get rid of excess iron, except by giving blood. That reminds me of medieval blood letting as a primitive “cure” for most diseases. There might actually be some benefits to such treatments.

Iron toxicity

Campylobacter

Bugs just love excess iron.

Iron toxicity occurs when there is free iron in the cell, which happens when iron levels exceed the capacity of transferrin to bind the iron. Damage to the cells of the gastrointestinal tract can also prevent them from regulating iron absorption leading to further increases in blood levels.

High blood levels of free ferrous iron react with peroxides to produce free radicals, which are highly reactive and can damage DNA, proteins, lipids, and other cellular components. Observational studies have tracked such changes to the development of  type 2 diabetes, heart disease, insulin resistance, inflammation, Alzheimer’s disease, hypertension, fatty liver, hypothyroidism, and arthritis. A daunting list of diseases connected to excess body stores of iron.

There is also the issue of the purported connection between red meat consumption and the development of colorectal cancer. One of the theories supporting this connection blame the high iron content of red meat.

Complicating things further, this is heaven for disease-causing bacteria. Like all living beings, bacteria need iron to survive and multiply. Excess iron promotes their growth and capacity to make you sick.

So what to do?

Let’s first look at iron intake. You can certainly get enough iron from food. Iron absorption is best (15-18%) from foods that contain haem iron. Red meat, seafood and poultry are the best sources of haem iron. Iron absorption from foods that contain non-haem iron is much lower (<5%). Non-haem iron is predominantly found in plant foods such as cereals, vegetables, legumes and nuts.

In case of a deficient diet it is also possible to use iron supplements to improve iron status. Iron supplements are often used to treat anaemia caused by pregnancy, heavy menstrual periods, kidney disease and chemotherapy. Iron supplements are commonly recommended for infants and toddlers, teenage girls, and women who are pregnant or of childbearing age to help prevent anaemia.

But if you actually need less iron?

coffee3

A cup of coffee after dinner can reduce iron absorption.

Phytonutrients like polyphenols, flavanols and other plant-derived antioxidant compounds inhibit iron absorption. They can be found in apples, onions, grapes, many other plant foods, and in most colourful spices and herbs.

Even low levels of phytates have a strong inhibitory effect on iron absorption. Phytates can be found in walnuts, almonds, sesame, dried beans, lentils, peas, cereals and wholegrain.

A cup of coffee after dinner is particularly good at inhibiting iron absorption with instant coffee the most effective. Tea might even be better. Tannins in coffee and tea bind the iron and prohibit absorption.

But there is more help at hand in a piece of cheese after dinner. The calcium it contains is a potent inhibitor of iron absorption. More than that, calcium reduces any carcinogenic interactions between haem iron and colonic cells.

If you’re going to drink alcohol, make it red wine and lean toward lower-alcohol wines. Its polyphenols inhibit iron absorption, while straight ethanol enhances iron absorption.

And if that is not enough you might try some ancient blood letting or in simple terms become a blood donor.

Can honey make you sick?

honey_(Hillary_Stein)

The safety of honey questioned (Photo: Hillary Stein)

Is the world mad when Irish scientists focus their attention on Australian honey and find high levels of pyrrolizidine alkaloids? And the results are sensationalised by the Australian press a year later, talk about a slow response! Headlines in January 2016 proclaimed that “Australian honey could make us sick” and the article stated that “Australian honeys are the most contaminated in the world with natural poisons linked to chronic disease including cancer”. If that didn’t frighten you, what would?

And truely, pyrrolizidine alkaloids are natural toxins linked to chronic disease including cancer. Typically the compounds affect the liver and in some cases the lungs causing serious illness. Animal experiments have also shown that certain pyrrolizidine alkaloids are genotoxic carcinogens, the worst of the worst of toxins.

So what are they?

Pyrrolizidine alkaloids are produced as a protection against herbivores by about 6,000 plant species, representing 3% of all flowering plants, most of which are weeds. There is a great variety of compounds with more than 500 different pyrrolizidine alkaloids known to date. Besides in honey, pyrrolizidine alkaloids in food have been detected in products of plant origin, for example, in herbal teas and supplements, cereals, and salads. Cases of elevated contamination in wheat are known to have occurred in Afghanistan associated with illness and similarly contaminated salad in Germany.

