Big Food’s resistance to health stars crumbling

Food industry resistance to the front-of-packet nutrition star rating system is crumbling, with cereal giant Kellogg’s the latest to adopt the labelling scheme for its products.

Almost two years after the Health Star Rating system was approved by the nation’s food and health ministers, Kellogg’s has announced that, from June, the labelling scheme would be introduced across all 37 of its cereal products.

Under the system, which the AMA was involved in developing, food is awarded between a half and five stars depending on its nutritional value. The label also includes a panel detailing sugar, saturated fat, sodium and energy content.

While some Kellogg’s products, including All Bran and Guardian, have been awarded five stars under the scheme, and the majority have four or more stars, several varieties aimed at children, including Coco Pops, Fruit Loops, Crunchy Nut and Nutri-Grain have just two stars and one, Crispix, has earned just 1.5 stars.

Assistant Health Minister Fiona Nash said that Kellogg’s adoption of the voluntary scheme meant that soon the vast majority of breakfast cereals would carry a Health Star Rating, making it easier for “time-poor parents [to] make quick, informed choices…without taking precious time reading labels”.

Monster Health Foods Company was an early adopter of the scheme, and other manufacturers has since joined them, including Sanitarium, Nestle/Uncle Toby’s, Food for Health, Goodness Superfoods, Freedom Foods, Greens General Foods, Coles home brand and Woolworths’ ‘Macro’ brand.

The increasing adoption of the scheme by industry has despite fierce resistance from some manufacturers.

Major food companies including McCain, Mars, PepsiCo, Mondelez, George Weston and Goodman Fielder are yet to implement the scheme.

A Mondelez spokeswoman told Fairfax Media the company, which owns of Kraft, Belvita and Philadelphia, was resisting the scheme because it was flawed.

“Our view is that the concept and formula underpinning the voluntary system fails to account for individuals’ dietary requirements and takes an unrealistic view of portion sizes,” she said.

The resistance has come despite industry’s close involvement in developing the scheme over a two-year period prior to its adoption by the nation’s food and health ministers.

Industry representatives publicly expressed dissatisfaction soon after the system’s formal adoption, and a Federal Health Department website promoting the Health Star Rating system was controversially taken down in early 2014 at the direction of Senator Nash’s office.

The Minister’s then-Chief of Staff, Alistair Furnival, who had directed the take-down, was subsequently forced to resign after it was revealed he co-owned a consultancy that had major food manufacturers among its clients.

The website was reinstated last December, a move welcomed at the time by AMA Vice President Dr Stephen Parnis, who said giving consumers quick and easy nutritional information was an important tool in helping improve food choices and reducing obesity.

Estimates suggest that almost two-thirds of adults, and a quarter of children, are overweight or obese, meaning a huge proportion of the population will be at risk of diabetes, heart disease, stroke and other complex, chronic and expensive health problems unless more is done to trim the nation’s waistline.

Dr Parnis said he hoped that the Health Star Rating scheme would encourage manufacturers to reformulate their products and make them more nutritious in order to earn more stars.

Manufacturers have four years to voluntarily adopt the system, and Dr Parnis said the AMA would support a move by the Government to subsequently make it mandatory.

The Health Star Rating System website can be viewed at:

http://www.healthstarrating.gov.au/internet/healthstarrating/publishing.nsf/content/home

Adrian Rollins

The global challenge of women’s health

Sierra Leone, a West African state of 6 million, saw 11 000 cases and over 3000 deaths during last year’s Ebola outbreak. A bitter civil war from 1991 to 2002, fuelled largely by fierce factions from neighbouring countries, led to 50 000 deaths and degradation of the country’s infrastructure and social fabric. Sierra Leone’s exports of diamonds and bauxite notwithstanding, the lack of a socially responsive polity and a largely agrarian population set the scene for the epidemic. Over 70% of its population live in extreme poverty.1

Sierra Leone also tops the 2013 chart when it comes to maternal deaths — 1100 per 100 000 live births.2 The comparable figure for Australia is six. UNICEF estimates that 88% of the women have been subject to genital mutilation.3

Improving maternal health

The Millennium Development Goals, promulgated by the United Nations in September 2000 and endorsed by 189 countries, sought to halve desperate poverty, defined as living on less than a dollar a day, by 2015. The metrics suggest that this goal has been achieved, and it is a remarkable tribute to international efforts. Among the eight goals, five concern health, and most have been achieved, including huge reductions in infant mortality.

