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

Pope Francis, food and the mystics

Almost every article I have read about the new Pope Francis mentions his humility, the simplicity of his home, his dedication to serving the poor and the fact that he cooks for himself.

This led me to wonder what he eats.

According to an article in the Argentinian newspaper La Nacion in 2009, he chooses healthy frugal food and occasionally drinks a glass of wine. He is said to like fruit, skinless chicken and salads. When in Buenos Aires, he apparently never ate out in restaurants. He would eat by himself and would not even join meals at parish churches in his diocese. On the rarest of occasions, he might break from his routine of eating in his own quarters to visit a nunnery to enjoy bagna cauda – a fondue of anchovies, garlic and olive oil.

The simplicity of Pope Francis’ diet reminds me of the story of Daniel and his friends in the Christian Bible (Daniel 1).

King Nebuchadnezzar of Babylonia attacked Jerusalem and surrounded the city. He captured King Jehoiakim and seized treasures from the Temple.

Nebuchadnezzar then ordered his chief official, Ashpenaz, to select some young men from the noble and royal families of the Israelite exiles to serve in his court. They had to be handsome, intelligent, well-trained, quick to learn, and free from physical defects. Ashpenaz was to teach them to read and write the Babylonian language. The king also gave orders that every day they were to be given the same food and wine as the members of the royal court. After three years of this training they were to appear before the king. Among those chosen were Daniel, Hananiah, Mishael, and Azariah, all of whom were from the tribe of Judah. The chief official gave them new names: Belteshazzar, Shadrach, Meshach, and Abednego.

Daniel made up his mind not to let himself become ritually unclean by eating the food and drinking the wine of the royal court, so he asked Ashpenaz to help him. Ashpenaz was sympathetic to Daniel but was afraid of the king. So he said to Daniel, “The king has decided what you are to eat and drink, and if you don’t look as fit as the other young men, he may kill me.”

So Daniel went to the guard whom Ashpenaz had placed in charge of him and his three friends. “Test us for ten days,” he said. “Give us vegetables to eat and water to drink. Then compare us with the young men who are eating the food of the royal court, and base your decision on how we look.”

He agreed to let them try it for ten days. When the time was up, they looked healthier and stronger than all those who had been eating the royal food. So from then on the guard let them continue to eat vegetables instead of what the king provided.

God gave the four young men knowledge and skill in literature and philosophy. In addition, he gave Daniel skill in interpreting visions and dreams.

At the end of the three years set by the king, Ashpenaz took all the young men to Nebuchadnezzar. The king talked with them all, and Daniel, Hananiah, Mishael, and Azariah impressed him more than any of the others. So they became members of the king’s court. No matter what question the king asked or what problem he raised, these four knew ten times more than any fortune teller or magician in his whole kingdom. Daniel remained at the royal court until Cyrus, the emperor of Persia, conquered Babylonia.

Daniel was not alone in his experience with food. Mystics of all traditions teach that diet influences spiritual awareness.

Many spiritual masters of the East, including Hindus, and various schools of yoga, divide foods into three basic categories: Sattvic (pure), Rajasic (kingly), and Tamasic (impure). They teach that this last category of foods, which includes all flesh foods and eggs, is to be completely avoided. A sattvic diet consists of fresh, simple foods including: grains, beans, vegetables, fruits, seeds, nuts, and dairy. Sattvic foods are said to promote mental clarity, relaxation, meditation, and spiritual experience including inner visions. A rajasic diet includes very rich, spicy food, and a tamasic diet includes meat and alcohol. These are said to stimulate passions, promote mental agitation, and have an adverse effect upon concentration in meditation.

Those who take up the practices concerning the lower centres in the body, do take meat … but those who are anxious to rise above body consciousness and go into the Beyond have of necessity to eschew all that. This is the Path I have put before you. Liberation or salvation is something which starts only when you rise above body consciousness. For that reason, vegetarianism is the first essential.

(Kirpal Singh, The Night is a Jungle, published by Sant Bani Ashram of New Hampshire).

Guru Kabir, a great Master from Northern India, loved by Sufis, Sikhs, Jains, and Hindus alike, said:

The man who eats meat is a demon in human form. Keep away from him – his company will ruin your meditation.

(Kabir: the Weaver of God’s Name, Radha Soami Satsang Beas).

According to these teachers, the bad karma and other negative effects of flesh-eating apparently to some degree darkens one’s inner vision, interfering with the quality of one’s meditation, making it more difficult to reach the required deep levels of tranquility, clarity and concentration.

The concept of diet affecting spiritual awareness is not confined to Eastern mystics.