To be fair to the Irish, the study was all about developing better analytical methods for detecting multiple pyrrolizidine alkaloids and the scientists probably selected Australian honey to be certain of having positive samples. They could as well have selected South American samples also known for containing high levels of pyrrolizidine alkaloids.

Nevertheless, their results showed that 41 of the 59 honey samples were contaminated by pyrrolizidine alkaloids with a mean total sum of 153 µg/kg. This is on average four times more pyrrolizidine alkaloids than in European honeys and is quite high as an average level. Echimidine and lycopsamine were most common and found in 76% and 88%, respectively, of the positive samples. The scientists also attempted to calculate possible average daily exposure based on the results and found that adults could have an exposure of 0.051 µg/kg bodyweight per day and children 0.204 µg/kg bodyweight per day of pyrrolizidine alkaloids.

What does it mean?

It is debatable if all pyrrolizidine alkaloids should be treated equally when considering their toxicity due to their expected cumulative effects or if some of the compounds could be considered to be less toxic.

laboratory

Scientists cannot agree on how to assess safety of honey.

Conveniently the Australian authority, Food Standards Australia New Zealand, considers that echimidine is less toxic and used a Tolerable Daily Intake approach in establishing a safe level of exposure of 1 µg/kg bodyweight per day. This was calculated by applying an uncertainty factor of 10 to what was considered to be a human no-observed-effect level of 10 µg/kg bodyweight per day for liver failure due to veno-occlusive disease. But carcinogenic effects were not considered. Using this approach the Irish exposure estimates are well within safe limits.

Not so says a number of national and international organisations like the World Health Organization International Programme on Chemical Safety, the Dutch Rijksinstituut voor Volksgezondheid en Milieu, the UK Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment, the German Bundesinstitut für Risikobewertung, and the CONTAM Panel of the European Food Safety Authority. They have all concluded that 1,2-unsaturated pyrrolizidine alkaloids may act as genotoxic carcinogens in humans (that is they may cause cancer and damage DNA, the genetic material of cells).

The safety of genotoxic carcinogens should be evaluated using the Margin of Exposure approach and not the Tolerable Daily Intake approach. A benchmark dose lower confidence limit for a 10% excess cancer risk (BMDL10) of 70 μg/kg bodyweight per day for induction of liver haemangiosarcomas by lasiocarpine in male rats was calculated as the reference point for comparison with the estimated dietary exposure. As a Margin of Exposure of 10,000 or higher, based on a BMDL10 from an animal study, is considered to be of low concern from a public health point of view, exposure to 0.007 µg/kg bodyweight per day or less of pyrrolizidine alkaloids would not be a worry. But the Irish presented much higher exposure estimates.

What margin is safe?

The different interpretations of what is a safe exposure to pyrrolizidine alkaloids is confusing to scientists and the public alike. Honey consumption has a long and varied history as a remedy for several health afflictions. Although, due partly to low numbers and questionable quality of human studies, some of the suggested health benefits of honey have been difficult to prove scientifically. Nevertheless, the public perception is that honey is a wholesome and natural product beneficial to health and a tastier alternative to refined sugar. There is a small committed group of consumers that regularly consume relatively large amounts of honey. So the findings of pyrrolizidine alkaloid contamination is disturbing.

Patersons

Paterson’s curse is a common source of pyrrolizidine alkaloids in honey.

However, there are som alleviating factors to reassure honey consumers. The presence in honey of lasiocarpine used to calculate the BMDL10 is rare and most other pyrrolizidine alkaloids are at least a magnitude less toxic. This could raise the level of exposure of no concern to 0.07 µg/kg bodyweight per day. Also retail honeys are often mixed from several sources to reduce the overall level of pyrrolizidine alkaloids in the consumer-ready product. And finally the Australian honey industry is claiming that they have reduced access of bees to Paterson’s curse, a main source of pyrrolizidine alkaloids in Australian honey. But the future will tell if that is right.

