Worried about PFAS?

Well, it is a bit complicated as we are talking about PFAS as the collective name for a huge group of chemicals that according to some counts include over 12,000 synthetic per-and polyfluoroalkyl substances that have unique chemical uses including as lubricants, sealants and for waterproofing and heat resistance. The real problem is that they are highly resistant to degradation both in the environment and in human bodies and have thus been dubbed forever chemicals.

Although they have been around since the 1950s, concerns about their presence and toxicity have been gradually increasing. The reason being that the physical and chemical properties that make PFAS persistent and mobile in the environment also make them particularly challenging to analyse. Analytical methods sensitive enough to detect environmentally relevant concentrations didn’t become widely available until the early 2010s.

Now PFAS contamination has been found to be global. PFAS have been detected in regions with little human activity, including the atmosphere of remote locations, the Arctic and Antarctic seas and remote soils of every continent.

But let’s start from the beginning

PFAS have existed for over 90 years with the first form, polychlorotrifluoroethylene (PCTFE), discovered in 1934 in Germany. Bought by 3M in 1957, it was commercialised under the name Neoflon for use in semiconductors, chemicals and electronic components.

In parallel and almost by accident, DuPont had in 1938 found that a frozen, compressed sample of the fluorocarbon tetrafluoroethylene had spontaneously formed a white, waxy solid that would be dubbed PTFE (polytetrafluoroethylene) and later trademarked as Teflon. It was initially used in the Manhattan Project in gaskets and valves to hold toxic uranium hexafluoride in pipes when building the first nuclear bomb. Over the next several years, the company expanded the chemical’s use into cookware, stain repellents in fabrics and textiles and industrial coatings.

Not to be beaten, 3M scientists continued their development of PFAS chemicals resulting in perfluorooctanoic acid (PFOA) in 1947 and perfluorooctane sulfonic acid (PFOS) in 1953. They were both resistant to heat, oil, stains, grease and water. In 1951, 3M provided PFOA to DuPont to be used as an aid when coating products with Teflon. Both PFOS and PFOA would go on to be used as a component in a wide variety of products for years, including Scotchgard, stain resistant carpets and later firefighting foam. The 3M company kept expanding the range of PFAS by introducing perfluorohexane sulfonic acid (PFHxS) in 1958, again to be used in stain-resistant fabrics, fire-fighting foams, food packaging, and as a surfactant in industrial processes.

Within 20 years of its initial discovery in 1934, PFAS in its many forms had gone from a laboratory accident, to an atomic bomb project component, to an ingredient in everyday household products.

The dangers of PFAS

You would have thought that when synthesising indestructible compounds they would be extensively tested for potential toxicity before being released. Very conveniently according to publicly released information PFAS were long presumed to be biologically inert. However, legal disclosures and investigative reporting later uncovered evidence that companies that manufactured PFAS knew of their toxic effects on human health and the environment by 1970, forty years before it was generally known in the public health community.

Their human toxicity and ecosystem impacts have since received extensive public, scientific and regulatory attention. Testing of human blood in the USA, starting in 1999, found PFOA, PFOS, and PFHxS, the worst of the worst, in 99% of the sampled population. By 2006, PFAS had been found in ground and surface water, in soil and sediments, and in wildlife. The toxic properties and their inability to break down in the environment and to build up in human blood had become more evident.

Mounting evidence of the adverse health effects of PFAS showed that exposure to certain levels of the forever chemicals increased cancer risk such as liver, kidney, and testicular cancers, lowered birth weight in babies, produced higher levels of cholesterol, reduced kidney function, caused thyroid disease, altered sex hormone levels, and damaged the immune system resulting in a reduced vaccine response.

In 2007 a concerned European Commission asked the European Food Safety Authority (EFSA) to review health aspects of some PFAS as there was a clear need to assess the potential risks associated with human exposure to this class of substances. EFSA, in its opinion published in 2008, concluded that it was unlikely that adverse health effects from dietary exposure to PFOS or PFOA were occurring in the general population but stressed that this opinion was based on very limited data.

However, the more we look, the more alarming the health threat appears to be. Emerging research found PFAS in consumer products such as cosmetics, packaging, waterproofing, inks, pesticides, medical articles, polishes and paints, metal plating, pipes and cables, mechanical components, electronics, solar cells, textiles and carpets. As a result two of the highest-profile compounds, PFOS and PFOA, were added to the Stockholm Convention for the protection of human health and the environment from persistent organic pollutants (POPs) in 2009 and 2019, respectively, limiting their use and production. PFHxS was added to the list in 2022. In 2023, the International Agency for Research on Cancer (IARC) declared PFOA a category one human carcinogen.

What about exposure from food and water?

Potential human exposure pathways for PFAS include inhalation, incidental soil and dust ingestion, dermal contact, diet and drinking water. Diet and drinking water are considered the main sources of human exposure to PFAS in the general population. Two main processes are thought to lead to PFAS contamination of food, namely bioaccumulation in aquatic and terrestrial food chains, and transfer from contact materials used in food processing and packaging. Local water supply is a special case with high levels of PFAS detected close to industrial sites, military institutions and fire training facilities. Apart from water, foods like fish, fruit and eggs and egg products have been shown to contribute the most to human exposure.

In 2018, EFSA changed their tune based on new information for dietary exposure and toxicity. In establishing a tolerable intake of 13 ng/kg body weight per week (TWI) for PFOS and 6 ng/kg body weight per week for PFOA, they now concluded that exposure of a considerable proportion of the population exceeded the proposed limits for both compounds.

This was further strengthened in the EFSA opinion from 2020 evaluating the combined exposure to the sum of the four most potentially dangerous compounds: PFOA, PFNA, PFHxS and PFOS. Effects on the immune system with reduced antibody response to vaccination were considered the most sensitive and thus the most critical for the risk assessment. Since accumulation over time is important, the tolerable intake was lowered to a combined 4.4 ng/kg body weight per week for the four PFAS, considered protective also to other potential adverse effects observed in humans. Unfortunately parts of the European population exceed this TWI, which EFSA concluded was a concern.

International focus on PFAS

Worldwide, regulatory PFAS guidance has been rapidly evolving, with the inclusion of a wider range of PFAS covered in advisories and a continued decrease in what is deemed safe PFAS concentrations. In the USA a recent extensive review was published in 2022 by the National Academies of Sciences, Engineering, and Medicine titled Guidance on PFAS Exposure, Testing, and Clinical Follow-Up. The review found that an estimated 2,854 U.S. locations (in all 50 states and two territories) have some level of PFAS contamination and almost 100 percent of the U.S. population is exposed to at least one PFAS. They concluded that although not all of the contamination exceed health advisories, the pervasiveness of the contamination is alarming.

In a 2023 response to the PFAS challenge, the Government of Canada published a Draft State of Per- and polyfluoroalkyl substances (PFAS) Report. The report provides a qualitative assessment of the fate, sources, occurrence, and potential impacts of PFAS on the environment and human health in Canada. With the application of precautionary assumptions that are protective of human health and the environment when addressing gaps in information, the report provides the basis for a class-based approach to inform decision-making on PFAS in Canada. The report also conclude that PFAS as a class are harmful to human health and the environment.