Many early Christians were vegetarian; also Clement of Alexandria, Origen, John Chrysostom, and Basil the Great. In some early church writings, Matthew, Peter and James (brother of Jesus and first leader of the Aramaic-speaking Jerusalem Church) were said to be vegetarian. According to the historian Eusebius, the Apostle “Matthew partook of seeds, nuts and vegetables, without flesh.” Many monasteries in ancient times practised vegetarianism and continue to do so.

Clement of Alexandria wrote,

It is far better to be happy than to have your bodies act as graveyards for animals.

Modern day Seventh Day Adventists, for example, advocate a vegetarian diet.

Most conventional world religions in the West condone flesh-eating, but many esoteric traditions which have practised various forms of mysticism, are consistent in their agreement about the need for contemplative mystics to abstain from the flesh. The list of Western vegetarian paths includes: the Pythagoreans, followers of the Hermetic philosophy of Egypt, the Sethians, Theraputae, Essenes, the original Jewish Christians called Ebionites, the Gnostic religions, Manichaeans, some Catholic monasteries, some monasteries associated with the Orthodox Church – including the great mystery school on Mount Athos in Greece – and the Sufi mystics of Islam.

It may be no coincidence that the predominantly plant-based diet of Daniel and spiritual masters of many traditions, is virtually identical to that advocated by modern science. A diet which is believed to enhance spiritual openness also protects against cancer, heart-disease, stroke, diabetes, dementia, arthritis and the general ravages of aging.

Pope Francis’s simple diet may not only have helped to deepen his spiritual practice but also given him the physical strength to take on this monumental role at the age of 76. May he prove to be as wise, knowledgeable and visionary as Daniel.

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Sugar in soft drinks

At one time humans obtained most of their calories from food.  That changed with the arrival of cheap sugar, and then cheaper high-fructose corn syrup.

In the late 16th century, a teaspoon of sugar cost the equivalent of ten pounds in London (1).  Nowadays, 1 teaspoon of sugar costs approximately one pence (2).

 

 

Sugar added to food now accounts for nearly 16 percent of the average American’s daily intake; sweetened soft drinks make up nearly half of that (3).

In Britain, government statistics indicate that 14.2 per cent of the calories in the average diet come from added sugars (4).

Researchers at Glasgow University asked 2,005 people from across the UK to estimate how many teaspoons of sugar were in some of the UK’s most popular drinks (5).  Those surveyed were also asked to estimate their average weekly liquid consumption in detail.

 

 

The findings suggest that the average person in the UK consumes 659 grams of sugar and 3,144 calories per week (which equates to 450 calories per day) through non-alcoholic liquid intake.  This is the equivalent of nearly a quarter of recommended daily calories for a woman and a fifth for men.

People underestimated the amount of sugar in a serving of pomegranate juice by an average of 17.9 teaspoons, while they overestimated the amount of sugar in a serving of fruit squash by almost seven teaspoons.

It is worth noting that a number of products state they contain “100% juice” or “100% pomegranate juice”. You need to read the product label carefully because most products contain only 20 to 30 per cent pomegranate, with the rest typically apple or grape juice.

 

Pomegranate juice

 

Professor Naveed Sattar said:

“While people sometimes overestimate the amount of sugar in carbonated drinks, they significantly underestimate the sugar levels in smoothies and fruit juices.

This analysis confirms that many people are perhaps not aware of the high calorie levels in many commonly consumed drinks.  Some varieties of drinks such as pure fruit juices and smoothies which are perceived as “healthy” options are also very high in sugar. For many people struggling with their weight, reducing their intake of such drinks and replacing with water or diet drinks would be a sensible first target to help them lessen their calorie intake.

For some, this change might seem difficult or impossible as they admit to having a “sweet tooth.”  However, it is now clear that our taste buds can be retrained over time to enjoy far less sugar in drinks (or no sugar at all).  But people deserve support and encouragement to make these changes and the soft drinks industry also has a role to play here by providing drinks with less sugar or offering cheaper diet versions.”

According to information from the British Soft Drinks Association, most soft drinks do not contain sugar.  Their data indicate that more than 60 per cent of the soft drinks market is now made up of diet, low calorie and no added sugar drinks, up from 30 per cent 20 years ago (6).

It is best to drink water but if you would like a fruit juice, here is a recipe for a watermelon, strawberry  and rose water crush, which is relatively low in sugars and calories.