Improving maternal health is one of the health-related goals that has proved harder to reach. Under Goal 5, countries committed to reducing maternal mortality by three-quarters between 1990 and 2015. Since 1990, maternal deaths worldwide have dropped by 45%.4

Maternal mortality — often due to blood loss and infection — has proved more resistant to efforts to substantially reduce it as a global health problem. It has been intractable in areas of poverty and social turmoil. There were 289 000 maternal deaths worldwide reported in 2013.4

The explanation for these disturbing figures has much to do with social attitudes and investment. When we encounter health disparities, the explanation is most often found outside the clinic, in society and politics. In preventing maternal death, strong investment in education for women is fundamental. Provision of the basic infrastructure necessary for safe childbirth comes next. But even more basic is a pathological view of women — that they are not a priority and that public resources should be invested elsewhere.

Broadening the focus

The World Health Organization draws our attention in 2015 to food security. Its importance is great for women’s health, before and during reproduction and throughout all adulthood, to reduce the risk of nutritional deficiencies, diabetes and heart disease.

When, in 2003–2004, my colleagues at Columbia University and I were examining cardiovascular disease in emerging economies, I was amazed to discover that it far outweighed obstetric and perinatal disorders, HIV and malaria as causes of death of women in the years of family formation and support. In seven out of nine developing countries that we studied, chronic diseases caused over 20% of deaths among women aged 15–34 years, while reproductive causes and HIV together accounted for about 10% of deaths.5 We questioned why the traditional conceptualisation of women’s health has more to do with disorders that impair their performance as reproductive machines than with the real threats to their wellbeing, including the precursors of cardiovascular catastrophe. Those who work on global programs to abate the scourge of diabetes make a major contribution to reducing deaths among women from cardiovascular disease.

Shaking stereotypic thinking

Even if our view of women’s health is restricted to an understanding of causes of death, it is clear we have a task to shake the stereotypic thinking and social relegation of women that foster a completely inadequate global response to their health needs.

There are tasks aplenty for those with advocacy in their blood at governmental, educational and individual levels. Heroic clinicians such as 91-year-old Dr Catherine Hamlin AC and her co-workers at the Addis Ababa Fistula Hospital, its five regional hospitals and the Hamlin College of Midwives set outstanding examples of other pathways.

Commercial in confidence: public health without confidence

Implementing public health measures with obvious benefits becomes a complex struggle when commercial interests are paramount

The evening of 25 March 2009 was cool for the community consultation — a necessary step before the implementation of fluoridation of the Cobram water supply. There were only a few people present in the Civic Centre, but they warmly applauded the initiative. None of the expected antifluoride lobby turned up, and the meeting was a short one …

After all, it is accepted that fluoridation of drinking water is an effective way to ensure the whole community can benefit from fluoride’s preventive role in reducing tooth decay.1,2

Thus, it was expected that Cobram would follow the path of nearby Yarrawonga and this seemingly routine adoption of a well researched public health measure would be quickly achieved.

Wrong! Over 5 years later, Cobram still has not had its water supply fluoridated.

The story so far

Cobram, a small country town on the Murray River in Northern Victoria, is where the Murray Goulburn Co-operative, one of the largest milk producers in Victoria, has existed since 1949. In 1951, the Co-operative diversified into cheesemaking. It is a major contributor to the local economy. In early 2014, the company announced that it would build a $74 million “world class cheese cut-and-wrap facility” in Cobram to serve Australian and Asian markets and, as part of a broader $38 million investment, it would increase the Cobram factory’s capacity to produce infant nutrition products — some for export.3

The reason for the inaction over water fluoridation? Murray Goulburn did not want fluoridated water in their milk products, including the infant formula preparations. This was not disclosed in any of the formal community discussions, and only came to light when the Department of Health enquired about the cause for the delay in fluoridation. It seemed that commercial considerations regarding fluoridation simply outweighed community dental health.

Although, perhaps it was not that simple. There were other options — one being whether the government was prepared to fund a separate water pipeline for the Co-operative’s use. The company argued that the options of either precipitating the fluoride out during the manufacturing processes or treating the factory water supply to remove fluoride were less cost-effective.

The possibility that fluoridation might not affect the product was not considered. One can only suspect that commercial motives were paramount. Asian countries are a large importer of dairy products, and these countries are, by and large, averse to fluoridated water. China has no fluoridation4 and Japan, almost none.

There is concern about dental fluorosis, but there is little evidence to suggest that fluoridated water, particularly in infant formulas, causes significant fluorosis.5 A significant number of the infant formulas sold in Australia are imported,6 but these have sufficiently low levels of fluoride for the Australian Research Centre for Population Oral Health and state health departments to deem them safe for reconstitution using water within the target range for fluoridation (0.6–1.1 mg/L). So, what is the fuss about?

Companies do not engage in public health debate about fluoridation. In fact, one international company that sells products on the Australian market refuses to indicate where its factories are; it does, however, admit that its products use unfluoridated water. The degree of secrecy about these matters can lead to comments layered with conjecture.