Japan is no stranger to chemical contamination. But despite the history, combined with Japan having one of the world’s largest chemical industries and many Japanese companies producing or using PFAS chemicals, the attention paid to these chemicals has been far less than in the USA and Europe, at least in the public domain. Some researchers have recently warned of adverse effects on humans after high concentration levels of PFAS were detected in various parts of the country, which fuelled concern among residents. A report from Japan’s Food Safety Commission proposes the first-ever daily intake limits for PFOS and PFOA linked to health risks, emphasising safety in food consumption. It suggests a tolerable daily limit of 20 ng/kg body weight for each compound.

Based on advice from EFSA, the European Commission in 2022 established maximum levels for PFOS, PFOA, PFNA, and PFHxS in eggs, fish and bivalve molluscs and meat and offal. The varying maximum levels are laid out in Regulation (EC) 2022/2388.

Regulators worldwide have proposed or regulated varying concentrations for some PFAS in drinking water. Suggested maximum levels vary from 4 ng/L in the USA to 560 ng/L in Australia. However, it is impossible to compare the suggested maximum levels between countries as they are based on coverage of different numbers of PFAS. Some limits only cover PFOS and PFOA while others include all measurable PFAS.

The future is still uncertain

To eliminate the threat posed by PFAS will not be easy as they are still used in many applications where the use is considered proprietary with information not readily available or public. Gaining a complete picture of the threat is also a challenge because of the chemical and toxicological differences among individual PFAS and uncertainty about the exposure level at which their adverse effects may occur. In addition, many of the chronic diseases associated with PFAS exposure have also myriad other causes.

Unfortunately for all of us, it is difficult to reduce exposure to PFAS through personal behaviour modifications. There are so many routes of potential dietary exposure to PFAS from non-stick cookware, grease-resistant paper, fast food wrappers, microwave popcorn bags, and retail and convenience packaging. Add to that the use of PFAS in our clothes, our furniture, cosmetics, sunscreens, shampoos, carpets, menstrual products, dental products and even in artificial turf.

The best we can do is to keep up the pressure on regulatory authorities to lower the PFAS limits in the water supply and look at banning their use in most consumer products and food packaging.

And finally let’s learn from the mistake of releasing chemicals before they have been tested for harmful effects to humans and the total environment.

Bananas vs. liquorice!

Should you have a banana with your liquorice? It might be a good idea and here we explain why. But first let’s start with the liquorice, and we are talking about the real stuff with the characteristic liquorice taste provided by glycyrrhizin and not sweets flavoured with aniseed or other similar flavourings.

Liquorice is the common name given to a flowering plant (Glycyrrhiza glabra) that grows in parts of Asia and Europe. The root of the liquorice plant is the source of a sweet, aromatic compound called glycyrrhizin, which is used as a flavouring in confectionery and drinks. It is over 50 times sweeter than succros. The root itself may also be used as a dietary supplement with claimed health benefits like anti inflammatory activities and respiratory health support.

Liquorice consumption considered safe

For most of us, the liquorice found in food is generally considered safe to eat and safe when consumed as a medicine for short periods of time. However, when taken in large amounts over an extended period, it may cause potassium levels in the body to fall and this may impact your blood pressure. Some people may be particularly sensitive to these effects, such as those with heart disease, kidney disease and high blood pressure. Daily consumption of 50 g or more of liquorice candy for as little as two weeks may increase blood pressure by a small amount. This in turn can trigger abnormal heart rhythms, oedema (swelling), lethargy, and congestive heart failure in some people.

The component glycyrrhizin is responsible for many of these side effects. Although the amount of glycyrrhizin varies depending on the manufacturer of the confectionary and country preferences, a recent Danish study established a typical mean content of around 2 mg/g. Safe intakes recommended by the European Union and the World Health Organization (WHO) are specified as up to 100 mg glycyrrhizin a day, equivalent to about 50 g of confectionary. The US FDA allows soft candy to contain a maximum of 3.1% of glycyrrhizin so a 100 mg limit would be reached after the consumption of only 4 g of confectionary.

Swedish study issues a warning

However, in a study published in 2024, Swedish researchers suggested that the safe limit for liquorice might need to be reconsidered after discovering a significant impact on blood pressure in healthy adults. The researchers recruited 28 healthy participants with an average age of 24 years. The study used a randomised crossover design, with participants either starting with a liquorice product containing 100 mg of glycyrrhizin or a control product. The first block consisted of a 1-week run-in, followed by the 2-week liquorice intervention, a 2-week washout, a 2-week control period and a further 2-week washout period. The second block reversed the sequence of 2-week periods.

The researchers observed significant increases in systolic blood pressure during the liquorice intervention period when compared to measurements in the control period. Blood pressure readings were found to show increases from day five, with a mean increase in systolic blood pressure of 3.1 mm Hg at day 14. In addition, renin and aldosterone were found to be suppressed during the liquorice intervention. Renin is a hormone made by the kidneys. It controls the production of aldosterone, a hormone made in the adrenal glands. Aldosterone helps manage blood pressure and maintain healthy levels of potassium and sodium in the body. These effects have not previously been demonstrated for such moderate amounts of daily intake of liquorice.

Thus the researchers indicated that liquorice seems to be a more potent substance than previously thought and that currently advised safe levels might need to be reconsidered.

And here is the saviour

So now we come to potential counter measures in case you cannot resist the temptation posed by liquorice candy. And bananas could be part of the answer.

Researchers at The George Institute of Global Health at Imperial College London analysed data from a five year monitoring study of 20,995 people in China where half of the participants had replaced the use of normal table salt in cooking with a “salt substitute” containing potassium-enriched salt. They found that a one gram increase in daily potassium intake lowered systolic blood pressure levels by 2 mm Hg on average.

As it happens consuming an extra gram of potassium is the equivalent of eating two medium-sized bananas, a cup of spinach or a large sweet potato. So eating bananas can actually be an effective way of reducing blood pressure similar to cutting down on salt intake.

A global collaboration of researchers from Australia, the US, Japan, South Africa and India have called for potassium to be added to international health guidelines, with just Chinese and European guidelines currently suggesting it as an effective way to reduce blood pressure.

So what are the lessons learned?

First up be careful with your liquorice intake. Maybe eating 50 g every day for two weeks is overdoing it a bit. And also we are talking about mean levels of glycyrrhizin in liquorice sweets while some products may have much higher levels.

On the other hand, it is possible to balance the potassium reducing effects of liquorice by consuming other potassium-rich foods. Bananas is a good choice as they have other beneficial health effects as well. And why not a cup of spinach on she side?

As always a balanced diet without excesses either way is the solution to a long and healthy life.

Toxic arsenic in rice

We have written about the toxicity of arsenic in food twice before. The first time was in 2012 covering a 2009 opinion from the European Food Safety Authority (EFSA) and a 2012 report from the US Food and Drug Administration. The second time was in 2020 based on research from the University of Washington covering the impact of climate change on further accumulation of arsenic in rice due to a warmer climate.

Previous problems in determining the chemical form of arsenic (arsenic speciation)

Arsenic exists in several different forms in nature bound to a number of other compounds resulting in varying toxicity. It is the inorganic arsenic (compounds that do not contain carbon) commonly found in water and rice that is particularly toxic. Soluble inorganic arsenic is rapidly and nearly completely absorbed after ingestion and widely distributed to almost all organs. Organic arsenic commonly found in fish and other seafood is far less toxic.