So some caution is justified for regular honey consumers. Vary your source of honey to limit exposure and hopefully you will be fine. For now.

 

Time to learn about carvone

Caraway seeds contain carvone (Photo: Wikimedia)

Caraway seeds contain plenty of carvone (Photo: Wikimedia)

To be brutally honest I have never heard of carvone before, have you? Maybe it’s time to get better acquainted with this chemical compound, at least that’s the view of the Scientific Committee of the European Food Safety Authority.

It is not that it hasn’t received attention before from different bodies, initially by the Joint FAO/WHO Committee on Food Additives (JECFA) between 1968 and 2000, then as a pesticide active substance by the European Commission in 2008, then by the EFSA Panel on Food Contact Materials, Enzymes, Flavourings and Processing Aids (CEF) in 2011 and the latest evaluation by EFSA’s Panel on Additives and Products or Substances used in Animal Feed (FEEDAP) in 2011.

So why a renewed attention now?

Carvone can be found in many places

Let’s first have a look at what carvone is since it is a little complex. Carvone is a member of a family of chemicals called terpenoids. It is a natural component in several food items such as mint and caraway but it may also be used as a pesticide, food and feed flavouring, in personal care products, or, together with other active substances, as a zootechnical feed additive. So it could be expected to be around a fair bit.

There are actually two varieties of carvone that are mirror images of each other, R-(-)-carvone (also called l-carvone) and S-(+)-carvone (also called d-carvone), which can be recognised by their smell. R-carvone smells like spearmint and S-carvone smells like caraway so there is no price for guessing that R-carvone is a principle component of oils extracted from several species of mint and S-carvone a principal component of caraway seed oil and also dill seed oil and mandarin peel oil.

Caraway is one of the oldest herbs cultivated in Europe and was used for medicinal purposes by the ancient Romans without knowing about the specifics of carvone. As the compound most responsible for the flavour of caraway, dill and spearmint, carvone has been used for millennia in food. Both carvones are now used in the food and flavour industry. Wrigley’s Spearmint Gum is soaked in R-carvone and powdered with sugar.

S-carvone is used to prevent premature sprouting of potatoes during storage while R-carvone has been proposed for use as a mosquito repellent. R-carvone is also used for air freshening products, in personal care products, in aromatherapy and in alternative medicines.

So what is the problem?

A little bit tricky since toxicity results are available only for S-carvone and we are exposed to much higher levels of R-carvone, about three times more. Although experimental animals died when given very high levels of S-carvone, more realistic dose levels caused damage to the liver. The Scientific Committee opinion used the liver damage to establish an Acceptable Daily Intake (ADI) of 0.6 mg/kg body weight per day for S-carvone, using an uncertainty factor of 100 based on the experimental animal results. An ADI for R-carvone could not be established because of the previously mentioned lack of toxicity data.

Question then is if we get close to the ADI for S-carvone and what to do with R-carvone. As a matter of fact children with the highest exposure to S-carvone come very close to the ADI. The largest contributors are food flavourings, personal care products and natural spices. The much higher intake of R-carvone, especially for adults, come from personal care products followed by food flavourings.

Toothpaste among the largest contributors to carvone exposure (Photo: Brandon Cripps)

Toothpaste among the largest contributors to carvone exposure (Photo: Brandon Cripps)

One culprit in particular is toothpaste followed by mouthwash. Carvones are commonly added to such personal care products. Toothpaste commonly contain 3-10% spearmint oil (80% R-carvone) which corresponds to an average content of 52,000 mg R-carvone/kg toothpaste + 1-2% dill or caraway oil (60% S-carvone) which corresponds to an average content of 9,000 mg S-carvone/kg toothpaste.

The carvone content in mouthwash has been estimated to be 1.5% R-carvone, which corresponds to 15,000 mg R-carvone/kg mouthwash.

Still uncertainties

Consumption of S-carvone seems to be within the ADI and safe for most people as long as there are no cumulative effects from simultaneous consumption of R-carvone. And this we will not know until results are in from further experiments.

So stay tuned and in the meantime you should probably continue to brush your teeth.

Ordinary salt a killer, or not!