 

Watermelon, strawberry and rose water crush

 

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References

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(1) http://www.sugarnutrition.org.uk

(2) http://www.tesco.com

(3) Malik VS, Schulze MB, Hu FB.  Intake of sugar-sweetened beverages and weight gain: a systematic review. American Journal of Clinical Nutrition. 2006; 84:274-288

(4) DEFRA Food Statistics Pocket Book 2011

(5) http://www.gla.ac.uk/news/headline_230642_en.html

(6) British Soft Drinks Association 2011 UK Soft Drinks Report, data from Zenith International

How to lose weight

Many people resolve to go on a diet and adopt a healthier lifestyle, only to give up a few weeks later. Good intentions are often hard to put into practice and sustain. Here are a few suggestions to help you move towards and maintain a healthier weight:

1. Be realistic

Many people set themselves goals they find hard to achieve, such as fitting into a size 8 dress or a dinner jacket from 25 years ago. It is far better to begin by aiming to reduce your weight by 5 to 10 percent of your current weight. This may not turn you into a glamour model in a hurry, but it can lead to important improvements in weight-related conditions such as high blood pressure and diabetes. Once you have achieved this goal, you can always continue and aim to lose another 5 to 10 per cent until you are happy with your weight. Breaking the target down into manageable stages increases your chance of success.

2. Be gentle on yourself

Crash diets may work in the short-term but typically people regain all the weight they have lost and even add some more. Crash diets can also be dangerous. Not only this, but it is usually miserable being on a diet. Depriving yourself of food and feeling hungry sets up cravings which can lead to binge-eating followed by feelings of guilt. Neither deprivation nor hunger are necessary to lose weight if you are willing to take time and do the right things. If you cut out just 100 calories per day, the equivalent of a single can of fizzy drink or a bedtime snack, you could lose about 10 lb (4.5 kg) in a year. If you also added a brisk walk for half an hour a day five days per week, the weight loss could increase to 20 lb (9 Kg) in a year.

3. Keep moving

Next to not smoking, regular physical activity is arguably the best thing you can do for your health. It lowers the risk of heart disease, diabetes, stroke, high blood pressure, osteoporosis, and certain cancers, and can help to control stress and boost mood. Contrary to popular belief, the evidence for a simple relationship between physical activity and weight loss is equivocal, with some studies showing that exercise helps and others suggesting that it does not, possibly due to complex interactions between physical activity, diet and genes. If moderate to vigorous over an extended period, physical activity can help to maintain a healthy weight, provided you do not compensate by eating more as a self-reward. You would have to walk for 98 minutes to burn off the calories in one Mars Bar or swim for 45 minutes to burn off one slice of a pepperoni pizza, for example. For general health, any amount of exercise is better than none. The more you do, though, the better. This does not have to mean joining a gym or jogging. Many activities count as exercise: dancing, skating, gardening, cycling, scrubbing floors, washing the car by hand, or playing with children. Incorporate activity into your day by taking the stairs rather than the escalator, getting off the bus one stop before your destination and walking the rest, cycling to do errands rather than taking the car, and cutting back on watching television, playing computer games and other sedentary activities. Start slowly and gradually build up to more vigorous activity when your fitness increases.

4. Keep track

Many of us eat without thinking and have no idea how much we have consumed. Such lack of awareness can result in us eating and drinking more than we plan to. Try keeping a daily food diary for a while. List everything that you eat or drink, no matter how insignificant it seems. The calories can really add up, even just with drinks – one can of Coca Cola contains 142 calories, for example.

5. Eat food as nature intended

Research shows that people who eat at fast-food restaurants more than twice a week are more likely to gain weight and show early signs of diabetes than those who only occasionally eat fast food.

Our bodies were designed to consume food in the form that nature provides, with nothing added and nothing taken away.

Vegetables, fruit, nuts, seeds and whole grains all contain protein, carbohydrates, essential fats, vitamins, minerals and fibre. Fibre makes the food bulkier and less nutrient dense than highly processed food. This means that you have to eat a greater quantity of unprocessed food, like vegetables, to obtain the same amount of calories as highly processed foods, such as ice cream.

In the stomach and the gut, there are stretch receptors and nutrient receptors which signal to the body that it has enough food and to stop eating. If you eat highly processed foods, which are rich in calories but poor in vitamins, minerals and essential fats, such as white sugar and white bread, your body’s mechanism for signaling that it is full does not work properly – the gut is neither fully stretched nor receives the nutrients the body needs – so you carry on eating. This increases the chance of you consuming too many calories and becoming overweight, whilst not obtaining enough vitamins, minerals and essential fats.

The more unprocessed foods, like whole grains, vegetables, nuts and seeds, you include in your diet, the easier it is for your body to obtain the nutrients it needs without over-eating. Even if all you do is have porridge for breakfast instead of eating a sugary cereal or drinking strong coffee, you will find it easier to lose weight.

6. Keep your blood sugar stable

Another advantage of a food like porridge is that it has a gentle effect on blood sugar, or what’s called a low glycaemic index. When you eat porridge, glucose is released slowly and steadily into the bloodstream which helps to maintain energy levels over a longer period of time. This reduces hunger and cravings, so you tend to eat less. Other examples include whole grains such as brown rice (especially basmati), quinoa and whole-grain breads and pasta, as well as beans, nuts, fruits, and vegetables.