And here we have a real problem in that arsenic analysis at speciation level has been very difficult. Unfortunately, the EFSA risk assessment in 2009 had to make assumptions about the proportion of inorganic arsenic in different food commodities based on the total arsenic levels reported to allow calculation of specific exposure to the toxic species. With an improved focus on arsenic speciation, the European Commission asked EFSA to first update the exposure assessment based only on inorganic arsenic results and secondly to update its risk assessment of inorganic arsenic to consider new studies on its toxic effects.

The new exposure results

In 2021, EFSA published an updated exposure assessment. It was based on a total of 13,608 analytical results on inorganic arsenic of which 7,623 covered drinking water and 5,985 covered different types of food, in particular rice and rice-based products. Samples were collected across Europe between 2013 and 2018. Consumption data from 23 different European countries and a total of 44 different dietary surveys (87,945 subjects) were used to better estimate the chronic dietary exposure of inorganic arsenic.

The highest dietary exposure to inorganic arsenic was seen in the young population (infant, toddlers and other children) with mean values in the different surveys ranging between 0.07-0.61 μg/kg bodyweight per day, and high exposure consumers (the 95th percentile estimates) between 0.17-1.20 μg/kg bodyweight per day. In the adult population (adults, elderly and very elderly), mean dietary exposure estimates ranged between 0.03-0.15 μg/kg bodyweight per day, and between 0.06-0.33 μg/kg bodyweight for high intake consumers (the 95th percentile estimates).

These dietary exposure estimates of inorganic arsenic were noticeably lower than previously reported, with the new estimates being around 1.5–3 times lower across the different age classes. This difference can be explained by the use of measured rather than previously calculated inorganic arsenic and more accurate consumption data. The higher dietary exposure seen in the young population is to a large extent due to consumption of rice-based foods for infants as well as biscuits, rusks and cookies for children.

And the new risk assessment results

In 2024, EFSA published a new risk assessment of inorganic arsenic in food based on the new exposure assessment and updated toxicity results. The latter used findings from existing human epidemiological studies not normally available, and not animal studies as proxies for human effects. The epidemiological studies showed that chronic intake of inorganic arsenic via diet and/or drinking water was associated with increased risk of several adverse outcomes including cancers of the skin, bladder and lung.

For its risk assessment, EFSA considered the increased incidence of skin cancers associated with inorganic arsenic exposure as the most relevant harmful effect. The experts concluded that ensuring protection against skin cancer would also be protective against other potentially harmful effects.

When assessing genotoxic and carcinogenic substances that are unintentionally present in the food chain, EFSA calculates a margin of exposure (MOE) for consumers. The MOE is a ratio of two factors: the dose at which a small but measurable adverse effect is observed called the reference point, and the level of exposure to a substance for a given population.

In its 2009 opinion, EFSA calculated the reference point as a range of values between 0.3 and 8 µg/kg bodyweight per day of inorganic arsenic associated with cancers of the lung, skin and bladder, as well as skin lesions. In the new opinion of 2024, the reference point was lowered to a single value of 0.06 μg/kg bodyweight per day using a case–control study of skin cancer (squamous cell carcinoma) carried out in the US. This is in the range of the new mean dietary exposure estimates for inorganic arsenic in adults (0.03–0.15 μg/kg bodyweight per day), and below any of the high exposure estimates in adults ( 0.07–0.33 μg/kg bodyweight per day). In adults, the calculated MOEs ranged between 2 and 0.4 for mean consumers and between 0.9 and 0.2 for high consumers, respectively. An MOE calculated from human data of 1 or less would correspond to an exposure level to inorganic arsenic that might be associated with an increased risk of skin cancer and thus raises a health concern.

The same conclusion applies to the younger age groups despite their higher exposure to inorganic arsenic as the harmful effect seen in adults are due to chronic exposure and the epidemiological studies would have captured their dietary exposure during early life.

So what can be done to limit the risk?

As has been indicated above, rice is a major contributor to inorganic arsenic exposure as it is a dietary staple for millions of people around the world. So what can be done to limit the risk?

Authorities could introduce maximum levels for arsenic in rice, consumers could look at rice types and try to buy rice from regions with less natural levels of arsenic, rice preparation in kitchens could be changed or rice consumption could be reduced if there are alternatives available.

Regulating inorganic arsenic levels

Unfortunately, regulating a naturally occurring element in such a widely eaten food as rice is no easy task. Arsenic levels can vary widely in rice from different countries and states, and among different rice cultivars. This raises difficult questions about how a regulated standard could be monitored and enforced.

Codex Alimentarius has adopted a recommended limit for inorganic arsenic of 200 μg/kg for polished rice, and 350 μg/kg for husked rice. In the European Union maximum levels for inorganic arsenic in rice was introduced in 2016 varying from 100-300 μg/kg depending on the specific product. The Australian guidelines are for total arsenic (organic and inorganic) in rice and set a maximum level of 1000 μg/kg.

However, looking at the reported inorganic arsenic levels in rice reported to EFSA only 15 samples exceeded European Union maximum levels and still a health concern was identified.

Buying rice with proven lower levels

The amount of arsenic in rice depends on the variety of rice and where it was grown. Brown rice has more arsenic than white rice since arsenic is accumulated in the outer layers of the grain, while basmati rice regularly has the lowest levels. Globally, inorganic arsenic in polished rice varied from < 2 to 399 μg/kg in a recent study. The lowest levels were found in East Africa followed by Indonesia and California, while West African rice had an order of magnitude higher inorganic arsenic followed by South America and Southern American states like Texas and Luisiana.

Although it can be quite difficult to know where the rice is grown, it is clear that basmati rice is a preferred choice and brown rice should be avoided despite its better nutritious profile.

Changing rice preparation

Rinsing rice before cooking has a minimal effect on the arsenic content of the cooked grain, but washes enriched iron, folate, thiamin and niacin from polished and parboiled rice. However, cooking rice in excess water efficiently reduces the amount of arsenic in the cooked grain by 40% to 60%. It is recommended to use six cups of water to one cup of rice. After boiling the rice, pour off the remaining water, then rinse the cooked rice again.

Unfortunately, this cooking method common in Asia will also reduce some of the nutrients but is recommended on balance to minimise arsenic toxicity.

Limit rice consumption

It is not necessary to eliminate rice completely from your diet, but If you eat a lot of rice eat it less often substituting rice with other whole grains, such as quinoa, barley, ferro, amaranth, bulgur and millet. They’ll be just as nutritious and don’t have arsenic in them because they don’t take up arsenic from the ground as they grow.

Arsenic in rice is a real concern. Be more choosey with the type and origin of your rice, always cook it with excess water, and be aware of how much you’re consuming. Try looking at other whole grain alternatives to keep your arsenic consumption to a minimum.

Baby food pouches criticised

Our very young children are precious. The first 1000 days of a child’s life is a crucial period of early life development. The establishment of healthy eating habits early in life provides a path towards the prevention of future diet-related chronic diseases. Introducing complementary food after exclusive breast feeding for six months as recommended by the World Health Organisation is not an easy period for parents. And of course the food industry has attempted to be the saviour by inventing the baby squeeze pouch.