Excess sodium can cause heart disease (Photo: Wolf Soul)

Excess sodium can cause cardiovascular disease (Photo: Wolf Soul)

Some simple facts:

  • Cardiovascular disease is the number one cause of death in the world
  • Excess sodium intake raises blood pressure
  • High blood pressure is one of the major contributors to the development of cardiovascular disease

Research just published modelling populations across 187 countries attributed more than 1.6 million cardiovascular-related deaths per year to sodium consumption above the World Health Organization’s recommendation of a maximum of 2.0 g per day.

The details of the study

The researchers collected and analysed existing data from 205 surveys of sodium intake in countries representing nearly three-quarters of the world’s adult population, in combination with other global nutrition data, to calculate sodium intakes worldwide by country, age, and sex.

The researchers found the average level of global sodium consumption in 2010 to be 3.95 g per day, nearly double the 2.0 g recommended by the World Health Organization. All regions of the world were above recommended levels, with regional averages ranging from 2.2 g per day in sub-Saharan Africa to 5.5 g per day in Central Asia.

The proportion of deaths from heart attacks and strokes attributable to sodium ranged quite a bit. In Canada, the United States, Australia and New Zealand, about 10% of cardiovascular deaths were linked to high salt intake. But in a wide band stretching from Eastern Europe all the way across into Central Asia and East Asia, the percentage of cardiovascular deaths attributed to sodium consumption jumped up to 20 to 25%. This happens to be the Old Silk Road, where people traveled vast distances on trade missions and needed salt to preserve their food. This tradition of eating salt-preserved foods has survived to our days.

The researchers found that reduced sodium intake lowered blood pressure in all adults, with the largest effects identified among older individuals, blacks, and those with pre-existing high blood pressure. They stated that because the study focused on cardiovascular deaths, the findings may not reflect the full health impact of sodium intake, which is also linked to higher risk of nonfatal cardiovascular diseases, kidney disease and stomach cancer, the second most-deadly cancer worldwide.

So that’s settled then, is it? Doom and gloom, since limiting salt consumption is difficult given that 80% of a person’s daily salt intake comes from the foods they eat, rather than the salt shaker.

Not so fast!

On the contrary, another recent study suggests that many dietary guidelines for sodium intake are unrealistic, and that the low recommended level of sodium could be associated with a higher risk of cardiac disease and mortality.

Although it has long been the view that eating too much salt will raise your blood pressure, a comprehensive global study now says that too little salt in your diet also can harm your heart health. There appears to be a “sweet spot” for daily sodium intake between 3 and 6 g (equal to 7.5 to 15 g of salt) associated with a lower risk of death and heart disease than either more or less.

The study included more than 100,000 adults from the general populations of 17 countries, providing a broad sample of people that varied greatly in socioeconomic, geographic and demographic makeup. The study found that those who consumed more than 6 g of sodium daily had higher blood pressures than those who consumed less sodium. Within this group, blood pressure increased with higher sodium intakes. The effect of dietary sodium intake on blood pressure was less dramatic for those in the medium (3 to 6 g) range of sodium intake and none for those in the low range of sodium intake (less than 3 g). However, sodium intake of less than 3 g per day was tied to a 27 percent increased risk of death and heart disease, according to their findings.

The study thus provided evidence that both high and low levels of sodium intake may be associated with an increased risk of death and cardiovascular disease and that healthy people probably can eat about twice the amount of salt compared to what is currently recommended — or about as much as most people consume anyway. Since only one in 20 people in the world currently eat what is recommended, it’s not a very practical recommendation.

The good news

Potassium in bananas can counter effects of sodium (Photo: Branko Collin)

Potassium in bananas can counter effects of sodium (Photo: Branko Collin)

But there is more. Before you start to worry too much about a futile effort of counting your exact intake of sodium think potassium. The study provided new evidence about the association of sodium and potassium intake with blood pressure, death and major cardiovascular events. It showed that consuming larger amounts of potassium counterbalanced the adverse effect of high sodium excretion on blood pressure. Potassium is a nutrient found in fruits, vegetables and beans. Rather than focusing on sodium, maybe it is better to focus on eating an overall healthy diet and pursuing healthy lifestyle changes.