In November last year, just before the Victorian state election, the member for Murray Valley finally announced a $4.1 million project including, inter alia, a 2.5 km pipeline carrying unfluoridated water from the Cobram water treatment plant to the Murray Goulburn dairy processing plant.7 The Co-operative agreed to make a contribution to the funding, and the project was expected to be completed in 2016.

The cost of living in a small community

This was a win-win situation for Cobram and the Co-operative, with most of the funding coming from the government.

But is it such a win? Cobram, and in particular its children, will have missed out for 7 years on fluoridated water. For the community at large, the Cobram imbroglio barely raised a policy ripple. Small communities of less than 1000 may miss out on fluoridation altogether because it is not regarded as cost-effective. However, these dismissed populations add up to 2 million people nationwide.8

The question, then, becomes one of assessing the effectiveness of advocacy when any proposed change is confronted by the fear, real or otherwise, of losing jobs. However, when advocacy becomes ineffective, change has to be achieved by subtler nagging of government, because there is virtually no sensible person who would disagree about the benefits of fluoride.9

Have we lost the plot?

It is all about cost; especially, as with all public health and commercial considerations, there is a further twist — in this case, the increase in the consumption of bottled water, almost all of which is suboptimally fluoridated. Bottled water is permitted to have the same level of fluoride recommended for drinking water — 0.6–1.1 mg of fluoride per litre. Since its introduction in the 1980s, bottled water has grown into a $500 million a year industry in Australia and has become the main source of drinking water in one in 10 households. However, as the chair of the Australian Dental Association’s Oral Health Committee said, “people who prefer bottled water … risk putting their dental health back to the 1960s, when tooth decay was widespread because there was no fluoride in the water”.10

The rise in bottled water production without any serious move by the multinational manufacturers towards fluoridation is presumably one of those awkward commercial-in-confidence matters. Without concerted nagging of the policymakers, such as occurred in Cobram, nothing happens.

In fact, fluoridation in Australia has gone backwards. In Queensland, where once it was obligatory, legislation has made it a voluntary responsibility. Many local governments have subjugated public health to the commercial imperative of it being “too costly”, despite evidence to the contrary.11

Fluoridation policy is in danger of degenerating into public health anarchy where commercial interests can shelter behind the mantra of freedom of choice with its rehearsed arguments of blind libertarianism, no matter how obvious the public good. Presumably none of these libertarians would want to advocate freedom of choice about a clean water supply.

Ignoring the bleeding obvious should not be allowed to make the community bleed the cost of appalling teeth, especially when there are continual complaints about how disadvantaged rural areas are with regard to dental health.

At least, the Cobram community will eventually know better times in dental health; but now, what about the fluoridation of bottled water?

The world we live in

Among the great mysteries of human existence, our uncertain relationship with our environment has been a constant source of puzzlement. In the days of the flat earth, when gods and planets needed constant placation and sacrifice lest the food supply fail and fertility fall, surging infections were thought to be a further manifestation of divine displeasure — something that the deities inflicted upon the people (demos) from above (epi) to chasten and punish. Yet the Old Testament book of Leviticus shows that, thousands of years ago, the need to quarantine people with rashes or swellings “like the plague of leprosy” was recognised (Leviticus 13: 2–5), implying that humans understood from early on that they had a measure of control over infective afflictions.

The path from primitive ignorance and fear to the understanding of the microbiological cause of infection is, as the cliche runs, history. Nevertheless, we continue to fear uncontrolled epidemics, despite our heavy investment in technology to hold them at bay.

Battling the threats

At the beginning of 2003, during the early phases of the severe acute respiratory syndrome (SARS) epidemic, I saw lights burning in the windows of Ian Lipkin’s microbiology laboratory at Columbia University, close to where I was working at the time, for 24 hours every day during the race to sequence the genome of the virus responsible. By May, the 29 751-base genome of the Tor2 isolate had been sequenced in British Columbia and published in Science.1 Fortunately, although SARS was a serious illness, as classical epidemiological data were assembled we recognised that it had low infectivity. We had come to know the enemy — quickly and in fastidious detail — yet we still needed traditional methods to prevent its spread.

Infection retains its character of surprise. Who would have guessed the story of Helicobacter pylori and peptic ulcers? As an intern in 1966–1967, peptic ulcer meant antacids, stress and socioeconomic status, vagotomies, pyloroplasties and heroic surgery for life-threatening haematemesis. What other disorders — cancer, coronary disease — may have an infective element in their aetiology? And, like the global financial crisis of 2008, the Ebola epidemic of 2013 caught us off guard. It also reminded us of how critical the social environment and poverty, in particular, are to the formation of modern infective epidemics.

