Angelina Jolie, cancer, your genes and your fate

Angelina Jolie

It must have taken courage for Angelina Jolie to tell the world, via an article in the New York Times, that she had undergone a preventive double mastectomy.  A-list actresses are usually judged on their body image as much as on their acting ability.

Angelina made this choice because her doctors had warned her that she has an 87% risk of developing breast cancer and a 50% risk of getting ovarian cancer because her mother died of breast cancer and she carries the BRCA1 gene.

I respect Angelina for making a choice which felt right for her and her family.

That is all any of us can do when faced with difficult decisions and the tsunami of judgement that has greeted her article is regrettable.

The story does, however, raise fascinating questions about whether we are really at the mercy of our genes.

Do our genes dictate our fate or do we have any power over them?

I want to tell you what I think and why.

In 1868, Friedrich Miescher discovered the presence of DNA, and in 1953, James Watson and Francis Crick discovered its molecular structure, with the help of Maurice Wilkins, Rosalind Franklin, Erwin Chargaff and Linus Pauling.

In the years that followed, scientists have learned a great deal about how this genetic code dictates who we are.

Our DNA – specifically the 25,000 genes identified by the Human Genome Project – is now widely regarded as the instruction book for the human body.

Genetic science has attracted billions of dollars of research funding and was heralded as the key to understanding and curing diseases like cancer.

The trouble is that despite all the money that has been poured into it, our knowledge of genetics has not yielded the promised revolutionary cures for cancer on a widespread scale.

Whilst the latest official report on the “War on Cancer” from America indicates that death rates for all cancers combined decreased by 1.5 percent per year from 2000 to 2009 [1], this is no greater than the previous five year period.

Deaths are still rising for certain cancer types including liver, pancreatic, uterus and, among men, melanoma.  Rates of human papillomavirus (HPV)–related cancers, such as oral, anal, vaginal, vulval, penis and cervical, also remain stubbornly high despite the availability of a vaccine.  And many epithelial cancers (carcinomas) and effectively all mesenchymal cancers (sarcomas) remain incurable.

There were decreases in new breast cancer cases about a decade ago, as many women stopped using hormone therapy after menopause.  Since then, overall breast cancer incidence has reached a plateau, and rates have increased among black women.

The decrease in cancer mortality is driven largely by the decrease in cancer incidence, which is mostly because of the decrease in smoking [1]. Smoking can cause more than a dozen cancers, including lung, head, neck, bladder and mouth.

Although improvements in screening and treatment for breast and some other cancers have cut death rates, most of the expensive new drugs prolong survival for no more than three or four months on average.

James Watson, famous for his part in the discovery of the structure of DNA, wrote in a recent edition of the Royal Society Journal “Open Biology”[2]:

Even though an increasing variety of intelligently designed, gene-targeted drugs now are in clinical use, they generally only temporarily hold back the fatal ravages of major cancers such as those of the lung, colon and breast that have become metastatic and gone beyond the reach of the skilled surgeon or radiotherapist.  Even though we will soon have comprehensive views of how most cancers arise and function at the genetic and biochemical level, their ‘curing’ seems now to many seasoned scientists an even more daunting objective than when the ‘War on Cancer’ was started by President Nixon in December 1971.

When we look at the decades of investments, the cost of treatments, the number of researchers and journals, and at the number of people who continue to die, we have to ask if we are barking up the wrong tree.

I believe we are.

The reality is that as fast as scientists find a ‘magic bullet’ to block a particular protein or cellular pathway to decimate cancer cells, the cancer cells find a way to circumvent the therapy, thrive and proliferate.

How do they do this?

Well it turns out that DNA, the genome, is only half the story.

This should not be a surprise given that chromosomes contain only 50 per cent DNA; the other 50 per cent is protein.

Within each chromosome, DNA is wrapped around proteins called histones.  Both DNA and histones are covered in millions of tiny chemical tags.

This second layer of structure comprising histones and chemical tags is called the epigenome – meaning literally “above the genome”.

The epigenome shapes the physical structure of the genome, the DNA.  It tightly wraps inactive genes making them unreadable.  It relaxes around active genes making them easily accessible.

Epigenome

Different sets of genes are active in different cell types.

A human liver cell, for example, contains the same DNA as a brain cell, yet somehow it knows to code only those proteins needed for the functioning of the liver.  Those instructions are found not in the letters of the DNA itself but on the array of chemical tags which are part of the epigenome.

The DNA code remains fixed for life but the epigenome is flexible.

Epigenetic tags react to signals within the cell environment and to signals from the outside environment, such as diet, stress and our thoughts.

The epigenome adjusts the expression of specific genes in response to our rapidly changing environment.

How does this work?

In the 1980s, researchers discovered that the answer to this question lay in specific chemical modifications to genomic DNA and its associated histone proteins, without changing the DNA itself at all.

What are these modifications?

In school biology lessons we learn that DNA is built from four different units called nucleotides: adenine, cytosine, guanine, and thymine.

In one type of epigenetic modification, a methyl group (one carbon atom linked to three hydrogen atoms -CH3) is added to specific cytosine bases of the DNA with help from enzymes.

DNA methylation. Credit: Adrian Bird

This process, called DNA methylation, is known to play a key role in both development and disease.

Methylation of DNA affects the way the molecule is shaped and, consequently, regulates which genes are available to be ‘read’ or transcribed.

Recently, another type of epigenetic modification of DNA was discovered: the addition of a hydroxymethyl group (–CH₂–OH) to specific cytosine bases of DNA.

Histone proteins can also be modified in a number of ways; in addition to methylation, they can be modified with acetyl groups (acetylation), phosphate groups (phosphorylation), ubiquitin proteins (ubiquitylation), and SUMO proteins (sumoylation).

But epigenetic phenomena are not restricted to DNA methylation and various types of histone modifications.

Scientists have found that RNA molecules themselves can also regulate DNA directly by physically blocking or influencing the reading of DNA sequences.