Squeeze pouches

Squeeze or spout pouches are a plastic retort baby food sachet or pouch containing pureed foods marketed as suitable for children aged between six months to five years. The pouches enable children to consume wet ready-to-use food directly from the packet through sucking on the spout. Food pouches for babies and toddlers were first launched in the USA around 2008 and has since taken off worldwide. The increased market share of squeeze pouch baby foods has been driven by changes in the labour market and ‘time-poor’ parents making life a little bit easier for them.

The global pouches market was valued at US$22 billion in 2021 and is expected to expand to around US$40 billion by 2030. Squeeze pouches are now the primary product sold in the Australian baby food market and have contributed to sales worth A$1.2 billion. The food industry calls it mobile food technology for the modern family. They are marketed as ‘convenient’ and ‘easy to feed’ to help parents on the run to select a product that they perceive as the healthiest food for their infant. But are they?

Nutritional composition

Nutritional composition analysis of squeeze pouch infant food undertaken in the US, Germany, Denmark, UK and New Zealand have a striking common finding. All pouch products were considered high in both total and added or free sugars when compared to other infant and toddler foods with most of the total energy provided from free sugars.

There was a predominance of apple, pear and sweet vegetable purees in squeeze pouches, and only small amounts of bitter vegetables and grains.

In the USA, the Baby Food Facts Report found that most infant squeeze pouches do not support recommendations for encouraging healthy eating habits, and the marketing of the pouches is misleading about the true nutritional content.

Similarly, in the UK, a report by First Steps Nutrition found that many product names did not reflect their actual content, with 30% of 188 products analysed failing to mention the main ingredient (e.g. fruit puree) in the product name.

In New Zealand it was found that squeeze pouches contained as little as 0.3 mg/100 g of iron, placing infants at risk of iron deficiency if complementary fed exclusively on commercial squeeze pouches

Recent Australian data

A team of Australian scientists from the Western Sydney University recently confirmed the findings of previous international studies when investigating product content and labelling of 276 ready-to-use infant food pouches available on the Australian market. Only two products were nutritionally adequate according to a nutrient profiling tool. Marketing messages included desirable ingredient emphasis, nutrient absence claims, claims about infant development and health, good parenting, and convenience. Claims of ‘no added sugar’ were made for 59% of pouches, despite the addition of free sugars through the use of fruit juice or syrup.

They concluded that squeeze pouch products available in Australia are nutritionally poor, high in sugars, not fortified with iron, and there is a clear risk of harm to the health of infants and young children if these products are fed regularly. The marketing messages and labelling on squeeze pouches are misleading and do not support official recommendations for the appropriate introduction of complementary foods and the labelling of products. There is an urgent need for improved regulation of product composition, serving sizes and labelling to protect infants and young children aged 0–36 months and better inform parents.

So what to do?

Feeding time can be a difficult mission and certainly requires patience and plenty of cleaning cloths and protecting the carpet is essential. None of these things are needed with pouches making them a great choice if you want to avoid spills and chaos that are often associated with feeding babies in a highchair.

Thus, infant pouches can make up over 70% of the baby food market and they dominate the baby food aisle in supermarkets in many countries. No doubt that’s because they are easy to carry, have a shelf life of at least 12 months and don’t produce a messy feeding situation. They clearly have their place for an occasional meal when out and about or taking to a special event where messy eating isn’t appropriate.

However, numerous studies have shown that the more variety of tastes, textures, colors, and mouth feels a baby is exposed to, the more likely those children are to accept new foods later on in life. Every time a baby or toddler sits down to eat presents a learning opportunity in more ways than one. And unfortunately, pouches detract from that learning more than they contribute to it. 

But don’t feel guilty when sneaking in a pouch or two now and then. Caring for an infant is a difficult task and occasionally some relief is necessary. Hopefully, food manufacturers can improve the nutritional composition of the food they put in their pouches to better justify their use.

Feeling energetic?

Are you counting your calories and limiting your energy intake from food and drink for a slimmer you? Or maybe just talking about calories in general terms as many of us do. Then you might like to know what you are talking about or counting so I thought a brief explanation would be useful. It is actually a little bit complicated as it has evolved over time.

Let’s start from scratch

It is self evident that food and drink provide the energy we need to stay alive and active. However, the standard measure of energy in the International System of Units or SI system is joules (although a derived unit from the seven defined SI base units) and not calories. The joule is named after James Prescott Joule. It is clearly defined as a unit of work or energy equal to the work done by a force of one newton acting through a distance of one meter.

So why do many of us still think in calories (or Calories as you will see below)?

It might be historical as the term calorie has been in use since the early 19th century when Nicholas Clément-Desormes in 1825 defined it as the amount of heat required to raise the temperature of a kilogram of water from 0°C to 1°C. However, scientists were not happy with this definition so changed it to the amount of heat required to raise the temperature of a gram (not kilogram) of water from 0°C to 1°C. So the initial calorie (now often expressed as the capitalised Calorie) is now equal to 1,000 new calories or 1 kilocalorie (abbreviated kcal). The concept entered the food world when W.O. Atwater used it in 1887 to describe food energy.

After that the Calorie became the preferred unit of potential energy in nutrition science and dietetics for a while.

But it didn’t stop there as in the early 20th century the calorie started to be defined in terms of joules. Thus the Committee on Nomenclature of the International Union of Nutritional Sciences changed the definition of the “small calorie” to the amount of heat required to raise the temperature of 1 g of water from 14.5 to 15.5°C, a 1% change from the previous definition. And the Calorie followed. This way a Calorie could be defined as equal to 4.184 kJ.

Slightly confusing?

To avoid further confusion most countries have officially adopted the joule as a measure of food energy, expressed as kilojoule (kJ) for convenience on food labels. However, a few countries (and maybe you and me) stick to Calories and the final say goes to the current US Dietary Reference Intakes that define 1 kcal (or Calorie) as 4.186 kJ, again slightly different to previous definitions.

So after all that feel free to think in Calories as long as you know that you can multiply your Calories by 4.2 to get to kJ or divide your kJ by 4.2 to get to Calories. Or for the lazy you can even use a simple 4 for the calculations to get to a close enough approximation.

Energy intake in practice

With that out of the way let’s get back to practical considerations in looking at energy intake. It is assumed that an average adult needs about 8,700 kJ (2,100 kcal) a day to maintain a healthy weight. But it varies quite a bit – some people need more and others less. It depends on age, gender, height and weight as well as how active we are. If consuming more energy than we use, the extra energy is stored as fat. To lose excess fat means you need to take in less energy (fewer kJ) or use more through exercise, or preferably both.

The energy is provided by the protein, carbohydrate and fat in the foods we eat and in drinks. These nutrients deliver energy in varying amounts. Fat is the most concentrated source of energy (37.7kJ/g), followed by protein and carbohydrate (both at 16.7kJ/g). Alcohol also provides energy (29.3kJ/g) while also increasing the amount of vitamins and minerals that the body requires. 

Although every person’s daily energy intake is highly variable, based on their personal goals and needs, the typical daily energy intake of 8,700kJ is often split with 1,800kJ for breakfast, 450kJ for a morning snack, 2,500kJ for lunch, 450kJ for an afternoon snack and 3,500kJ for dinner.