Complex relationships

In recent years, dramatic developments in our exploration of the universe of infection have led us to the human microbiome — the “organ” that has 10 times as many cells as does the whole of the rest of the human body — that inhabits our gut, skin and other surface tissues, and about which new knowledge is coming to us daily. A 2012 Spanish study described a changing microbiome profile in human breast milk over the months after birth that involved over 700 species of microorganisms.2

I had a glimpse of the importance of the human microbiome in 1968 when working at Baiyer River in the western highlands of Papua New Guinea. We were visited by Eben Hipsley, a nutrition scientist from Canberra, who had an interest in understanding how the local Enga people, naturally muscular and fit, kept their metabolism going without eating much more than sweet potato.3 What about essential amino acids? In private conversation, Eben conjectured that their gut flora generated the molecules missing from this people’s natural diet. Today’s experts in this field presumably have a much better idea of Papua New Guinean nutrition, but Hipsley respected what he knew, even then, of the human microbiome. Contemporary experts now agree that while human microbiota do not fix atmospheric nitrogen, they can upgrade dietary nitrogen-containing compounds into essential amino acids.4

Together, we triumph

In terms of infection control, the global response to HIV has been an astounding exercise that combined technology, preventive science, biological insight, social understanding, philanthropy and dogged global political action. This, together with the GAVI Alliance (made up of such heavyweights as the World Health Organization, UNICEF, the World Bank, the Bill & Melinda Gates Foundation and donor countries), the Global Fund to Fight AIDS, Tuberculosis and Malaria, and the elimination of smallpox, should surely give heart to those who doubt the value of medical research and action. Rather than lamenting what we can’t do, these achievements signal what amazing things we can do together when we try.

Domestically acquired hepatitis E successfully treated with ribavirin in an Australian liver transplant recipient

We describe a rare case of domestically acquired hepatitis E in Australia and the first in an Australian liver transplant recipient. The infection was successfully treated with ribavirin.

Clinical record

A 48-year-old Australian man of European ancestry received his third liver transplant in February 2013 for hepatic failure precipitated by ischaemic cholangiopathy and secondary biliary cirrhosis. His first liver transplant was performed 10 years earlier for complications of cirrhosis arising from autoimmune hepatitis – primary sclerosing cholangitis overlap syndrome, but required retransplantation after 3 months due to hepatic vein thrombosis and hepatic infarction. The second liver transplant was complicated by hepatic artery thrombosis, resulting in ischaemic cholangiopathy.

For his third transplant, from 13 days before to 13 days after transplantation, the patient received blood products from 22 individual donors. His initial immunosuppressive regimen comprised cyclosporin 150 mg twice daily, prednisolone 20 mg once daily and mycophenolate mofetil (MMF) 500 mg twice daily. Subsequently, moderate renal impairment (creatinine, 170 µmol/L; reference interval [RI], 60–110 µmol/L) and cytopaenias prompted gradual cyclosporin and MMF dose reductions. Blood products were not required, and results of liver function tests (LFTs) remained normal.

Ten weeks after transplantation, an elevation in LFT levels occurred (alanine aminotransferase [ALT], 131 U/L [RI, < 40 U/L]; aspartate aminotransferase [AST], 53 U/L [RI, < 45 U/L]; γ-glutamyltransferase [GGT], 76 U/L [RI, < 60 U/L]). Abdominal ultrasound was unremarkable, and the raised LFT results gradually settled without adjustment of the immunosuppressive regimen.

Twenty-two weeks after the patient’s transplantation, he developed significant transaminitis (ALT, 338 U/L; AST, 215 U/L; GGT, 183 U/L; alkaline phosphatase, 126 U/L [RI, 35–135 U/L]; total bilirubin, 13 µmol/L [RI, < 20 µmol/L]) (Box 1).

The patient adhered to his immunosuppressive regimen and had not commenced other medications. Physical examination was unremarkable and abdominal ultrasound did not show biliary or hepatic vascular abnormalities. A liver biopsy was performed and reported as consistent with moderately active acute rejection. This prompted methylprednisolone therapy (500 mg once daily for 3 days) followed by prednisolone (50 mg once daily) and replacement of cyclosporin with tacrolimus (3 mg twice daily). MMF was continued unchanged. A second liver biopsy was performed 1 week later due to a further rise in the ALT level (456 U/L), which demonstrated non-specific hepatitis without definite features of rejection or an autoimmune aetiology (Box 2). Subsequent comparison of these biopsies by a specialist histopathologist confirmed acute hepatitis in both samples, without significant features of rejection on either biopsy.