These RNA molecules aren’t the classic messenger RNA (mRNA) molecules we learn about in school biology that carry the information from DNA in the nucleus to the cytoplasm of a cell.  Rather, these RNA molecules – called antisense RNAs, microRNAs, and noncoding RNAs – stay primarily within the nucleus, where they induce changes in DNA function.

It is not yet fully understood how these RNA molecules work but it appears they may bind to histone proteins and/or help to turn off gene promoters.

So how does the environment interact with the epigenome and influence our genes?

One of the most exciting discoveries of modern science is that our DNA, the genome, responds dynamically to the environment.

Stress, diet, behaviour, toxins and other factors activate the chemical tags or switches that turn our genes on and off.

Nutrition is one of the easier environmental factors to study with respect to epigenetic changes and is receiving considerable research effort.

One of the most stunning examples of the effect of nutrition on gene expression was an experiment conducted at Duke University in 2000 [3].

Randy Jirtle and his postdoctoral student Robert Waterland took pairs of fat, yellow mice which carry the agouti gene, which is also found in humans.  This gene makes the rats extremely hungry and renders them prone to obesity, diabetes and cancer.

Typically, when agouti mice breed, most of the offspring are identical to the parents: yellow, fat and susceptible to disease.

In this experiment, the researchers simply changed the diet of the mothers.

Before conception and during pregnancy, one set of mice were fed a diet containing nutrients rich in methyl groups, for example, folate and the B vitamins.  These molecules are found in many plant foods and in supplements given to pregnant women.  The other set of genetically identical mice were fed a regular diet low in these nutrients over the same time period.

Mice with the agouti gene (picture from University of Utah)

To the researchers’ amazement, the mothers fed the methyl rich diet produced brown, slim, healthy offspring, whereas the mothers on the normal diet produced the typical yellow, fat and sickly offspring.  The only difference between the two was the diet the mothers were given.

Methyl groups from the dietary supplements (folic acid, vitamin B₁₂, choline, and betaine) bound to the DNA of the mice, increasing DNA methylation and preventing the agouti gene from being expressed.

Chemicals and additives that enter our bodies can also affect the epigenome.

Bisphenol A (BPA) is a compound used to make polycarbonate plastic.  It is in many consumer products including water bottles and the lining of tin cans.

When pregnant yellow agouti mothers were fed BPA, more yellow, unhealthy babies were born than normal.  Exposure to BPA during early development had caused decreased methylation of the agouti gene.

However, when BPA-exposed, pregnant yellow mice were fed a diet containing B vitamins, folate, choline and betaine, which are rich in methyl groups, the offspring were predominantly brown.  The maternal nutrient supplementation had counteracted the negative effects of exposure to a genotoxic chemical [4].

Mice with the agouti gene fed with Bisphenol A

The father’s diet may be important too.

A Swedish paper published in 2007 [5] provided evidence from historical records that a shortage of food for grandfathers was associated with extended lifespan of their grandchildren.  Food abundance, on the other hand, was associated with a greatly shortened lifespan of the grandchildren due to diabetes and heart disease.

This suggests the possibility that during this critical period of development for the grandfather, epigenetic mechanisms are “capturing” nutritional information about the environment to pass on to the next generation.

Honey bees, too, provide a beautiful example of the power of nutrition over gene expression.

The larvae that develop into workers and queens are genetically identical.  Larvae destined to become queens, however, are fed a diet of royal jelly in a special compartment in the hive called a queen cup.

Queen cup

Royal jelly is a complex, protein-rich substance secreted from glands on the heads of worker bees.   Consumption of royal jelly enables the queen to develop functional ovaries and a larger abdomen for egg laying, while worker bees remain sterile.

The queen also develops different behaviours from those of the workers, becoming more aggressive, looking for mates and communicating using sounds.  The queen is fed royal jelly exclusively for the rest of her life.

In a recent series of experiments, scientists determined that royal jelly silences a key gene (Dnmt3), which codes for an enzyme involved in genome-wide gene silencing [6].  When Dnmt3 is active in bee larvae, the queen genes are epigenetically silenced and the larvae develop into the default “worker” variety.  But when royal jelly turns Dnmt3 off, certain genes jump into action that turn the larvae into queens.

This is all very interesting but how is it relevant to cancer?

Cancer develops when a cell becomes abnormal and begins to grow out of control.

Normal cells and cancer cells (picture from University of Utah)

Cancer can begin when a mutation changes a cell’s DNA sequence.  We know that mutations in at least several hundred human genes (out of a total of 25 000 genes) can lead to the abnormal cell growth and division process that generates human cancer [7].

But cancer cells also have abnormal epigenomes.

In many cancers, some genes are turned up and some are turned down – often in the same cells.  Cancer is just one in a growing number of diseases that are being linked to changes in the epigenome.

Some cancer cells have a lower level of methylation (more active DNA) than healthy cells.

Too little methylation causes:

• activation of genes that promote cell growth
• chromosome instability – highly active DNA is more likely to be duplicated, deleted and moved to other locations
• loss of imprinting.  For most genes, we inherit two working copies – one from each parent. But with imprinted genes, we inherit only one working copy. Depending on the gene, either the copy from your mother or your father is epigenetically silenced.  Silencing usually happens through the addition of methyl groups during egg or sperm formation.

Cancer cells can also have genes that have more methyl (are less active) than normal.

The types of genes that are turned down in cancer cells:

• keep cell growth in check
• repair damaged DNA
• initiate programmed cell death

But here is the real magic.

Unlike mutations, DNA methylation and histone modifications are reversible.

Researchers are thus exploring drug therapies that can change the epigenetic profiles of cancer cells.  One challenge with epigenetic therapies is figuring out how to target drugs to the right genes in the right tissues.

It is for example possible to reactivate dormant tumour-suppressor genes with drugs which remove methyl groups from histone proteins [8].