Eating foods that make your blood sugar and insulin levels shoot up and then crash may contribute to weight gain. Insulin tells the body to store surplus glucose as fat, so constantly excessive levels of glucose and insulin in the blood lead to weight gain. Such foods include white bread, white rice, and other highly processed grain products. So this is another good reason to increase the amount of unprocessed whole foods in your diet and reduce the amount of processed foods rich in calories.

7. Do not be afraid of good fats

Fat in a meal or in snacks such as nuts gives the food taste and helps you to feel full. Good fats, such as olive oil, have many benefits for health, including helping to improve your cholesterol levels when you eat them in place of saturated or trans fats or highly processed carbohydrates, like sugar and white flour products.

8. Drink water rather than fizzy drinks

Drinking juice or cans of sugary drinks can give you several hundred calories a day without even realising it. Several studies show that children and adults who consume sugar-sweetened beverages are more likely to gain weight than those who don’t, and that switching from these to water can reduce weight.

Using artificial sweeteners in soft drinks instead of sugar or high-fructose corn syrup seems like it would sidestep any problems with weight or diabetes. Artificial sweeteners deliver zero carbohydrates, fat, and protein, so they can’t directly influence calorie intake or blood sugar. Over the short term, switching from sugar-sweetened soft drinks to diet drinks cuts calories and leads to weight loss. Long-term use, though, may be a different story.

Some long-term studies show that regular consumption of artificially sweetened beverages reduces the intake of calories and promotes weight loss or maintenance. Others show no effect, while some show weight gain.

One concern about artificial sweeteners is that they uncouple sweetness and energy. Until recently, sweet taste meant sugar, and thus energy. Glucose is critical for the human brain to function, so the body has delicate feedback mechanisms involving the brain, stomach, nerves and hormones, to ensure that there is always a steady supply. When we eat something sweet, the human brain responds with signals – first with signals to eat more, and then with signals to slow down and stop eating. By providing a sweet taste without any calories, artificial sweeteners could confuse these intricate feedback loops. This could potentially throw off the body’s ability accurately to gauge how many calories are being taken in. Studies in rats support this idea. Researchers at Purdue University have shown that rats eating food sweetened with saccharin took in more calories and gained more weight than rats fed sugar-sweetened food. In addition, a long-term study of nearly 3,700 residents of San Antonio, Texas, showed that those who averaged three or more artificially sweetened beverages a day were more likely to have gained weight over an eight-year period than those who didn’t drink artificially sweetened beverages. At present, research findings are mixed, but there is a possibility that diet drinks may lead to weight gain in the longer term.

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References

Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: the evidence report. National Institutes of Health, National Heart, Lung, and Blood Institute, Obesity Education Initiative

Haskell WL, Lee IM, Pate RR, et al. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Med Sci Sports Exerc. 2007; 39:1423–34

Pronk NP, Wing RR. Physical activity and long-term maintenance of weight loss. Obes Res. 1994 Nov;2(6):587-99

Fogelhom M, Kukkonen-Harjula K. Does physical activity prevent weight gain – a systematic review Obesity Reviews, Volume 1, Issue 2, 95–111, October 2000

Pereira MA, Kartashov AI, Ebbeling CB, et al. Fast–food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis. Lancet. 2005; 365:36–42

Bellisle F, Drewnowski A. Intense sweeteners, energy intake and the control of body weight. European Journal of Clinical Nutrition. 2007; 61:691-700

Swithers SE, Davidson TL. A role for sweet taste: calorie predictive relations in energy regulation by rats. Behavioral Neuroscience. 2008; 122:161-173

Fowler SP, Williams K, Resendez RG, Hunt KJ, Hazuda HP, Stern MP. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity (Silver Spring). 2008; 16:1894-1900

Frank GK, Oberndorfer TA, Simmons AN, et al. Sucrose activates human taste pathways differently from artificial sweetener. Neuroimage. 2008; 39:1559-1569

Willett, W. Eat, drink and be healthy. Harvard Medical School Guide to Healthy Eating. The Free Press; Free Press Trade Pbk. Ed edition (April 2005). ISBN: 978-0743266420.

Lisle D, Goldhamer A. The Pleasure Trap – Mastering the Hidden Force that Undermines Health and Happiness.  Healthy Living Publications, 30 March 2006

Do high fat diets make us stupid and lazy?

Rats fed a high-fat diet show a stark reduction in their physical endurance and a decline in their cognitive ability after just nine days, a study by Oxford University researchers has shown.

The research, funded by the British Heart Foundation and published in the FASEB Journal, may have implications not only for those eating lots of high-fat foods, but also athletes looking for the optimal diet for training and patients with metabolic disorders.