Investigation for infectious causes excluded hepatitis A, hepatitis B, hepatitis C, Epstein–Barr virus, cytomegalovirus, and human herpesvirus 6. Anti-hepatitis E IgG antibody (HEV ELISA, MP Biomedicals Asia Pacific) was not detected, but an in-house hepatitis E virus (HEV) reverse transcription polymerase chain reaction (RT-PCR) assay (Appendix) detected HEV RNA in the patient’s blood. HEV RNA was also detected at the Victorian Infectious Diseases Reference Laboratory (VIDRL), and nucleotide sequencing demonstrated genotype 3 HEV. Paraffin-embedded liver tissue from the biopsy collected 22 weeks after transplantation was HEV RNA positive, as were blood samples collected 22 and 23 weeks after transplantation. Retrospective testing of the patient’s and liver donor’s blood at the time of transplantation was negative for anti-HEV IgG antibody and HEV RNA. A biopsy of the donor liver, collected at the time of transplantation, was also HEV RNA negative.

Stored blood from all donors of the blood products were tested for anti-HEV IgG antibody by two assays (HEV IgG ELISA, Genelabs Diagnostics; HEV-IgG ELISA, Beijing Wantai), anti-HEV IgM antibody (HEV-IgM ELISA, Beijing Wantai) and by in-house (VIDRL) and commercial (RealStar HEV RT-PCR 1.0, Altona Diagnostics) HEV RT-PCR. All 22 donors’ samples were negative for anti-HEV IgM antibody and HEV RT-PCR. Three donors were found to have detectable anti-HEV IgG antibody levels. Two of these donors were found to have detectable IgG anti-HEV antibody levels in both assays; one was born in South Africa but had not left Australia in 6 years, and the second had travelled frequently to India in the past 5 years, most recently 8 months before donation. The third donor had never travelled outside of Australia, but had worked in a piggery. Repeat samples collected 9 months after donation from these donors and 18 of the 19 seronegative donors produced the same serological results.

The patient was born in Australia, had not recently travelled overseas, and worked in a city office. He had no contact with overseas travellers, and had not visited rural areas, farms or had any livestock exposure. He consumed pork regularly, which was sourced from local supermarkets.

Despite reducing the patient’s immunosuppression, the hepatitis continued to worsen over the next 5 weeks (ALT, 669 U/L) and HEV RNA remained detectable (Box 1). Ribavirin at a dose adjusted for his renal impairment (200 mg once daily) was commenced with an immediate improvement of his liver function. HEV RNA was last detected 17 days after commencement, and HEV RT-PCR was negative after 24 days. Pegylated interferon alfa was not used due to pre-existing cytopaenia and the risk of precipitating acute rejection. The patient received a 12-week course of ribavirin and remained HEV RNA negative 15 weeks after cessation. The patient had not developed anti-HEV IgG antibody 7 months after onset of hepatitis.

Discussion

HEV is a non-enveloped RNA virus identified in 1980 as the cause of “epidemic, non-A, non-B hepatitis”, a waterborne illness similar to hepatitis A.1 After an incubation period of 2–9 weeks2 the illness is usually self-limiting, but can progress to severe disease, particularly during advanced pregnancy, and among very young children and those with pre-existing chronic liver disease.3

There are four human HEV genotypes. Genotypes 1 and 2 cause large outbreaks in Asia, Africa and Central America via contaminated water. Genotypes 3 and 4 are predominantly swine viruses causing sporadic zoonotic disease in Europe, the United States and Eastern Asia.4

Acute hepatitis E is most reliably diagnosed either serologically by IgG anti-HEV antibody seroconversion,1,3 or by detection of HEV RNA in blood or faeces. HEV RNA is detectable in blood samples from up to 2 weeks before and 1 week after the onset of jaundice, and in stool it is detectable for up to 3 weeks after the onset of jaundice.

In developed countries, genotype 3 HEV is mostly transmitted by the consumption of undercooked pork or raw offal,3 and occasionally from animal contact or blood transfusion.1,4 The seroprevalence in Europe and the US is lower than for hepatitis A, but higher than for hepatitis B and hepatitis C.1,3 However, the incidence of acute hepatitis E in developed countries is unknown, with only five US cases of domestically acquired acute hepatitis E reported from 1997 to 2006.3

The source for HEV infection in our patient was unknown, but the donor liver, blood products, or contaminated food or water could have been responsible. Solid organ donors are not routinely screened for HEV infection in Australia, although this is recommended where HEV is endemic.4 Donor liver transmission of HEV, presenting 5 months after transplantation from an anti-HEV antibody negative but HEV RNA positive donor has occurred,5 but in our case both donor blood and liver tested negative for anti-HEV IgG antibody and HEV RNA. The blood donor who had travelled to India is a possible source as this donor’s anti-HEV IgG antibody sample-to-cut-off ratio was high in both IgG assays, which has been correlated with a recent illness compatible with hepatitis E and overseas travel.2 A contaminated food source cannot be excluded, as anti-HEV seropositive pigs have been found in Australian piggeries6 and, although processed, up to 80% of the ham, bacon and smallgoods sold in Australia is made from imported pig meat, mostly from the US, Canada and the European Union.7