DNA demethylating drugs in low doses have clinical activity against some tumours, for example, leukaemia, but have not yet been shown to have activity against solid tumours [9].

A key problem is that these demethylating agents are non-specific, often toxic and can potentially exert their effects in healthy tissues paradoxically causing new tumours to develop.

Other drugs targeted at the epigenome are the histone deacetylase (HDAC) inhibitors.

These can induce differentiation, cell-cycle arrest, and programmed cell death (apoptosis) in vitro, although it has not been possible to pinpoint a specific mechanism that explains these effects [10].

In clinical trials, HDAC inhibitors are associated with a low incidence of adverse events.  The first drug of this type, suberoylanilide hydroxamic acid (vorinostat),has been approved by the Food and Drug Administration for the treatment of cutaneous T-cell lymphoma [11].  The efficacy of HDAC inhibitors in the treatment of other tumours is limited.

Research on manipulating specific targets in the epigenome with drugs is, in my view, likely to be as doomed to failure as the decades of research looking for drugs which target the genome.

This is because complex biological systems like the human body operate through a large number of simultaneous reactions occurring in a highly integrated and concerted manner.

The body has multiple back-up systems in case one system is bypassed.

Nutrition, epigenetics and cancer

In addition to drug research, there is also considerable interest in the way nutrients affect the epigenome in relation to cancer [12] [13] [14] [15].

Extensive review of the highest quality papers in the scientific literature by a team of international experts on behalf of the World Cancer Research Fund has led to the view that at least 30-40 per cent of cancers potentially can be avoided through dietary modification [16].

Many bioactive components have been identified in food, which are protective at different stages of cancer formation.  Diet has been implicated in many pathways involved in carcinogenesis, including apoptosis, cell cycle control, differentiation, inflammation, angiogenesis, DNA repair, and carcinogen metabolism [12].  These are also processes likely to be regulated by DNA methylation and other epigenetic events.

A host of bioactive substances in the diet, from alcohol to zinc, have been shown to modulate DNA methylation and cancer susceptibility [12] [16].

Dietary factors that are involved in one-carbon metabolism provide the most compelling data for the interaction of nutrients and DNA methylation because they influence the supply of methyl groups and therefore the biochemical pathways of methylation processes. These nutrients include vitamin B12, vitamin B6, folate, methionine, and choline.

A large number of epidemiologic and clinical studies suggest that dietary folate intake and blood folate concentrations are inversely associated with colorectal cancer risk [17].

Alcohol consumption increases breast cancer incidence by 41 percent for women consuming 30-60 g/day alcohol compared to non-drinking women [18].  Alcohol consumption has been shown to alter folate metabolism and increase cancer susceptibility [19] [20].

Sulforaphanes from broccoli, diallyl disuphides from garlic and resveratrol in wine, have been shown (in vitro and in vivo) to alter epigenetic processes with positive consequences for cell function, including control of proliferation, upregulated apoptosis and a reduction in inflammation [21].

Green tea polyphenols have been shown to inhibit carcinogenesis through effects on DNA methylation in many animal models [22].

Soy phytoestrogens, such as genistein, have been shown to prevent certain mammary and prostate cancers via protective DNA methylation [12].

Apigenin in parsley, curcumin in turmeric, and coffee polyphenols are reported to inhibit DNA methyltransferase enzyme activity in various cancer models [23] [24].

Zinc deficiency, selenium deficiency and vitamin A excess have been associated with DNA hypomethylation in rat liver, whilst vitamin C deficiency caused hypermethylation in lung cancer cells [12].

There are many more examples but these few serve to illustrate the fact that many dietary components interact in a complex and dynamic manner with the epigenome to alter gene expression and susceptibility to cancer and other diseases.

Whilst studying the effect of individual nutrients on epigenetic processes is instructive, it is far too simplistic.  Food contains an extraordinary array of nutrients and other substances that work together in concert to create health or disease.

Professor T. Colin Campbell’s thought-provoking book “The China Study” opened up the scientific literature on the effect of diet on health to a wide audience.  He explained the evidence showing that a plant-based diet is the healthiest way to eat, dramatically reducing the risk of a range of chronic diseases, such as arthritis, diabetes, heart disease and many cancers.

This dietary effect is due to the consumption of myriad beneficial substances found in whole plant foods, which interact with the epigenome to ensure that our genes are switched on and off correctly. 

Colin Campbell expands on this theme in his new book “Whole: Rethinking the Science of Nutrition”, due out on 23 May 2013.  He argues that nutritional science, long stuck in a reductionist mindset, is at the cusp of a revolution.  He writes:

The traditional “gold standard” of nutrition research has been to study one chemical at a time in an attempt to determine its particular impact on the human body. These sorts of studies are helpful to food companies trying to prove there is a chemical in milk or pre-packaged dinners that is “good” for us, but they provide little insight into the complexity of what actually happens in our bodies or how those chemicals contribute to our health.

Diet is, however, only one of many environmental influences on the way our genes behave.

There is also a growing body of scientific research surfacing from the medical literature showing that our thoughts and emotions directly affect expression of our genes.

Lissa Rankin MD’s new book “Mind over Medicine” is an excellent and readable synopsis of some of the key studies in this area and is thoroughly recommended.

David Hamilton PhD is an organic chemist who used to work in pharmaceutical research inventing drugs for cardiovascular disease.  He left his job because he became more interested in the placebo effect than the effect of drugs he was trying to invent.  David has also written some fascinating books on the science of how the mind affects the body, including “How Your Mind Can Heal Your Body”.

Bruce Lipton PhD, a developmental cell biologist and former Professor of Anatomy at University of Wisconsin School of Medicine, was one of the original researchers in the field of epigenetics and opened my eyes to its exciting advances in his book “The Biology of Belief”.

Dean Ornish MD, Clinical Professor of Medicine at the University of California, San Francisco, has been actively researching the effects of lifestyle factors, including diet, thoughts, social interactions and love, on cancer and other diseases for over 35 years.