Spending the daily energy intake

Preferably we should balance our energy intake with our energy expenditure. Metabolism is the process by which the body changes food and drink into energy. During this process, nutrients in food and drinks mix with oxygen to liberate the energy the body needs. Digesting, absorbing, moving and storing food burn energy. About 10% of daily energy consumed are used for digesting food and taking in nutrients. This can’t be changed much.

Then we have the basal metabolism. Even at rest, a body needs energy for all it does. This includes breathing, sending blood through the body, maintaining body temperature, keeping hormone levels even, and growing and repairing cells. The amount of energy a body at rest uses to do these things is known as basal metabolic rate. Our basal metabolism makes up about 60-70% of the energy we burn and again can’t be changed much although it is partly related to muscle mass. That is:

• people who are larger or have more muscle burn more energy, even at rest;
• men usually have less body fat and more muscle than do women of the same age and weight and thus burn more energy;
• with aging, people tend to lose muscle and more of the body’s weight consists of fat slowing energy burning.

Adding all this up we have already spent 6,000 to 7,000kJ and we haven’t accounted for all of our incidental activities that can be changed a lot. These include things such as housework, walking around the house, gardening, walking to a shop, hanging out the washing or even fidgeting. These activities are collectively called non-exercise activity thermogenesis and accounts for about 500 to 3,000 kJ used daily.

We are now hopefully in energy balance.

Surplus energy

But how well do we stick to the average energy intake of 8,700kJ? Not so sure about that!

We have the morning break and go for a coffee and order a large flat white (this is Australia) and an apple danish without considering the energy content. The apple danish will actually contribute 1,100kJ and the coffee 670kJ, well above our indicated average of 450kJ for the morning snack.

We might feel a bit tired in the afternoon and go for another coffee. This time we pick a cappuccino (only Italians limit a cappuccino to before 11am) and a blueberry muffin. Now we have added another 1,600kJ to our energy intake. On second thought we could replace the large blueberry muffin with a mini muffin to limit the energy intake to 850kJ for the afternoon snack, still above the suggested 450kJ.

After a long day we sit down for dinner. As we had a really successful day we share a bottle of red wine with our partner. If you share it equally you’ve had 1,260kJ even before you start to consider the energy content of the first bite of food. That’s the equivalent of a cup of chunky vegetable soup, a slice of wholemeal bread with a teaspoon of butter, and two slices of prosciutto. You skip the wine and instead go for a 375mL bottle of 4.5% strength beer. That way you limit the extra energy intake to 400kJ as long as you stick to only one beer.

We could go on with many other examples. Adding a chocolate croissant to our normal breakfast would contribute about 1,000kJ. A gin and tonic to relax in the evening provide 715kJ. A medium sized glass of a cola soft drink would add a further 750kJ. If you want to get more bad news you can search for the energy content of many other food and drinks on the excellent fatsecret Australia website.

Spending the extra energy

But even with the extra energy intake all is not lost as we can become more physically active. This is the form of energy expenditure that we have real control over. This is the energy used by physical movement and it varies the most depending on how much energy you use each day. Physical activity includes planned exercise like walking the dog, going for a run or playing sport.

Just standing for an hour working at your desk and your muscles have spent 600kJ to keep you upright. A walk with the dog for an hour would consume 1,000kJ or if you are power walking it could be close to 2,000kJ per hour. During strenuous or vigorous physical activity, our muscles may burn through as much as 3,000kJ per hour. If you are the one mowing the lawn (if you have one) you would spend 1,500kJ for an hour’s work. Fast step dancing, shovelling snow (not needed here in Sydney), using an exercise machine, or playing basketball all four half an hour and you have spent close to 1,000kJ.

As you can see there are many ways to spend excess energy intake so a little indulgence now and then wouldn’t go astray while still keeping your energy intake and expenditure in balance. Keep your brain working by reading a captivating book for an hour and you have spent 600kJ.

A matter of balance

Of course there is much more to consider when consuming food and drink. Empty calories (see there I can’t get myself to stick to kJ) are the worst, that is food and drink which mainly provide energy and few nutrients. Candy, pastries, chips, bacon, and sugar-sweetened beverages are less nutrient dense. These foods contain added sugar, solid fats, and refined starch, and they provide few essential nutrients.

On the other hand there should also be pleasure in eating. Food can nourish our body in a lot of different ways. In fact, experts often indicate that eating for pleasure not only fuels the body but the mind as well. When people feel satiated, they are less likely to feel deprived or restricted.

So we are back to the balanced diet concept with the last word going to the Verywell Fit website. The best you can do is to find a balance between enjoying food and life, feeling good, and enjoying the best health we can.

What more can we ask for?

Satisfying saffron!

Mmm … saffron, such a flavoursome and useful spice, but there is more to it than that so read on.

Initially it is worth noting that saffron is the most expensive spice in the world. Nevertheless, it has a long history of use as a flavouring agent essential to a broad range of dishes from Swedish saffron buns to Spanish paella, Persian rice dishes and Indian curries.

Actually, saffron use dates back 3000–4000 years with records found in Persian, Greco–Roman and Egyptian cultures. From here it spread first to India and China and much later to other parts of North Africa and Europe. While saffron’s origin is still debated, it most likely originated in old Persia. There, as in other countries, it was revered not only for its flavour but also for its perceived medicinal properties. People would eat saffron to enhance libido, boost mood, and improve memory. Cleopatra used it to infuse her bathwater. Alexander the Great bathed his battle wounds with it and drank saffron tea.

So what is saffron?

Saffron is derived from the saffron crocus plant (Crocus sativus) related to the lily. It is a domesticated autumn-flowering perennial plant unknown in the wild. Being sterile, its purple flowers fail to produce viable seeds. Instead reproduction depends on humans digging up and replanting bulb-like organs called corms. A corm survives for one season, producing via vegetative division up to ten cormlets that can grow into new plants in the next season.

The dried thread-like parts of the flower called stigmas are used to make saffron spice, food colouring and medicine.

The high retail value of saffron is maintained on world markets because of labour-intensive harvesting methods, which makes its production costly. One freshly picked crocus flower yields on average 30 mg of fresh or 7 mg of dried saffron threads. Some forty hours of labour are needed to harvest 150,000 flowers and hand-pick 440,000 red stigmas from the flowers that after heating and curing yield a kilogram of dried saffron.

Iran produces some 90% of the world total of saffron. At $10,000 per kg or even higher, saffron has long been the world’s costliest spice by weight.

Health impact of saffron

Saffron has long been used in traditional medicine to treat menstrual problems, depression, asthma and sexual dysfunction. It contains an impressive variety of plant compounds acting as antioxidants – molecules that protect cells against free radicals and oxidative stress. These compounds include crocin and crocetin that are carotenoid pigments responsible for saffron’s red colour, safranal that gives saffron its distinct aroma and picrocrocin producing the bitter taste, among several other compounds. Together they are believed to be responsible for the observed beneficial effects identified in initial scientific trials covering conditions from memory loss to cancer.

Although early evidence has been inconclusive, this is starting to change with reports of results from new scientific studies.

A review of ten randomised controlled trials involving unhealthy subjects showed that saffron supplementation clearly improved oxidative stress through its antioxidant activity, a general indicator of beneficial health effects.

Summarising nineteen studies, more specific results indicated that saffron significantly reduced fasting blood glucose, waist circumference, diastolic blood pressure, concentrations of total cholesterol and low-density lipoprotein cholesterol, and improved symptoms of depression, cognitive function and sexual dysfunction compared with controls (mainly placebos).