Chronic hepatitis E can develop in solid organ transplant recipients, patients receiving cancer chemotherapy, and people with HIV. About two-thirds of solid organ transplant recipients infected with HEV develop chronic disease,8 which can be severe and cause significant inflammation and fibrosis.1 In our patient, the undetectable anti-HEV IgG antibody is likely a reflection of his immunosuppression.9

Management options for hepatitis E in solid organ transplant recipients include reducing immune suppression, pegylated interferon alfa or ribavirin therapy, or a combination of these. Reduction of immunosuppression alone can clear HEV in a minority of solid organ transplant recipients and pegylated interferon alfa has been used effectively to treat chronic hepatitis E after transplantation, but may precipitate donor organ rejection.4,8 Although not approved for this use in Australia, ribavirin for at least 3 months has been shown to produce sustained virological responses in at least two-thirds of patients with chronic hepatitis E,8 and is recommended as first-line treatment in solid organ transplant recipients who do not clear the virus despite reducing the immunosuppression.4

Domestically acquired hepatitis E has been reported rarely in Australia since the mid 1990s.1 0–12 To our knowledge, this is the first case of an Australian organ transplant recipient with hepatitis E successfully managed with antiviral therapy. Domestically acquired cases in Australia may be missed due to infrequent HEV serological testing in the absence of a travel history and the relative unavailability of HEV RNA testing. Hepatitis E should be considered in patients with unexplained hepatitis, and solid organ transplant recipients or those with compromised immune systems with hepatitis should be tested for HEV RNA because anti-HEV antibody tests may be negative in these patients.

1 Timeline of laboratory test results and treatment

HEV = hepatitis E virus. PCR = polymerase chain reaction. RI = reference interval, < 40 U/L.

2 Liver biopsy findings 5 months after transplant

A: Mild portal tract inflammation with interface and lobular hepatitis (haematoxylin and eosin stain [H & E], x20). B: Lobular disarray with spotty necrosis (H & E, x40). C: Portal tract expansion by early fibrosis with extension into the lobule (Masson trichrome, x10).

The effect of fasting diets on medication management

To the Editor: Fasting diets have been used by humans for millennia for religious and medical purposes and are now gaining popularity for wellbeing and weight loss purposes. With increasing use of short- and long-term courses of medication to manage a multitude of conditions, a question that needs to be asked is will fasting diets impact on medication regimens?

The 5 : 2 diet, where calorie intake is unrestricted 5 days a week and limited to 500 calories for women and 600 calories for men 2 days a week, is becoming increasingly popular due to widespread publicity. In humans, there is some evidence that intermittent fasting (mainly alternate day fasting rather than the 5 : 2 regimen) could lead to weight reduction, decreased insulin resistance and prevention of type 2 diabetes.1,2

It is possible that patients who are taking medication and intermittently fasting each week could encounter adverse effects or therapeutic failure. Medications of concern generally fall into two categories: those for which absorption may be significantly altered by administration on an empty stomach, and those for which increased gastrointestinal3 or other4 adverse effects may result when taken on an empty stomach (Box).

For example, the bioavailability of telaprevir when taken while fasting is 27% of that when taken with a standard meal.5 As telaprevir needs to be taken three times a day for 12 weeks for treatment of chronic hepatitis C, treatment failure may result with intermittent fasting.

On a similar note, while the absorption of warfarin is not adversely affected by fasting, it is possible that an altered diet (particularly a diet that is high in vitamin K-containing foods) in patients taking warfarin may lead to volatility in international normalised ratio.6

Caution is warranted for patients with diabetes who wish to embark on these fasting diets, despite the appeal in terms of weight loss and reduced insulin sensitivity.2 Glibenclamide, glimepiride and insulin carry a high risk of hypoglycaemia if continued as normal when fasting.7

We urge all health professionals to consider the possible impact of fasting diets on medications and investigate further where required. Information regarding potential clinical significance of the diet may be evaluated via the full product information for individual medications and through community and hospital pharmacies.

Medications that warrant further investigation in patients undertaking fasting regimens*

Medications for which adverse effects may be increased if taken while fasting

Medications for which there may be clinically significant alterations in absorption if taken while fasting

Corticosteroids, mycophenolate, tacrolimus

Itraconazole capsules, posaconazole

Doxycycline, metronidazole, sodium fusidate, tinidazole, sulfamethoxazole–trimethoprim

Atazanavir, darunavir, tenofovir, etravirine, ritonavir, saquinavir, valganciclovir, telaprevir, boceprevir

Clomipramine, fluvoxamine, paroxetine, venlafaxine

Acitretin, isotretinoin, tretinoin

Amantadine, bromocriptine, levodopa

Albendazole (for systemic infections only), griseofulvin, ivermectin, mebendazole, praziquantel

Baclofen, betahistine, cyproheptadine, dapsone, lithium, sodium valproate, tiagabine

Mefloquine, artemether–lumefantrine, atovaquone

Imatinib

Ivabradine, labetalol

Cinacalcet, spironolactone

* This list is not exhaustive.