The research that he and his colleagues conducted has been published in the Journal of the American Medical Association, The Lancet, Proceedings of the National Academy of Sciences, Circulation, The New England Journal of Medicine, the American Journal of Cardiology, The Lancet Oncology, and elsewhere.

This research is not pseudoscience woo-woo.  It is high quality, properly designed and controlled, peer-reviewed science published in some of the most prestigious medical journals in the world.  And it is only the tip of the iceberg.

The knowledge and understanding we are gaining from modern scientific research in the field of epigenetics has profound implications.

It demonstrates that we do not have to be the victims of our genes.

Genes may predispose us to certain health conditions but their presence does not inevitably determine our health outcomes.

Our environment and lifestyle choices – the thoughts we think, the food and drink we consume, our physical activity, whether or not we smoke, our relationships, our work, our finances, our level of stress, our stewardship of the earth – all interact with our genes to determine our fate.

The truth is that all of us will die one day.

While we are here, though, it is about having a life, not just living.

So embrace your power, trust your instincts about what is best for you, and do not allow fear-mongers on both sides of controversial debates, like the one about Angelina Jolie, scare you to death.

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References

[1] Jemal, A. et al (2013).  Annual Report to the Nation on the Status of Cancer, 1975–2009, Featuring the Burden and Trends in Human Papillomavirus (HPV)–Associated Cancers and HPV Vaccination Coverage Levels.  JNCI J Natl Cancer Inst (2013) doi: 10.1093/jnci/djs491 First published online: January 7, 2013

http://m.jnci.oxfordjournals.org/content/early/2013/01/03/jnci.djs491.full

[2] Watson, J.  Oxidants, antioxidants and the current incurability of metastatic cancers.  Open Biol. 2013 3, 120144, published online 8 January 2013

[3] Waterland RA, Jirtle RL. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol 2003;23(15):5293–5300

[4] Dolinoy D.C., Huang D., Jirtle R.L. (2007). Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. PNAS, 104: 13056-13061.

[5] Kaati G., Bygren L.O., Pembrey M., Sjostrom M. (2007). Transgenerational response to nutrition, early life circumstances and longevity. European Journal of Human Genetics, 15: 784-790.

[6] Kucharski R., Maleszka J., Foret S., Maleszka R. Nutritional Control of Reproductive Status in Honeybees via DNA Methylation (2008). Science, 319: 1827-1830 (registration required).

[7] Jones S, Vogelstein B, Velculescu VE, Kinzler KW. 2008 Core signaling pathways in human pancreatic cancers revealed by global genomic analyses. Science 321, 1801. (doi:10.1126/science.1164368)

[8] Esteller, M.  Epigenetics in cancer.  N Engl J Med 2008;358:1148-59.

[9] Mack GS. Epigenetic cancer therapy makes headway. J Natl Cancer Inst 2006; 98:1443-4.

[10] Bolden JE, Peart MJ, Johnstone RW.Anticancer activities of histone deacetylase inhibitors. Nat Rev Drug Discov 2006;5:769-84.

[11] Marks PA, Breslow R. Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug. Nat Biotechnol 2007;25:84-90.

[12] Davis, C.D and Uthus, E.O. DNA Methylation, Cancer Susceptibility and Nutrient Interactions. Exp Biol Med November 2004 vol. 229 no. 10, 988-995

[13] Khan, S.I. et al (2012). Epigenetic Events Associated with Breast Cancer and Their Prevention by Dietary Components Targeting the Epigenome. Chem. Res. Toxicol. 2012, 25, 61–73

[14] Liu, L. Et al. Aging, cancer and nutrition: the DNA methylation connection. Mechanisms of Ageing and Development Volume 124, Issues 10–12, December 2003, Pages 989–998

[15] Su, L.J. et al.  Epigenetic contributions to the relationship between cancer and dietary intake of nutrients, bioactive food components, and environmental toxicants. Frontiers in Genetics, Vol 2, Article 91, 1-12,, 09 January 2012 | doi: 10.3389/fgene.2011.00091

[16] World Cancer Research Organisation. 2^nd Expert Report: Food, Nutrition, Physical Activity and the Prevention of Cancer: A Global Perspective. Washington DC: AICR, 2007. http://www.dietandcancerreport.org/expert_report/report_contents/index.php

[17] Kim Y.-I.  Folate and DNA methylation: a mechanistic link between folate deficiency and colorectal cancer? Cancer Epidemiol Biomarkers Prev 13:511–519, 2004.

[18] Smith-Warner, S.A. et al.  Alcohol and breast cancer in women.  A pooled analysis of cohort studies.  JAMA 279 (1998), 535-540.

[19] van Engeland M, Weijenberg MP, Roemen GM, Brink M, de Bruine AP, Goldbohm RA, van den Brandt PA, Baylin SB, de Goeij AF, Herman JG. Effects of dietary folate and alcohol intake on promoter methylation in sporadic colorectal cancer: the Netherlands cohort study on diet and cancer. Cancer Res 63:3133–3137, 2003

[20] Choi SW, Stickel F, Baik HW, Kim YI, Seitz HK, Mason JB. Chronic alcohol consumption induces genomic but not p53-specific DNA hypomethylation in rat colon. J Nutr 129:1945–1950, 1999.

[21] Ross SA, Dwyer J, Umar A et al. (2008) Diet, epigenetic events and cancer prevention. Nutr Rev 66 (Suppl. 1), S1–S6.

[22] Fang MZ, Wang Y, Ai N, Hou Z, Sun Y, Lu H, Welsh W, Yang CS. Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer celllines. Cancer Res 63:7563–7570, 2003.

[23] Meeran, S. M., Ahmed, A., and Tollefsbol, T. O. (2010) Epigenetic targets of bioactive dietary components for cancer prevention and therapy. Clin. Epigenetics 1, 101–116.