‘We found that rats, when switched to a high-fat diet from their standard low-fat feed, showed a surprisingly quick reduction in their physical performance,’ says Dr Andrew Murray, who led the work at Oxford University and has now moved to the University of Cambridge. ‘After just nine days, they were only able to run 50 per cent as far on a treadmill as those that remained on the low-fat feed.’

High-fat diets, such as those that are prevalent in Western countries, are known to be harmful in the long term and can lead to problems such as obesity, diabetes and heart failure. They are also known to be associated with a decline in cognitive ability over long time spans. But little attention has been paid to the effect of high-fat diets in the short term.

Physical endurance – how long we can keep exercising – depends on how much oxygen can be supplied to our muscles and how efficiently our muscles release energy by burning up the fuel we get from the food we eat. In particular, using fat as a fuel is less efficient than using glucose from carbohydrates, but the metabolic changes induced by different diets are complex and it has been controversial whether high-fat feeding for a short time would increase or decrease physical performance.

The Oxford team set out to investigate whether rats fed a high-fat diet for just a few days showed any change in their physical and cognitive abilities.

All 42 rats were initially fed a standard feed with a low fat content of 7.5 per cent. Their physical endurance was measured by how long they could run on a treadmill and their short-term or ‘working’ memory was measured in a maze task. Half of the rats were then switched to a high-fat diet where 55 per cent of the calories came from fat. After four days of getting used to the new diet, the endurance and cognitive performance of the rats on the low- and high-fat diets was compared for another five days.

‘With the standard feed, 7.5 per cent of the calories come from fat. That’s a pretty low-fat diet, much like humans eating nothing but muesli,’ says Dr Murray. ‘The high-fat diet, in which 55 per cent of the calories came from fat, sounds high but it’s actually not extraordinarily high by human standards. A junk food diet would come close to that.

‘Some high-fat, low-carb diets for weight loss can even have fat contents as high as 60 per cent. However, it’s not clear how many direct conclusions can be drawn from our work for these diets, as the high-fat diet we used was not particularly low in carbs,’ he adds.

On the fifth day of the high-fat diet (the first day back on the treadmill), the rats were already running 30 per cent less far than those remaining on the low-fat diet. By the ninth day, the last of the experiment, they were running 50 per cent less far.

The rats on the high-fat diet were also making mistakes sooner in the maze task, suggesting that their cognitive abilities were also being affected by their diet. The number of correct decisions before making a mistake dropped from over six to an average of 5 to 5.5.

The researchers also investigated what metabolic changes the high-fat diet was inducing in the rats. They found increased levels of a specific protein called the ‘uncoupling protein’ in the muscle and heart cells of rats on the high-fat diet. This protein ‘uncouples’ the process of burning food stuffs for energy in the cells, reducing the efficiency of the heart and muscles. This could at least partly explain the reduction in treadmill running seen in the rats.

The rats that were fed a high fat diet and had to run on the treadmill also had a significantly bigger heart after nine days, suggesting the heart had to increase in size to pump more blood around the body and get more oxygen to the muscles.

While this research has been done in rats, the Oxford team and Andrew Murray’s new group in Cambridge are now carrying out similar studies in humans, looking at the effect of a short term high-fat diet on exercise and cognitive ability.

The results will be important not only in informing athletes of the best diets to help their training routine, but also in developing ideal diets for patients with metabolic disorders such as diabetes, insulin resistance or obesity. People with such conditions can have high levels of fat in the blood and show poor exercise tolerance, some cognitive decline, and can even develop dementia over time.

‘These are startling results,’ says Professor Kieran Clarke, head of the research team at Oxford University. ‘It shows that high-fat feeding even over short periods of time can markedly affect gene expression, metabolism and physical performance. By optimising diets appropriately we should be able to increase athletes’ endurance and help patients with metabolic abnormalities improve their ability to exercise and do more.’

‘In little more than a week, a change in diet appears to have made the rats’ hearts much less efficient,’ says Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, who funded the research. ‘We look forward to the results of the equivalent studies in human volunteers, which should tell us more about the short-term effects of high-fat foods on our hearts. We already know that to protect our heart health in the long-term, we should cut down on foods high in saturated fat.’

For more information about the effect of diet on health, plant-based diets, recipes and tips please sign up for my free newsletter and visit my website.

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Journal reference:

Murray et al. Deterioration of physical performance and cognitive function in rats with short-term high-fat feeding. The FASEB Journal, 2009; DOI: 10.1096/fj.09-139691

Oily fish may prevent dementia

Experts estimate that over 24 million people worldwide suffer from dementia, and many of these people live in low- and middle-income countries. Recently, there has been growing interest in whether dietary factors, particularly oily fish and meat, might influence the onset and/or severity of dementia. Oily fish are rich in omega-3 long-chain polyunsaturated fatty acids, which some studies suggest are positively related to cognitive function in later life. 