It is probably safe to say that if you don’t already have high blood pressure and you’re not over 60 or eating way too much salt, salt won’t have much impact on your blood pressure.

But this is controversial news that could potentially undercut current public health messages about salt. It will take some further time before scientists can agree on the way forward.

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Red hot findings indicate new dangers with bisphenol A

Hormon disturbing chemicals (Photo: Sooz)

Hormon disturbing chemicals can be dangerous (Photo: Sooz).

Endocrine disruptors interfere with our bodies’ finely tuned hormonal regulation systems. Unfortunately, human exposure to endocrine disruptors, and particularly to bisphenol A commonly found in food packaging materials, is omnipresent in our daily lives. The potential risks to consumer health of such chemical contaminants have been the subject of many contradictory reports with science divided over how to handle the findings. Now there seems to be a link between bisphenol A exposure and food intolerance. More than 20% of the global population suffer from food allergy or intolerance making this an important issue.

Scientific controversy

The French are hellbent on proving that bisphenol A is a dangerous chemical that should not even come close to food of any sort. And they might be right. In the USA it is the opposite situation with federal agencies protecting the use of bisphenol A in food applications at any cost. They cannot both be right though. The arbiter is sitting on the fence. This is the European Food Safety Authority that recently completed a new draft assessment of bisphenol A but decided to consult extensively with external stakeholders before making a final decision. It is not going to be easy.

To start in France,  the French Agency for Food, Environmental and Occupational Health and Safety (ANSES) published an opinion on bisphenol A in April 2013 which recommended limiting exposure to this substance and lowering the toxicological thresholds on which risk evaluations were based. This resulted in the French government deciding to ban the use of bisphenol A in all food packaging from 2015. And new research findings are accumulating showing new dangers.

New scientific results published

Using female rats exposed to bisphenol A at low doses during pregnancy and early suckling, scientists at INRA’s Joint Research Unit for Food Toxicology in Toulouse demonstrated that it affected development of the immune system in the off-spring of the exposed rats and predisposed their progeny to food intolerance in adulthood. The scientists tested different doses (0, 0.5, 5 and 50 μg/kg body weight per day) and demonstrated a non-linear relationship between the bisphenol A doses and the undesirable effects observed. In particular, the most marked disturbances were observed at a dose of 5 μg/kg body weight per day. This is of course confusing but in line with the low dose hypothesis suggesting that there can be different reactions at different dose levels. At the low-dose level the scientists found that when challenged with ovalbumin, an egg white protein not previously included in their diet, an immune reaction was seen directed against ovalbumin which induced colonic inflammation that testified to a food intolerance. However, rats descending from the control group developed a food tolerance to ovalbumin, which resulted in a lack of immune response.

This is the same dose of 5 µg/kg body weight per day that is proposed by EFSA to be safe. The new findings highlight the problem of determining a safe and tolerable dose for bisphenol A. EFSA is still to make up their mind but has so far used the expression “as likely as not” for many negative findings to indicate an uncertainty around the real health impact of current human exposure levels.

Laboratory findings questioned

Laboratory findings questioned because of contamination.

Americans have been more gung ho about the safety of bisphenol A. To be fair there is an ambitious ongoing U.S. research project known as “CLARITY-BPA” into the safety of bisphenol A funded to the tune of US$32 million. But scientists from the National Center for Toxicological Research in Arkansas preempted this research by publishing interim findings in Oxford Journals’ Toxicological Sciences claiming that only very high doses of bisphenol A are dangerous, and that the “low levels” in common circulation through plastic bottles, thermal paper receipts, tin can linings and other sources are not a threat. These findings have since been heavily criticised because of bisphenol A contamination also of the control group.

Is there a safe level?

So what to believe? It seems pretty clear that not even 5 µg/kg body weight per day is a safe level. But actual exposure might be much less than this according to EFSA’s new exposure calculations as long as you don’t live exclusively on canned food. We have to wait until the end of 2014 until we can get access to EFSA’s conclusions. Agony for us and for the scientists grappling with the final opinion.

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