[24] Lee, W. J., and Zhu, B. T. (2006) Inhibition of DNA methylation by caffeic acid and chlorogenic acid, two common catechol-containing coffee polyphenols. Carcinogenesis 27, 269–277.

Whoppers in the NHS

Burger King, Level C, Southampton General Hospital

I locked my car and headed down the steps of the car park towards the main entrance of Southampton General Hospital.

Waves of anxiety swept over me.

I had come to visit a dear friend who is very poorly and I wasn’t sure what to expect.

Over the last two weeks things had taken a turn for the worse.

What could I say?  What should I say?

I just didn’t know.

My heart was heavy as I approached the main hospital building.

An ambulance raced past, siren blaring, blue lights flashing.

Glancing round I noticed people in pyjamas sitting on benches in the paved area opposite the entrance.

My nostrils twitched and involuntarily I held my breath; the warm air was thick with the stench of cigarette smoke.

Stubbing out her fag, a woman with long greasy hair, a pink dressing gown and fluffy slippers, grabbed her drip stand and shuffled across the zebra crossing and through the sliding door into the hospital.

I followed.

Inside, as my eyes adjusted to the light, I searched for signs. Costa Coffee. Reception. Hospital Security. Claims Solicitors. Outpatients.  Childrens Outpatients. Neurosciences. Emergency Department. X-Ray. Oncology. Burger King.

Burger King?

I walked closer.

Burger King?

Two kind faces watched as I approached.

“Do you need any help?” asked one with a friendly smile – hospital volunteers on ‘meet and greet’ duty.  The smile was genuine and I remembered to breathe properly again.

“I’m looking for Ward C4, but first I need a toilet, a cash point and a cup of tea”.

They gave me directions and another reassuring smile.

All around me were reminders of the frailty of the human body, my own frailty. Wheelchairs, walking sticks, grey faces, worry. Fear gripped me again.

Taking a deep breath, I pressed the buzzer for entry to the ward.

Several hours later I emerged from the hushed efficiency of the clinical suites, a little more relaxed than I had entered.

I wished with all my heart that everything was back to normal.  But it wasn’t.  Nevertheless, there was no doubt about it – my friend was receiving the best possible medical, nursing and personal care.  The ward was spotlessly clean and every member of staff I had met, from the tea lady to the Consultant, had behaved with kindness, compassion and professionalism.

There is so much to be proud of in the NHS.

Back outside, a queue was forming at Burger King.

Furtively, I pulled my iPhone out of my pocket and took a picture.  I had to convince myself that I hadn’t imagined it, that the cortisol coursing through my veins hadn’t scrambled my senses.

But there it was – plain to see – Home of the Whopper.

University Hospital Southampton NHS Foundation Trust is, according to its annual report:

…a centre of excellence for training the doctors and nurses of the future and developing treatments for tomorrow’s patients. Its role in research and education, developed in active partnership with the University of Southampton distinguish it as a hospital that works at the leading edge of healthcare developments in the NHS and internationally.

I believe them.  But given these credentials, surely they must know that diet is a key determinant of long-term health?

Reports by the World Health Organisation describe in detail how, in most countries, a few major risk factors account for much of the illness and death (1).

For non-communicable diseases, the most important risks include high blood pressure, high concentrations of cholesterol in the blood, inadequate intake of fruit and vegetables, overweight or obesity, physical inactivity and tobacco use.

These risks arise predominantly from elevated consumption of energy-dense, nutrient-poor foods that are high in fat, sugar and salt; reduced levels of physical activity at school, work, and home; and smoking.

There, in front of my eyes, was evidence that one of the most prestigious teaching hospitals in the UK is not only ignoring public health research, it is encouraging its patients, carers and staff to indulge in food and drink that is scientifically proven to damage human health.

At this point, I must stress that NHS patients are not given fast food by hospital staff when they are on the ward.  They are offered three meals a day, with choices from an extensive menu of hot and cold dishes.  My friend had eaten a Cornish pasty followed by a yoghurt, for example.

This food is not, however, available for visitors or staff.  Furthermore, as I had witnessed myself, patients are able to leave the wards during the day and wander around the shopping area.  Outside, I had seen some of them eating burgers whilst smoking.

Two weeks ago, a Health and Wellbeing Summit was convened by NHS Employers and Dame Carol Black.  It brought together a range of senior NHS leaders to demonstrate their commitment to the health and wellbeing of the NHS workforce.

The Boorman Review published in 2009 had already highlighted both the individual and business value of healthier NHS employees.

Steve Boorman concluded:

We believe that the NHS can reduce current rates of sickness absence by a third, and doing so would mean:

• 3.4 million additional available working days a year for NHS staff

• equivalent to an extra 14,900 whole-time equivalent staff

• with an estimated annual direct cost saving of £555 million

At the NHS Employers Summit, Dame Carol Black said:

The benefits of strong health and wellbeing programmes in the NHS go far beyond the individual. Staff whose wellbeing and health is well supported deliver better care and are more resilient and better engaged with their role. At a time when the NHS is striving to make the absolute most of its resources, getting this right is crucial. I am very pleased that the NHS leaders in the new system are getting behind this agenda so quickly.

Participants signed a pledge to continue to improve the health and wellbeing of staff who work in healthcare.

We will:

• foster a culture that promotes better physical and mental health and wellbeing for staff in all workplaces used by our organisation
• work to strengthen staff engagement both in and through these endeavours
• include measures of employee health and wellbeing within Key Performance Indicators and other performance monitoring systems within our organisation
• sign up to the relevant parts of the Public Health Responsibility Deal for our staff
• exploit the relationships we have with other NHS organisations, sharing expertise and experience in ways of safeguarding and improving staff health and wellbeing

Where does Burger King in a hospital fit into this, I wonder?

America has the same problem but the tide is turning.

After 34 years at the Children’s Hospital of Philadelphia, McDonald’s closed its doors last September.