Conversely, there is a suggestion from some studies that increased meat consumption may be related to cognitive decline. To examine this, a group of international researchers studied older people in 7 middle- to low-income countries. You can read the results of their study in the August 2009 issue of the American Journal of Clinical Nutrition. 

Data from 14,960 participants (≥65 y of age) living in China, India, Cuba, the Dominican Republic, Venezuela, Mexico, and Peru were analyzed. Dietary habits were assessed by using standard, culturally appropriate face-to-face interviews, and dementia was diagnosed by using validated culturally and educationally fair criteria. 

In each of the study countries, except India, there was an inverse association between fish consumption and dementia prevalence. These data extend to low- and middle-income countries previous conclusions from industrialized countries that increased fish consumption is associated with lower dementia prevalence in later life. 

The authors propose that this relation is not due to poor overall nutritional status in those with dementia, because meat consumption tended to be higher in this group. The relation between meat consumption and dementia remains unclear. 

To learn more about the effect of what we eat on the function of our brain, please come along to a Cooking for Health class on Food and Emotions, led by nutrition expert, Dr Jane Philpott

Alzheimer’s Disease, metabolic disorders and the role of diet

Accumulating evidence for the role of metabolic disorders such as insulin resistance, diabetes, obesity and hypertension in increasing the risk of Alzheimer’s disease and vascular dementia, is reviewed in a new paper published this month in the Archives of Neurology.

In the same journal, compelling evidence is presented that higher pre-diagnosis total cholesterol, low-density lipoprotein cholesterol, and diabetes are associated with faster cognitive decline in patients with incident Alzheimer’s disease.

A cohort of 156 patients with incident Alzheimer’s Disease (mean age 83 years) were followed for up to 10 years.  Changes in a composite score of cognitive ability were monitored from diagnosis onwards.

“These findings indicate that controlling vascular conditions may be one way to delay the course of Alzheimer’s, which would be a major development in the treatment of this devastating disease as currently there are few treatments available to slow its progression,”

said Yaakov Stern, Ph.D., a professor at the Taub Institute for the Research on Alzheimer’s Disease and the Aging Brain and director of the Cognitive Neuroscience Division of the Gertrude H. Sergievsky Center at Columbia University Medical Center, and senior author of the paper.

“Preventing heart disease, stroke and diabetes – or making sure these conditions are well managed in patients diagnosed with them – can potentially slow the disease progression of Alzheimer’s,” said Dr. Stern.

Diets high in fruit, vegetables, fibre and unsaturated fats, and low in sugar, salt and saturated fat are known to reduce the risk of a range of chronic conditions, such as diabetes, heart disease and stroke.  This means eating more plant-based foods and less processed and animal-based foods.

Stabilising blood sugar is crucial.  This may be done by eating a diet with a low glycaemic load, that is, one that includes moderate quantities of complex carbohydrates which release glucose slowly into the bloodstream.  Whole grains, such as whole-wheat bread, brown rice, quinoa, millet and buckwheat are valuable for helping to ensure smooth regulation of blood sugar.  In contrast, highly refined carbohydrates, such as white bread, white rice, white pasta and table sugar, create a roller-coaster of blood sugar highs and lows, which if left unchecked, can ultimately give rise to insulin resistance and eventually to diabetes.  Potatoes release sugar into the bloodstream almost as fast as table sugar and thus should be eaten sparingly, unless you are lean and exercise regularly.  Consuming protein with carbohydrates at every meal has also been found to help regulation of blood sugar.

Increasing the quantity of vegetables and fruit in the diet is also vital.  Blood sugar levels are easier to maintain if vegetables are emphasized more than fruit, as some fruit contains a lot of sugar.  A minimum of 5 portions of fruit and vegetables per day is recommended.  For easy tips for increasing the amount of fruit and vegetables in your diet please click here.

Unsaturated fats found in plant oils, such as olive oil and the oils of nuts and seeds, and in oily fish, are beneficial for preventing heart disease and other vascular health conditions.  For practical suggestions for ways to incorporate more healthy unsaturated fats in your diet please click here.

For information and practical tuition in how to put all these recommendations together to create fabulous food that protects you from diabetes, heart disease and Alzheimer’s Disease, please come to a Cooking for Health course, run by nutrition expert, Dr Jane Philpott.

Long term health is affected by maternal nutrition

This month, the British Medical Association (BMA) Board of Science has published a report on Early Life Nutrition and Lifelong Health.  The report reviews the evidence that the diets of women of reproductive age, and those of their foetuses and young children, are significant factors in influencing the risk of chronic diseases such as heart disease, diabetes, obesity, brittle bone disease and even some forms of cancer and mental illness, later in those children’s lives.