[Perspectives] Christina Roberto: taking a broad view on combating obesity

PEACH Lab—the Psychology of Eating and Consumer Health—is the intriguingly named research centre which is home to the work of Christina Roberto, a key figure behind a new Lancet Series on obesity. “There has been limited and patchy progress on tackling obesity globally”, says Roberto, who is Assistant Professor of Social and Behavioural Sciences and Nutrition at the Harvard T H Chan School of Public Health.

[Series] Smart food policies for obesity prevention

Prevention of obesity requires policies that work. In this Series paper, we propose a new way to understand how food policies could be made to work more effectively for obesity prevention. Our approach draws on evidence from a range of disciplines (psychology, economics, and public health nutrition) to develop a theory of change to understand how food policies work. We focus on one of the key determinants of obesity: diet. The evidence we review suggests that the interaction between human food preferences and the environment in which those preferences are learned, expressed, and reassessed has a central role.

[Series] Child and adolescent obesity: part of a bigger picture

The prevalence of childhood overweight and obesity has risen substantially worldwide in less than one generation. In the USA, the average weight of a child has risen by more than 5 kg within three decades, to a point where a third of the country’s children are overweight or obese. Some low-income and middle-income countries have reported similar or more rapid rises in child obesity, despite continuing high levels of undernutrition. Nutrition policies to tackle child obesity need to promote healthy growth and household nutrition security and protect children from inducements to be inactive or to overconsume foods of poor nutritional quality.

What proof is in your Christmas pudding? Is caring under the influence possible?

The humble Christmas pudding began as a traditional porridge full of raisins and dried fruit that people shared during the Christmas festivities. It was only in the 16th century that butter, eggs and flour became part of the recipe, resulting in a boiled pudding.1 Since then, there have been many variations that have incorporated all forms of fortified spirits, such as brandy, sherry and whisky. Secret recipes are age-old traditions passed down from generation to generation.

The traditional method allows the flavour to mature over a period of months, during which time the alcohol content of the moist pudding mixture preserves the ingredients. At the completion of flavour maturation, the pudding is boiled in a sealed container.

Controversy exists over the alcohol content of the Christmas puddings enjoyed on the 25th of December. Previous reports have listed the potential for the alcohol content of Christmas puddings to raise the blood alcohol content (BAC) to more than the legal driving limit.2,3 Due to the uncertain validity of these references, we conducted a systematic review of the literature on PubMed and Embase using the terms “Christmas pudding” or “Christmas cake” and “alcohol” or “blood alcohol concentration”. This search produced five studies that were reviewed by two independent researchers. None of these publications investigated the alcohol content and likely effects on BAC of ingestion of a typical slice of Christmas pudding.

We aimed to determine the ethanol concentration of a selection of Christmas puddings in Australia, and to extrapolate the BAC of a typical health care professional at our institution after lunch on Christmas Day. We hypothesised that any change in BAC would be negligible and unlikely to affect work performance and safety.

Methods

Fractional distillation

To simulate real-world experience, we used commonly available Christmas puddings for this study (Box 1).

A 100 g sample of each pudding was weighed and blended with 100 mL of sterile water to create a slurry for heating. Fractional distillation was conducted by heating the slurry in an electronically controlled water bath to the boiling point of ethanol (78.37°C) and held at that temperature for 10 minutes. Volume of the distillate was measured, and it was transferred to a watch glass. The weight of ethanol in each distillate was determined by the mass difference after combustion of the retrieved distillate.

Ethics approval was not required for this study. No commercial agreement was undertaken. The clinicians involved provided all funding required for the purchase of the puddings. All chemistry laboratory time and equipment were supplied by the School of Science and Health at the University of Western Sydney.

Estimated blood alcohol concentration

To calculate the estimated peak BAC immediately after the enjoyment of Christmas pudding and at the completion of a 30-minute lunch break, we adapted the Widmark formula4 as:

where AC is the alcohol content (g) of a standard 125 g slice of Christmas pudding, BW is the body water constant (0.58 for men and 0.49 for women), Wt is body weight (kg), MR is the metabolism constant (0.017) and IP is ingestion period (min).

We assumed that hospital staff at the Christmas lunch would share a 1 kg Christmas pudding cut into eight slices of 125 g each; and that typical male and female health care professionals weigh 70 kg and 60 kg, respectively.

Since ingested ethanol has a rapid and 100% absorption from the gastrointestinal tract,5,6 we calculated the consumption peak BAC from complete instantaneous absorption and assumed no other ethanol-containing food or drink were consumed over the lunch break.