Scientists studying the effects of saffron on sleep quality in healthy adults with self-reported poor sleep completed a randomised, double-blind, placebo-controlled trial. Saffron intake was associated with larger improvements in sleep quality in adults than the placebo.

A further overview of the scientific literature pointed to a consistent and significant improvement of depression, anxiety, and cognitive impairment associated with the daily intake of moderate quantities of saffron extracts. The effects seemed to be comparable to those of specific pharmacological treatments and appeared to be generally well tolerated with no major adverse effects associated with its daily consumption.

Indeed, it is now beyond doubt that saffron and especially its main constituent molecules (crocins, crocetin, picrocrocin and safranal) exert beneficial effects on frequent neuropsychiatric (depression, anxiety, schizophrenia, etc.) and age-related diseases (cardiovascular, ocular, neurodegenerative diseases and sarcopenia).

So all fine then?

Well yes, it seems to be fine from a scientific point of view. Saffron provides clear health benefits in reasonable doses of 20, 30 or 50 mg per day in the trials. But there is one remaining problem apart from the price and it is saffron adulteration.

Despite attempts at quality control and standardisation, an extensive history of saffron adulteration continues into modern times. Adulteration was first documented in Europe’s Middle Ages, when those found selling adulterated saffron were executed under the Safranschou code.

Typical methods include mixing in extraneous substances like beetroot, pomegranate fibres, red-dyed silk fibres, or the saffron crocus’s tasteless and odourless yellow stamens. Other methods included dousing saffron fibres with viscid substances like honey or vegetable oil to increase their weight. Powdered saffron is more prone to adulteration, with turmeric, paprika, and other powders used as diluting fillers. Safflower is a common substitute sometimes sold as saffron.

In recent years, saffron adulterated with the colouring extract of gardenia fruits has been detected in the European market. This form of fraud is difficult to detect due to the presence of flavonoids and crocines in the gardenia-extracts similar to those naturally occurring in saffron. Detection methods have been developed by using HPLC and mass spectrometry to determine the presence of geniposide, a compound present in the fruits of gardenia, but not in saffron.

Counter methods you can take!

All is not lost if you’re a little clever about it.

First, don’t buy bargain saffron as there is a reason for the high price of high quality saffron. The adage ‘you get what you pay for’ is most relevant in this case.

Second, check that the saffron strands are frayed at one end and look for a deep red hue that colours water orangey-yellow when submerged.

Finally, smell it and put it on your tongue – fake saffron has very little aroma or flavour while real saffron will smell slightly fruity and floral and taste sweet and bitter at the same time.

And after all that you can enjoy the wonderful taste of your saffron dishes and potential health benefits at the same time.

Tainted spinach

Spinach (Spinacia oleracea) is a leafy green vegetable that originated in Persia. It belongs to the amaranth family and is related to beets and quinoa.

Popeye, a pugnacious, wisecracking cartoon sailor popularised the beneficial effects of spinach by showing superhuman strength after ingesting an always-handy can of spinach.

And it’s true, spinach is considered very healthy, as it’s loaded with nutrients and antioxidants and is also high in insoluble fibre. Eating spinach, as part of a generally healthy diet, may benefit eye health, reduce oxidative stress, help prevent cancer, and reduce blood pressure levels.

There is a small caveat about the fairly high levels of nitrate in spinach. But nothing to worry too much about as we have previously explained.

So all good?

Well, that is until December 2022 when about 200 Australians were reported as being poisoned with symptoms typically occurring within one hour after eating fresh baby spinach leaves. They were reported to show quite serious symptoms including nausea, blurred vision, delirium, confusion, hallucinations, rapid heartbeat, flushed face and dried mouth and skin. Quite a list!

While there were several hospitalisations, most people affected were experiencing symptoms for a short time and recovered fairly quickly. After some considerable detective work the baby spinach was found to be contaminated with the leaves of the noxious weed thornapple, a poisonous invasive species that is found across Australia and in several other countries. 

Thornapple, also known as Jimson weed, devil’s snare and devil’s trumpet, with the scientific name Datura stramonium, belongs to the Solanaceae family of plants. This family includes both healthy kitchen staples like tomatoes and potatoes but also highly poisonous plants such as thornapple, mandrake (Mandragora officinarum) and belladonna (Atropa belladonna) that all contain a group of toxins called tropane alkaloids. This group comprises more than 200 different compounds with limited data on their occurrence in food and feed and their toxicity.

As usual it is the dose that makes the poison. As a matter of fact, small amounts of plant extracts containing tropane alkaloids have been used for centuries in human medicine and are still used, like atropine, hyoscyamine and scopolamine. These uses include for example the treatment of wounds, gout and sleeplessness, and pre-anaesthesia. Extracts from belladonna were used to dilate pupils for cosmetic reasons and to facilitate ophthalmological examination. In India, the root and leaves of thornapple were burned and the smoke inhaled to treat asthma. Some of these poisonous plants have also been used as recreational drugs, although under such less controlled circumstances ingestion could be deadly.

The thornapple culprit!

Thornapple is cultivated worldwide for its chemical and ornamental properties. The plant is one of the 50 fundamental herbs used in traditional Chinese medicine, where it is called yáng jīn huā. It prefers warm-temperate and sub-tropical regions, and as an invasive weed is often found on river flats, roadsides and agricultural lands where it competes with summer crops. It spreads by seed, with each plant producing up to 30,000 seeds and living for up to 40 years in the soil.

The active constituents in thornapple include scopolamine, atropine and other tropane alkaloids acting on the nervous system. Combined they cause stimulation of the nervous system in low doses and depression of the system at higher doses. Ingestion of plant parts may lead to generalised confusion, delirium and powerful hallucinations that often leave the person in a state of panic and severe anxiety.

All parts of the plant contain the highly poisonous tropane alkaloids. They are toxic also in tiny quantities with symptoms like flushed skin, headaches, hallucinations, and possibly convulsions or even coma. Eating a single leaf can lead to severe side effects as was noted in the Australian outbreak.

How did it get into spinach?

The baby spinach producer confirmed that when checking they found thornapple leaves in its baby spinach fields. It is likely that the high amount of rainfall during 2022 in Australia had contributed to the spread of the weed. A few young leaves that would have been looking like baby spinach leaves at that stage of growing were picked up during spinach harvest.

This is not a unique occurrence as seeds of tropane alkaloid-producing plants have been found as impurities in other important agricultural crops such as linseed, soybean, millet, sunflower and buckwheat. The consumption of a few berries from henbane (Hyoscyamus niger) or from belladonna has previously caused severe intoxication, including deaths in young children.

What can we learn?

From this incident we can learn that vigilance is important to avoid contamination of toxic weeds in agricultural crops.

It is also important to have an efficient reporting and tracing system of food related toxic events to capture outbreaks early.

However, fortunately it’s all clear for the baby spinach itself.

Consuming micro- and nanoplastics

We seem quite good at inventing ‘things’ and we rush them to market before giving enough thought to potential negative consequences. The question is will we ever learn? Ulrich Beck, a past sociology professor at the University of Munich, pointed to inherent long-term risks with new products that are often disregarded by an enthusiastic subordination of nature by science and technology. (Image by storyset on Freepik)

There are many examples of how this can backfire.