But as fast as some hospitals are ending contracts with fast food outlets, others are starting them.  Chick-fil-A recently set up shop in several facilities, including the Texas Medical Center’s St. Luke’s Episcopal Hospital and the Medical University of South Carolina University Hospital in Charleston, S.C.

Of the 14,000 McDonald’s in the United States, the company says there are 27 in hospitals.  They say that fast food outlets can be a convenience and a comfort for patients. The food may also appeal to some patients’ picky tastes when undergoing difficult treatments.

The Physicians’ Committee for Responsible Medicine surveyed hospital food at 100 US hospitals in 2011.  Some had as many as five fast food outlets.

Many clinicians feel that the presence of such outlets sends an inconsistent message to patients, staff and the community and have campaigned to remove them.  It has not always been easy.

Ten years ago, the Cleveland Clinic in Ohio tried in vain to terminate its contract with McDonald’s.  At the time, the clinic’s lead heart surgeon (and now hospital CEO), Delos Cosgove, proposed removing all fast food vendors.

The Pizza Hut did close. But McDonald’s stayed and remains a tricky relationship for the hospital, which is a pioneer in whole environment approaches to employee wellness.

Despite their failure to eliminate McDonald’s from their campus, the Cleveland Clinic, which has 37,000 employees, pressed ahead with other actions focused on the four big public health issues: tobacco, food choices and portion size, physical inactivity and stress.

Here is their timeline:

• July 2005: Designated all Cleveland Clinic campuses smoke-free
• January 2007: Offered free smoking cessation services to all Cuyahoga County residents for six months
• February 2007: Banned trans-fats from all public and patient menus
• May 2007: Began converting vending machines to replace unhealthy food items with healthy snack choices
• September 2007: Stopped hiring smokers
• November 2007: Created the country’s first Chief Wellness Officer position, with the appointment of Michael F. Roizen, MD
• January 2008: Established the Wellness Institute
• May 2008: Began free yoga classes for employees
• July 2008: Launched weekly farmers market for employees and community
• August 2008: Implemented free Weight Watchers services for EHP member employees
• October 2008: Welcomed first class of Lifestyle 180 participants, a lifestyle modification program for patients with chronic conditions like high blood pressure, diabetes, and heart disease
• November 2008: Initiated free memberships to Curves and Cleveland Clinic-owned fitness centers for EHP member employees
• January 2009: Rolled out GO Foods healthy labeling in all Cleveland Clinic cafeterias – GO foods contain nothing that can harm your body.
• August 2010: Banned sugared beverages from all cafeterias and vending machines

What are the results?

1. Over 10 years, their no-smoking policy and programme has achieved a 6 to 1 return on investment, reducing the percentage of smokers to 2.1%
2. US$36 million has been saved from smoking quitters
3. US$114 million has been saved from not hiring smokers
4. It is difficult to quantify savings from avoiding second-hand smoking, but it could be as much as the above, says Michael Roizen MD, Chief Wellness Officer
5. Since 2008, nearly 300,000 lbs. have been lost by Cleveland Clinic employees.  It is estimated that this equates to US$14-15 million in healthcare cost savings.
6. Memberships and visits at Cleveland Clinic-owned fitness centers have increased by 358%, with total visits now averaging over 20,000 per month.
7. Registration for Sunrise/Sunset Yoga continues to grow with nearly 50 classes and 3,300 registered participants in 2011.
8. Since 2009, more than 30,000 unique employees have enrolled in Shape Up and GO!

Dr Michael Roizen MD, Head of the Cleveland Clinic Wellness Institute, says:

Emotions and facts cannot change people’s behaviour.  But changing the environment can.  Organisations need to change the environment so that it is easy to do healthy things and hard to do unhealthy things.

This is easy to say but hard to do.

I wouldn’t mind betting that the Board responsible for Southampton General Hospital is facing a similar dilemma to that of Croydon University Hospital Trust in Surrey, which received negative media coverage when they had to pay £24,000 to shut down a Burger King restaurant inside their hospital.

£24,000 is enough to cover the salary of a low-grade nurse for a year

bleated the Daily Mail, without considering the long-term costs to the health service of people consuming Burger King’s products.

It may also be the case that they do not have direct control over which businesses operate in the entrance area if this is handled by a landlord.

At some point, however, someone within the NHS needs to demonstrate leadership, courage and imagination and set about creating hospital environments which make it easy for people to make healthy choices, as they have done at the Cleveland Clinic in the USA.

Will Southampton General Hospital, excellent in so many ways, take up the challenge?  I hope so.

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References

1. World Health Report 2002. Reducing risks, promoting healthy life. Geneva, World Health Organization, 2002.  http://www.who.int/whr/2002/en/whr02_en.pdf

An idealist is one who, on noticing that a rose smells better than a cabbage, concludes that it will also make better soup

I came across this little poem the other day:

I wonder if the cabbage knows

He is less lovely than the Rose;

Or does he squat in smug content,

A source of noble nourishment;

Or if he pities for her sins

The Rose who has no vitamins;

Or if the one thing his green heart knows

That self-same fire that warms the Rose?

This made me think.

Is it true that the rose has no vitamins?

The Chinese were the first to experiment with flowers as food and their many and varied recipes can be traced back as far back as 3,000 B.C.

In Roman times, the edible flowers of pinks, violets and roses were used in dishes, and lavender in sauces.

Gardeners and cooks over 1000 years ago were already using pot marigolds and orange blossom in their cooking and edible flowers were especially popular in the Victorian era.

After falling out of favour for many years, flower cookery is now back in vogue.

Innovative chefs in fancy restaurants have taken to garnishing their entrees with flower blossoms for a touch of elegance.

But do flowers only have aesthetic value in cooking?

Or do they have nutritive value too?

Broccoli flowering

Of course, this is a bit of a trick question because we are already familiar with eating flower heads.

Broccoli and cauliflower are good examples and we know that they are packed with vitamins, minerals and other beneficial substances which act as antioxidants.

But what about the sort of flowers which are usually grown for ornamental purposes, like roses and pansies?