Impairment

In accordance with work safety legislation and our institution’s local policy,7–9 we deemed the maximum BAC unlikely to impair health workers’ performance and safety to be 0.05 g/dL.

Results

Each of the Christmas puddings had ethanol in the mixture, with a wide range in concentrations (Box 1).

The estimated BAC calculated using the adjusted Widmark formula for each pudding is shown in Box 2. After applying our assumptions, we found that the peak BAC did not exceed 0.05 g/dL at any stage. While the female BAC levels were higher, due to variations in body water composition and weight, neither the male nor female staff had a predicted BAC > 0.000 g/dL by the end of the lunch break.

Discussion

Christmas pudding is traditionally soaked in ethanol for flavour maturation and to retard the rate and chance of spoilage. Despite previous research in this field,10 it is a common misconception that all the alcohol evaporates during the cooking process. We have shown in this study that this is not the case. While we found that some alcohol evaporated during the cooking process, we believe this correlated with the difference between the quantity specified on the packaging ingredients table and the quantity of alcohol distilled from the sample. Our fractional distillation did not recover greater levels of alcohol from the products where the alcohol concentration was specified. Interestingly, the two products sold by charities (Father Mac’s Heavenly Pudding and Lion’s Traditional Pudding) did not stipulate the amount of alcohol content, only that it was contained therein.

We used standard physiological and pharmacological assumptions and adapted the Widmark formula4 to show that after the consumption of a 125 g slice of pudding during a 30-minute Christmas Day lunch, a health care professional will not elevate his or her BAC by more than a very small amount. We have supported our hypothesis that consumption of Christmas pudding is unlikely to affect work performance or safety or impair a health worker’s ability to make complex decisions.

Our study had some limitations, including the breadth of Christmas pudding market coverage. Due to limited funding, we were not able to assess every pudding on the market, only those that were most readily accessible. In addition, we did not include homemade pudding, which theoretically would contain ingredients of a higher quality and potentially higher alcohol content. As such, the results of our study may not be representative of the BAC levels obtained after ingestion of homemade pudding.

Although the fractional distillation used in this research was robust, future work may focus on more sophisticated chemical analysis of the pudding slurry. To complete the calculations of BAC for this study, we made substantial assumptions regarding the typical size of Christmas pudding slices and the average weights of male and female health care professionals at our institution. These are avenues of research that could be clarified in future assessment.

It is reassuring to note that to obtain a BAC > 0.05 g/dL under the physiological parameters defined in our study, the average health care professional would need to eat in excess of 1 kg of the most potent Christmas pudding in a single sitting — a feat infrequently seen in our institution.

In conclusion, we found that the rise in BAC after ingestion of a typical slice of Christmas pudding is negligible and completely metabolised by the end of a 30-minute lunch break. Hospital staff should feel confident that the enthusiastic consumption of Christmas pudding at work in the festive season is unlikely to affect their work performance or safety, impair their ability to make complex decisions or compromise the standard of patient care.

1 Alcohol content listed on package and results of fractional distillation for Christmas puddings tested

Pudding brand	Package-listed alcohol content	Pudding sample weight in solution (g)	Volume of distillate (mL)	Combustion mass difference alcohol (g)

Newcastle’s Pudding Lady	4.0 mL/100 g	101.06	2.76	0.80
Coles Matured Christmas Pudding	3.5 mL/100 g	100.61	2.75	0.83
David Jones Christmas Fruit Pudding	3.0 mL/100 g	100.07	1.10	0.37
Woolworths Select Festive Sparkle Christmas Pudding	1.9 mL/100 g	100.16	3.80	1.35
Father Mac’s Heavenly Pudding	Not listed	100.93	1.40	0.21
Lion’s Traditional Pudding	Not listed	100.90	1.10	0.30

2 Typical health care professionals’ blood alcohol content (BAC) after ingestion of Christmas pudding

		Calculated BAC (g/dL)
		After ingestion		End of lunch break		Time to zero BAC (min)
Pudding brand	Ethanol per 125 g slice (g)	Male	Female	Male	Female	Male	Female

Newcastle’s Pudding Lady	0.990	0.002	0.003	0.000	0.000	8	11
Coles Matured Christmas Pudding	1.031	0.002	0.003	0.000	0.000	9	12
David Jones Christmas Fruit Pudding	0.462	0.001	0.002	0.000	0.000	4	5
Woolworths Select Festive Sparkle Christmas Pudding	1.685	0.004	0.006	0.000	0.000	14	20
Father Mac’s Heavenly Pudding	0.260	0.001	0.001	0.000	0.000	2	3
Lion’s Traditional Pudding	0.372	0.001	0.001	0.000	0.000	3	4