Lead author Professor Mark Hanson, director of the Centre for the Developmental Origins of Health and Disease at the University of Southampton, comments:

“Society and public health organisations need to pay much greater attention to these issues if the rising epidemic of these diseases is to be prevented. Tackling the diseases once children reach adulthood is often too late. By taking steps to improve maternal nutrition we could save many people from a lifetime of ill health.”

Unbalanced nutrition can result from both inadequate and excessive dietary intakes, and both can exist at the same time in many populations. Moreover diets which lead to over-nutrition (e.g., excess calories) are often micronutrient poor.

There is strong evidence that undernutrition (stunting or wasting) during the first two years of life leads to impaired adult cognitive, physical and economic capacity, which cannot be repaired even if nutrition improves later in childhood.

Improved availability of energy-rich foods has however, enabled large numbers of people to escape from hunger. This has brought considerable benefits, but is already giving rise to obesity and obesity-related disease. Developing countries are reporting high rates of coronary heart disease (CHD) and type 2 diabetes that have appeared in one or two generations to become leading causes of morbidity and mortality. These epidemics are expected to intensify.  By the year 2030, the prevalence of diabetes is predicted to rise by over 100 per cent in India, China, sub-Saharan Africa, Latin America, the Caribbean and the Middle East; an increase far exceeding that in high-income countries (54%).

There is good evidence that an increased deposition of fat tissue in foetuses and babies is an outcome of both undernutrition and excessive nutrition.  Low birth weight babies born to underweight women in India have proportionately more fat than would be expected for their body weight.  Maternal obesity, another form of maternal malnutrition, also increases the fat tissue of the foetus and newborn baby. This phenomenon is exacerbated further if maternal obesity is complicated by gestational diabetes.

Extremes of maternal body composition, either excessive thinness or obesity, are associated with adverse patterns of foetal and infant development leading to poorer long-term health.

“It’s not only women who need to be careful about the quality of their food intake. Prospective fathers should also eat well and steps need to be taken to ensure that young people understand the importance of good nutrition as part of their lifestyle choices.”

The numbers of women who breastfeed their infants is still too low, with many women starting to breastfeed but then stopping too soon, and many infants being fed inappropriate foods at the weaning stage.  Breastfeeding rates in the UK are much lower than in many European countries. Less than1 per cent of mothers in the UK are exclusively breastfeeding at six months.

While there are gaps in the evidence about the long-term consequences of poor maternal and infant nutrition, and we do not as yet understand the mechanisms fully, it is clear that steps need to be taken to promote healthy diets in young women and their families, to encourage breastfeeding and the use of appropriate complementary foods.

More advice could be given to people with young children about the importance of a balanced diet for those children and more support could be given to women to help them start breastfeeding and to continue with it.

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Weight loss diets – a new study asks which are the best?

Many popular diets emphasize either carbohydrate, protein or fat as the best way to lose weight.

Advocates of high protein diets claim that our Paleolithic ancestors obtained the majority of their calories from meat and thus our bodies have evolved to require a high protein intake.  There is much scientific controversy over the relative importance of animal and plant foods in the early hominid diet.  Direct evidence in the form of food remains is meagre or, at best, equivocal.  Most research relies on inference through dietary studies of other primates and archaeological evidence.  Most scientists now agree that plant foods contributed much more to the early hominid diet than did the flesh of animals. 

Humans have adapted to their environments wherever they have settled and the balance between meat-eating and plant-eating varies substantially between populations.  Some of the leanest and healthiest societies in the world, such as in the Mediterranean and Japan, consume a diet where the majority of energy comes from carbohydrates, mainly in the form of complex carbohydrates from whole grains and vegetables.  This has led some researchers to propose that a high carbohydrate diet is better for maintenance of a healthy weight than a high protein diet.

Controversy about the role of fat in the diet has raged since the 1950s, when Ancel Keys published his landmark “Seven Countries” study and highlighted that coronary heart disease is strongly related to diet.  Low-fat diets have therefore been promoted by governments and health professionals for several decades.

With the prevalence of obesity increasing at an alarming rate, everyone wants to know which of these dietary approaches – high protein, high carbohydrate, low fat – is the most successful for weight loss.

The scientific research conducted to date does not help much.  Some trials have shown that low-carbohydrate, high-protein diets resulted in more weight loss over the course of 3 to 6 months than conventional high-carbohydrate, low-fat diets, but other trials have not shown this effect.

A smaller group of studies that extended the follow-up to 1 year did not show that low-carbohydrate, high-protein diets were superior to high-carbohydrate, low-fat diets.  In contrast, other researchers found that a very-high-carbohydrate, very-low-fat vegetarian diet was superior to a conventional high-carbohydrate, low-fat diet.  Among the few studies that extended beyond 1 year, one showed that a very-low-fat vegetarian diet was superior to a conventional low-fat diet, one showed that a low-fat diet was superior to a moderate-fat diet, two showed that a moderate-fat, Mediterranean-style diet was superior to a low-fat diet, one showed that a low-carbohydrate diet was superior to a low-fat diet, and another showed no difference between high-protein and low-protein diets.