Chive and viola flower salad (theedibleflowershop.co.uk)

Nutrient content of edible flowers

I have searched high and low in the scientific literature for quantitative data on the nutrient content of flower petals. There are relatively few references, particularly in English.

Most of the literature is focused on evaluating flowers for their sensory characteristics, such as appeal, size, shape, colour, taste, and above all, aroma, which is important for the cosmetic and perfume industry.

The references I have found in journals from researchers in Turkey, Bosnia, Poland, South Korea and China among others, suggest that the common components – proteins, fats and carbohydrates – are present in similar amounts to those in other plant organs, e.g., in leaf vegetables (1).

Available data on a number of edible flowers show that petals also contain an array of vitamins and minerals, particularly vitamins A and C, various B vitamins, folic acid, and minerals including calcium, magnesium, potassium, iron and phosphorus.

The data in this table were compiled from sources in the list of references below (1-7).

Flower	Protein	Carb	Fat	Vit A	Folate	Vit C	Ca	Fe	Mg	K
	g/100g			IU	μg/100g	mg/100g
Chives	3.07					108.5
Pumpkin	1.03	3.28	0.07	1947	59	28	39	0.7	24	173
Sesbania	1.28	6.73	0.04	0	102	73	19	0.84	12	184
Hawthorn						900
Banana	2.07	91.4	0.4				33	43	34	571
Gourd	0.62	3.39	0.02	16	6	10.1	26	0.2	11	150
Broccoli	2.98	5.24	0.35	150	71	93.2	48	0.88	25	325

Flower colour is determined by many chemical compounds but carotenoids and flavonoids are the most important.  The flavonoids in particular have been shown to give flowers high antioxidant capacity (1).

Dandelions, for example, contain numerous flavonoids and carotenoids with antioxidant properties, including four times the beta carotene of broccoli, as well as lutein, cryptoxanthin and zeaxanthin. They are also a rich source of vitamins, including folic acid, riboflavin, pyroxidine, niacin, and vitamins E and C.

Violets contain rutin, a phytochemical with antioxidant and anti-inflammatory properties that may help strengthen capillary walls.

Rose petals contain bioflavonoids and antioxidants, as well as vitamins A, B3, C and E (6,7).

Nasturtiums contain cancer-fighting lycopene and lutein, a carotenoid found in vegetables and fruits that is important for vision health.

Lavender contains vitamin A, calcium and iron, and is said to benefit your central nervous system.

Chive blossoms contain vitamin C, iron and sulphur, as well as many antioxidants, and have traditionally been used to help support healthy blood pressure levels.

So, to answer my original question – yes – roses and other flowers do contain vitamins.

Practical considerations

When collecting flowers for eating, keep the following in mind;

• Accurate identification of flowers is essential – if you are in doubt, DO NOT EAT
• Pick young flowers and buds on dry mornings, before the sun becomes too strong, so the colour and flavours will be intense
• Use flowers immediately for best results or refrigerate in a plastic bag for a couple of days. Dried or frozen flowers are best used in infusions or cooked
• Generally, only the petals are used, so discard stamens, pistil and calyx of large flowers like hollyhocks, roses, lilies and hibiscus. The bitter ‘heel’ at the base of the petal should be removed
• Petals of daisies, borage and primroses can easily be separated from the calyx
• Smaller flowers in umbels like fennel and dill can be cut off and used whole

There are some poisonous flowers you definitely cannot eat, for example, daphne, foxglove, daffodils, hyacinths and all members of the nightshade family. Consult a reference book, or ask an expert in this area, before being too adventurous.  If you are not sure, DO NOT EAT.  I have included a list of books on edible and poisonous flowers below.

Edible ornamental flowers

Many garden favourites are edible and a few are listed below:-

• Alpine pinks (Dianthus) – a clove-like flavour ideal for adding to cakes as flavoured sugar, oils and vinegars
• Bergamot (Monardia didyma) – a strong spicy scent, makes good tea and complements rice and pasta
• Chrysanthemum (Chrysanthemum) – petals flavour and colour cream soups, fish chowder and egg dishes in the same way as calendula
• Daisy (Bellis perennis) – not a strong flavour but petals make an interesting garnish for cakes and salads
• Day lily (Hemerocallis) – add buds and flowers to stir fry, salads and soups. Crunchy with a peppery after taste but may have a laxative effect. Avoid buds damaged by gall midge
• Elderflower (Sambucus nigra) – used to make wine and cordials, or place in a muslin bag to flavour tarts and jellies but removed before serving. Elderflowers can be dipped in batter and deep fried
• Hibiscus (H. rosa-sinensis) – refreshing citrus-flavoured tea enhanced by rosemary
• Hollyhock (Alcea rosea) – remove all traces of pollen and decorate cakes with crystallized petals
• Lavender (Lavandula augustifolia) – flavoured sugar, honey or vinegar can be used in cakes and biscuits and dried flowers used as tea
• Nasturtium (Tropaeolum majus) – brightly-coloured, peppery flowers are good in salads and pasta dishes. The whole flower, leaves, and buds can be used or just the petals for a milder flavour
• Pot marigold (Calendula officinalis) – intense colour and a peppery taste useful in soups, stews and puddings. Petals can be dried or pickled in vinegar or added to oil
• Primrose (Primula vulgaris) – decorate cakes with crystallized or fresh primrose or cowslip flowers. They can be frozen in ice cubes
• Rose (Rosa) – all roses are edible with the more fragrant roses being the best. Petals can be crystallized, used to flavour drinks, sugar and even icing for summer cakes
• Scented geraniums (Pelagonium) – flowers are milder than leaves and can be crystallized or frozen in ice cubes for summer cordials
• Sunflower (Helianthus annuus) – blanch whole buds and serve with garlic. Petals can be used in salads or stir fries
• Sweet violet (Viola odorata) – delicate flavour suitable for sweet or savoury dishes as well as tea. Use candy violets and pansies as a garnish on cakes and soufflés
• Tiger lily (Lilium leucanthemum var. tigrinum) – delicate fragrance and flavour enhances salads, plus can be used to stuff fish

Edible flowers from your vegetable patch and herb garden

Herb flowers like basil, chives, lavender, mint, rosemary and thyme impart a more subtle flavour to food than the leaves. By adding sprigs of edible herb flowers like basil or marjoram to oils the delicate flavours can be used over a longer period.