DDT was hailed as a wonder chemical that would revolutionise agriculture until Rachel Carson published her book ‘Silent Spring’ in 1962. It is now known that DDT caused direct mortality of some birds by poisoning their nervous system, caused bird eggs to have thin shells and reduced levels of a hormone necessary for female birds to lay eggs. It could indeed lead to a silent spring.

PFAS are a large, complex group of manufactured chemicals that are ingredients in various everyday products. They are used to keep food from sticking to packaging or cookware, make clothes and carpets resistant to stains, and create firefighting foam that is more effective. Now we know of numerous human health effects including altered metabolism and fertility, increased risk of being overweight or obese, and reduced ability of the immune system to fight infections. Something we have to live with as PFAS are persistent chemicals spread everywhere in nature.

Neonicotinoids are insecticides that have been repeatedly called ‘perfect’ for use in crop protection. Since their introduction in the early 1990s, neonicotinoids have become the most widely used insecticides in the world on a variety of crops. However, in a 2013 report by the European Food Safety Authority it was stated that neonicotinoids pose an unacceptably high risk to honey bees, and that the industry-sponsored science upon which regulatory agencies’ claims of safety have relied may be flawed and contain data gaps not previously considered. As bees, consisting of around 20,000 species worldwide, are one of the primary pollinators of both native plants and agricultural crops the impact of neonicotinoids could spell disaster for worldwide food production. Bumblebees are also economically important pollinators and appear to be particularly sensitive to neonicotinoid pesticides, which affect both bumblebee colony growth and foraging efficiency. It is clear that we overuse pesticides at our own peril because human and natural environments are unquestionably linked. And still many countries have no restrictions on neonicotinoid use.

Do you want some plastics with that?

And so we come to plastics, such a useful innovation for many aspects of life. Attempts to produce plastic materials started already in the middle of the 19th century. However, the world’s first fully synthetic plastic was Bakelite, invented in New York in 1907. Many chemists have since contributed to the science of developing a variety of plastic materials. Over 9 billion tonnes of plastics are estimated to have been made over the last 70 years.

The success of plastics has caused widespread environmental problems due to their slow decomposition rate in natural ecosystems. At the macro level, plastic pollution can be found all over the world creating garbage patches in the world’s oceans and contaminating terrestrial ecosystems.

Of all the plastics discarded so far, OECD calculated that only 19% had been incinerated and 9% recycled. However, the real problem can be found at the micro (or even the smallest nano) level.

Microplastics can either come from a primary source like microfibers from clothing, microbeads in cosmetics, and plastic pellets. Or there are secondary microplastics arising from the degradation of larger plastic products through natural weathering processes after entering the environment. Microplastics can now be found wherever we look and will find their way into the food we eat.

Studies have found microplastics in foods including tea, salt, seaweed, milk, seafood, honey, sugar, beer, vegetables, fruit and soft drinks. It has been estimated that 5 g of plastic particles on average enter the human gastrointestinal tract per person per week. A recent Australian survey of microplastics in rice found that consumption of a single serve of rice may contribute 3-4 mg of microplastics, equivalent to an intake of around 1 g per person annually. Even tap water contains microplastics while bottled water contains even more.

So what’s the problem?

The actual plastic polymers are not the problem although residues of the monomers used in the manufacture of the complex polymers may be toxic. What is more of a problem is the variety of additives used to change the properties of the plastic, some of which can be quite toxic. These include plasticisers, flame retardants, heat stabilisers and fillers among many others.

According to current knowledge, microplastics at 0.001 to 5 millimetres in size are considered to pose a comparatively low risk to human health as they are considered to be too ‘bulky’ to be absorbed by human cells and are largely excreted again. However, experimental studies indicate that such particles passing through the gastrointestinal tract can lead to changes in the composition of the gut microbiome and in turn the development of metabolic diseases such as diabetes, obesity or chronic liver disease.

The situation is different with smaller particles, submicro- and nanoplastics. These particles are less than 0.001 millimetre in size. A laboratory study by the German Federal Institute for Risk Assessment found that the smaller the particles, the more they were absorbed. While microplastics only “seeped” into the cell to a small extent, particles in the submicrometre range could be measured in larger quantities in intestinal and liver cells.

Whether ingested micro- and nanoplastics pose a health risk is being investigated in numerous studies but is largely unknown to date. Using specific analyses there are indications that they could activate mechanisms involved in local inflammatory and immune responses and could crucially be involved in carcinogenesis.

What to do?

Not easy to say at this stage. We could of course try to reduce the use of plastics to diminish future contamination, but this is easier said than done with the ubiquitous use of plastics for all kinds of applications.  Some reduction can be achieved by washing fruit and vegetables before consumption. Washing rice before cooking reduced the microplastic content by around 25%.

American researchers pointed out that without a well-designed and tailor-made management strategy for end-of-life plastics, humans are conducting a singular uncontrolled experiment on a global scale, in which billions of metric tons of plastic material will accumulate across all major terrestrial and aquatic ecosystems on the planet.

We can do better!

Nothing wrong with cranberries

Sure there is nothing wrong with eating cranberries. Although the same thing could be said of consuming any fruits as they are all considered healthy so there is some competition. That might be the reason why the Cranberry Institute felt obliged to provide funding for two recent studies showing the beneficial effects of cranberry consumption on memory and blood flow.

But can you believe the conclusions of studies tainted by respective industry contributions? Read on so you can judge for yourself.

Cranberries might improve cardiovascular health

The Cranberry Institute provided financial support to a recent clinical trial which found that daily consumption of cranberries for one month improved cardiovascular function in healthy men.

The study included 45 healthy men who consumed 9g of freeze-dried cranberry powder equivalent to a cup of 100g of fresh cranberries per day or a placebo for one month. Incredibly, the study found that those consuming cranberries showed significant improvements in flow-mediated dilation of blood vessels already two hours after first consumption and after one month of daily consumption indicating both immediate and long-term benefits. The researchers claimed that consumption of cranberries as part of a healthy diet can help reduce the risk of cardiovascular disease by improving blood vessel function.

Sure there is evidence that links polyphenols from berries with heart health benefits. And as it happens, cranberries are rich in unique proanthocyanidins that have distinct properties compared to polyphenols found in some other fruits.

Cranberries might also improve memory

The Cranberry Institute wanted more good news by financially supporting a study investigating the impact of cranberry consumption on memory and brain function. Past studies have shown that higher dietary flavonoid intake is associated with slower rates of cognitive decline and dementia. And foods rich in anthocyanins and proanthocyanidins, which give berries their red, blue, or purple colour, have been found to improve cognition.

Thus, the commercially funded research team from the University of East Anglia (UK) investigated the impact of eating cranberries for 12 weeks on brain function and cholesterol among 60 cognitively healthy participants between 50 to 80 years old. Again, half of the participants consumed freeze-dried cranberry powder, equivalent to a cup of 100g of fresh cranberries, daily. The other half consumed a placebo.

The study, one of the first to examine cranberries and their long-term impact on cognition and brain health, showed that consuming cranberries significantly improved memory of everyday events (visual episodic memory), neural functioning and delivery of blood to the brain (brain perfusion).