Small samples, underrepresentation of men, limited generalizability, a lack of blinded ascertainment of the outcome, a lack of data on adherence to assigned diets, and a large loss to follow-up limit the interpretation of many weight-loss trials.  The novelty of the diet, media attention, and the enthusiasm of the researchers may affect the adherence of participants to any type of diet.

There have been few studies lasting more than a year that evaluate the effect on weight loss of diets with different compositions of those nutrients. In a randomized clinical trial led by researchers at the Harvard School of Public Health (HSPH) and Pennington Biomedical Research Center of the Louisiana State University System, a comparison of overweight participants assigned to four different diets over a two-year period showed that reducing calories achieved weight loss regardless of which of the three nutrients was emphasized. The study, which was funded by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health, appears in the February 26, 2009 issue of The New England Journal of Medicine.

“This is important information for physicians, dieticians and adults, who should focus weight loss approaches on reducing calorie intake,” said Frank Sacks, professor of cardiovascular disease prevention at HSPH and lead author of the study.

The trial included 811 men and women who were randomly divided into four diet groups with different target nutrient compositions:

• Low-fat, average protein: 20% of calories from fat, 15% of calories from protein, 65% of calories from carbohydrate
• Low-fat, high-protein: 20% fat, 25% protein, 55% carbohydrate
• High-fat, average protein: 40% fat, 15% protein, 45% carbohydrate
• High-fat, high-protein: 40% fat, 25% protein, 35% carbohydrate

The participants were diverse in age, sex (62% women, 38% men), geography and income. The diets followed heart-healthy principles, replacing saturated with unsaturated fat and were high in whole cereal grains, fruits and vegetables. Each participant received a diet prescription that encouraged a 750-calorie reduction per day, however none were less than 1,200 total calories per day. Participants were asked to do 90 minutes of moderate exercise each week. They recorded their daily food and drink intake in a food diary and in a web-based program that provided information on how closely they were meeting their dieting goals. Individual counselling was provided every eight weeks over two years and group sessions were held three out of four weeks during the first six months and two out of four weeks from six months to two years.

The results showed that, regardless of diet, weight loss and reduction in waist circumference were similar. Participants lost an average of 13 pounds at six months and maintained a 9-pound loss at two years. Weight loss primarily took place in the first 6 months; after 12 months, all groups began to slowly regain weight, a finding consistent with other diet studies. However, the extent of weight regain was much less, about 20%, of the average regain in previous studies. Waistlines were reduced by an average of two inches at the end of the two-year period.

Most risk factors for cardiovascular disease improved for dieters at six months and two years. HDL (“good”) cholesterol increased and LDL (“bad”) cholesterol, triglycerides, blood pressure and insulin decreased. The metabolic syndrome, a group of coronary heart disease risk factors including high blood pressure, insulin resistance and abdominal obesity, also decreased.

The main finding from the trial was that diets with varying emphases on carbohydrate, fat and protein levels all achieved clinically meaningful weight loss and maintenance of weight loss over a two-year period.

“These results show that, as long as people follow a heart-healthy, reduced-calorie diet, there is more than one nutritional approach to achieving and maintaining a healthy weight,” said Elizabeth G. Nabel, M.D., Director, NHLBI.

Another important finding was that participants who regularly attended counselling sessions lost more weight than those who didn’t. Dieters who attended two thirds of sessions over two years lost about 22 pounds of weight as compared to the average weight loss of 9 pounds.

“These findings suggest that continued contact with participants to help them achieve their goals may be more important than the macronutrient composition of their diets,” said Sacks.

Have you spent years embarking on every weight-loss diet going?  Have you tried cutting out entire food groups?  Have you spent a fortune on miracle foods or diet powders?  Have you eaten nothing except cabbage soup for weeks?  Have you driven your friends mad with your fervour over food combining?  Have you become obsessive about counting calories or points?  Have you spent hours jumping on and off your bathroom scales?  Do you feel hungry much of the time, exhausted and beset by cravings?

You can learn how to lose weight effortlessly without feeling hungry, whilst gaining health and vitality, at a Cooking for Health course on Managing Your Weight Naturally.  We explore why so many diets fail and explode many of the weight loss myths.  We look at cravings – how they arise and how to overcome them – and we discuss which foods the body needs to create energy and burn fat in the most efficient way.  We create a delicious meal with an array of different dishes designed to illustrate how it is possible to eat plenty without gaining weight.  The vital role of exercise in maintaining a healthy weight is also emphasised.

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