• Borage (Borago officinalis) – the cucumber flavour of these attractive blue flowers adds interest to cakes, salads and pate. Flowers are easily removed and can be frozen in ice cubes or crystallized
• Basil (Ocimum basilicum) – sweet, clover-like flavour compliments tomato dishes as well as oils, salad dressings and soups. Use aromatic leaves of both green and purple in Mediterranean dishes
• Dill (Anethum graveolens) – aniseed flavour, ideal addition to salads, vegetables and fish dishes. Add flowers to mayonnaise, white sauce and pickles
• Chives (Allium schoenoprasum) – mild onion flavour, good in salads, egg dishes and sauces for fish
• Clover (Trifolium pratense) – both red and white clover flowers can be used to garnish fruit and green salads or make wine from whole red flowers
• Courgette or marrow flowers – can be eaten hot in a tomato sauce or cold stuffed with cooked rice, vegetables and nuts. Use male flowers so as not to reduce yield
• Fennel (Foeniculum vulgare) – all parts are edible and enhance salmon, pâtés and salads. Flowers preserved in oil or vinegar can be used in winter
• Garden pea (Pisum sativum) – add flowers and young shoots to salad for a fresh pea taste
• Mint (Mentha sp) – Apple, pineapple and ginger mint, plus peppermint and spearmint flowers can all be used in oil and vinegar for both sweet and savoury dishes
• Rosemary (Rosmarinus officinalis) – a sweet flavour similar to the leaves can be used fresh to garnish salads and tomato dishes or to flavour oil
• Salad rocket or arugula (Eruca vescaria) – adds sharp flavour to salads or preserve in oil

Recipe

Here is a recipe using nasturtium flowers from one of my favourite cookery books – “Purple Citrus and Sweet Perfume” by Silvena Rowe.  Although not all of the recipes are plant-based, I love Silvena Rowe’s creative combinations of flavours and colours.

Pink Grapefruit, Avocado and Pomegranate Salad with Nasturtium Flowers

Serves 4

Ingredients

• 2 pink grapefruits
• 2 large avocados, stones removed, peeled and sliced into thin wedges
• 1/2 large bunch of fresh purple basil, leaves only
• seeds of 1 large pomegranate
• 3 tablespoons white wine vinegar
• 4 tablespoons olive oil
• 1 teaspoon mild mustard
• 1 teaspoon pomegranate molasses
• 1 teaspoon ground sumac
• 6-8 nasturtium flowers

Method

Peel the pink grapefruits, making sure you cut away all the pith, then cut them into individual segments. Place in a large bowl along with any juice, add the avocado, basil and pomegranate seeds, and season. Whisk together the vinegar, olive oil, mustard and pomegranate molasses and pour over the salad. Toss gently to combine, sprinkle with the sumac and serve garnished with the nasturtium flowers.

Books on poisonous and edible flowers

• Poisonous Plants by Elizabeth A. Dauncey
• The Edible Flower Garden by Kathy Brown
• Edible flowers by Kathy Brown
• The Edible Flower Garden by Rosalind Creasy
• Cooking with Edible Flowers by Miriam Jacobs
• Good Enough to Eat by Jekka McVicar
• Edible Flowers, Desserts & Drinks by Cathy Wilkinson Barash
• Edible Flowers from Garden to Palate by Cathy Wilkinson Barash

References

1. Otakar Rop, Jiri Mlcek, Tunde Jurikova, Jarmila Neugebauerova and Jindriska Vabkova. Edible Flowers — A New Promising Source of Mineral Elements in Human Nutrition. Molecules 2012, 17, 6672-6683; doi:10.3390/molecules17066672
2. Monika Grzeszczuk, Aneta Wesołowska, Dorota Jadczak, Barbara Jakubowska.  NUTRITIONAL VALUE OF CHIVE EDIBLE FLOWERS. Acta Sci. Pol., Hortorum Cultus 10(2) 2011, 85-94
3. USDA National Nutrient Database.http://ndb.nal.usda.gov/ndb/search/list
4. Azra Tahirović, Amira Čopra – Janićijević, Nedžad Bašić, Lela Klepo, Mirel Subašić1. DETERMINATION OF VITAMIN C IN FLOWERS OF SOME BOSNIAN CRATAEGUS L. SPECIES. Works of the Faculty of Forestry University of Sarajevo No. 2, 2012 (1-12)
5. Zhan-Wu Sheng, Wei-Hong Ma, Zhi-Qiang Jin1, Yang Bi, Zhi-Gao Sun, Hua-Ting Dou, Jin-He Gao, Jing-Yang Li and Li-Na Han.  Investigation of dietary fiber, protein, vitamin E and other nutritional compounds of banana flower of two cultivars grown in China.  African Journal of Biotechnology Vol. 9(25), pp. 3888-3895, 21 June, 2010
6. Alejandra Mabellinia, Elisabeth Ohacoa, Mónica Roselva Ochoaa, Alicia Graciela Kesselera, Carlos Alberto Márqueza, Antonio De Michelisb. Chemical and Physical Characteristics of Several Wild Rose Species Used as Food or Food Ingredient. Int. J. Ind. Chem., Vol. 2, No. 3, 2011, pp. 158-171
7. Hanan M. K. E. Youssef, Rasha M. A. Mousa. Nutritional Assessment of Low-Calorie Baladi Rose Petals Jam. Food and Public Health 2012, 2(6): 197-201. DOI: 10.5923/j.fph.20120206.03

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