The cranberry group also exhibited a significant decrease in LDL or ‘bad’ cholesterol levels, known to contribute to the thickening or hardening of the arteries caused by a build-up of plaque. The researchers claimed that the potentially improved vascular health may have in part contributed to the improvement in brain perfusion and cognition.

Of course the researchers considered the findings encouraging, especially as a relatively short 12-week cranberry intervention was able to produce significant improvements in memory and neural function. They see it as an important foundation for future research in the area of cranberries and neurological health.

Ocean Spray Inc. also at it

The U.S. cranberry juice giant, Ocean Spray Inc., has spent millions of dollars funding research to try to prove the health aspects of consuming cranberry juice. There has long been a myth that cranberry juice can prevent urinary tract infections (UTIs). Back in the day, before antibiotics were a thing, acidification of the urine was a recommended treatment for UTI. It was believed that because cranberries are acidic, they would make urine more acidic to fight off bacteria. This was attributed to formation of hippuric acid through metabolism of the quinic acid present in cranberry juice.

Unfortunately, later studies reported that the concentration of hippuric acid in the urine was insufficient for an antibacterial effect unless very large volumes of cranberry juice were ingested.

Subsequently, proanthocyanidins present in cranberries as well as blueberries were reported to inhibit binding of the type 1 P-fimbriae of Escherichia coli to uroepithelial cells, preventing bacterial adherence within the urinary tract.

However, researchers from the University of Manitoba found that the two proposed mechanisms for a beneficial effect of cranberries on UTIs had not yet been shown to have a role in human infection.

EFSA and FDA dismisses cranberry health claims

In 2009, Ocean Spray Inc. submitted a health claim for cranberry juice to the European Food Safety Authority (EFSA) supported by several scientific studies. However, the EFSA Panel concluded that the evidence provided was not sufficient to establish a cause and effect relationship between the consumption of Ocean Spray cranberry products and the reduction of the risk of UTIs in women by inhibiting the adhesion of certain bacteria in the urinary tract.

In 2017, Ocean Spray Cranberries Inc. tried again, this time logging a health claim for cranberry juice with the U.S. Food and Drug Administration (FDA). After reviewing the petition and other evidence related to the proposed health claim, the FDA determined that the scientific evidence supporting the claim did not meet the “significant scientific agreement” standard required for an authorized health claim. However, at the same time FDA announced that it does not intend to object to the use of certain ‘qualified health claims’ regarding consuming certain cranberry products and a reduced risk of recurrent urinary tract infection (UTI) in healthy women. As long as a qualifying statement was included on the label stating that FDA has concluded that the scientific evidence supporting this claim is limited and inconsistent.

Not looking convincing?

It’s up to you to decide what you think. As I said in the beginning there is nothing wrong in eating cranberries as they would be as healthy as any other berries.

To help you make up your mind here is a quote from the well known nutrition expert Marion Nestle:

“Without even getting into whether cranberry powder is equivalent to cranberries, whether anyone can eat cranberries without adding their weight in sugar, or whether any other fruit might have similar effects, we should ask whether it makes any sense at all to think that any one single food could boost memory and prevent dementia in the elderly.”

So there you have it.

The Coffee Consumption Genes

Are you desperate for a cup of coffee just now? The urge might be determined by your genes. I almost didn’t believe it when the newspaper reported that scientists had explored the genes of pregnant women to predict the amount of coffee they consume and its potential impact on their pregnancy.

I have been heavily involved in developing elaborate protocols to explore population food consumption in detail. And now all you have to do is look at the genes. So I did some research and it seems to be true that coffee drinking behaviour is at least partly due to genetics, with a specific set of genetic variants affecting how much coffee we drink.

What the researchers found

In the reported findings, researchers at the University of Queensland used a method called Mendelian randomisation which used eight genetic variants that predicted pregnant women’s coffee drinking behaviour and examined whether these variants were also associated with birth outcomes. Current World Health Organization guidelines say pregnant women should drink less than 300mg of caffeine, or two to three cups of coffee per day. However, the researchers through their genetic analyses found that coffee consumption during pregnancy might not itself contribute to adverse outcomes such as stillbirth, sporadic miscarriages and pre-term birth or lower gestational age or birthweight of the offspring.

As a caveat just to be on the safe side, the researchers emphasised that the study only looked at certain adverse pregnancy outcomes, and it might be possible that coffee consumption could affect other important aspects of foetal development. 

This has been known for some time

The important outcome is that genetics can be used to estimate the amount of coffee consumed. This has actually been known for some time. Heritability refers to degree of genetic influence and can vary from 0 (not heritable) to 1 (completely inherited).

A review published in 2010, reported that twin studies had estimated heritability of coffee consumption by comparing monozygotic twins, who share the common familial environment and the same genes, to dizygotic twins, who also share common familial environment but only half of the genetic material. These studies found that heritability of coffee consumption varied from 0.30 to 0.60 in different populations. Heavy consumption, defined as more than 6 cups of coffee daily, had a heritability of 0.77. A few conclusions can be drawn. First, heavy consumers seem to differ from moderate and light coffee users on several accounts. Secondly, heavier coffee users appear to be more influenced by genetics than lighter caffeine users. 

So far the studies confirmed the possibilities of coffee consumption inheritance without identifying the individual genes responsible for such differential inheritance pattern. 

And the complicated stuff

So genetics have long been suspected of contributing to individual differences in coffee consumption. However, pinpointing the specific genetic variants has been challenging. Thus, researchers as part of the Coffee and Caffeine Genetics Consortium conducted a genome-wide meta-analysis of more than 120,000 regular coffee drinkers of European and African American ancestry. They identified two variants that mapped to genes involved in caffeine metabolism, POR and ABCG2 (two others, AHR and CYP1A2 had been identified previously). Two variants were identified near genes BDNF and SLC6A4 that potentially influence the rewarding effects of caffeine. Two others – near the GCKR and MLXIPL genes involved in glucose and lipid metabolism – had not previously been linked to the metabolism or neurological effects of coffee.

The findings suggest that genes drive people to naturally modulate their coffee intake to experience the optimal effects exerted by the caffeine in coffee and that the strongest genetic factors linked to increased coffee intake likely work by directly increasing caffeine metabolism.

But there is more

People who like to drink their coffee black also prefer dark chocolate, a new Northwestern Medicine study found. The reason is also in their genes.

The scientists found that coffee drinkers who have a genetic variant that reflects a faster metabolism of caffeine prefer bitter, black coffee. And the same genetic variant is found in people who prefer the more bitter dark chocolate over the more mellow milk chocolate.

The reason is not because they love the taste, but rather because they associate the bitter flavour with the boost in mental alertness they expect from coffee.

It is interesting because these gene variants are related to faster metabolism of caffeine and not related to taste. These individuals metabolise caffeine faster, so the stimulating effects wear off faster as well. So, they need to drink more. They learn to associate bitterness with caffeine and the boost they feel. When they think of coffee, they think of a bitter taste, so they enjoy dark coffee and, likewise, dark chocolate.

A new era

In the past, when scientists studied the health benefits of coffee and dark chocolate, they had to rely on epidemiological studies, which only confer an association with health benefits rather than a stronger causal link. The new research shows these genetic variants can be used more precisely to study the relationship between coffee and health benefits.

And who knows, in the future there might be other genetic markers found that drive our food consumption behaviour.