The NHS turns 70 this year, and it’s Britain’s greatest medical innovation

Our health service stands alongside other brilliant inventions, such as penicillin, IVF and artificial hips. We must make sure it is fit for the decades to come

The NHS will celebrate its 70th birthday in 2018, after a difficult decade since the global financial crisis culminating in one of the most testing years in our history. The terrorist attacks in London and Manchester, along with the Grenfell Tower tragedy, saw all emergency services, including NHS staff, respond with skill and bravery.

In 1948, at the NHS’s founding, there were no routine antibiotics, anti-cancer drugs or blood pressure treatments, and infectious diseases were common. This has all changed, thanks in part to British science, which has brought the world vaccination, penicillin, IVF, stem cell transplants, artificial hips and MRI scanners, and knowledge of the structure of DNA.

But our greatest innovation by far, with the most far-reaching impact on the health of our nation, has been the NHS. It embodies the British social conscience. Since resources are very stretched, some may question the funding model, and suggest the NHS is not fit for the future. Nothing could be further from the truth. Scientific advances mean it is needed more now than ever before.

Growing up in Africa in the 1960s, I dreamed of moving to Britain and working for its health service. Fulfilling that dream has been a huge privilege. As national medical director I have learned that the NHS will always need to change to match emerging science and shifting disease profiles, and to meet increasing demand within a set budget.

So in the next two years alone we’ll deliver cutting-edge genomic testing for personalised cancer care, a 10% reduction in hepatitis C deaths, and advanced proton beam therapy. And as individual treatments continue to change, so too must the way we provide services: hospitals and GP surgeries still look much as they did when the NHS was founded.

Over the next 12 months we will step up efforts to get different parts of the NHS working better together. Technology will play a part, with more appointments bookable online and greater access to patient records.

Already, in Rushcliffe, Nottinghamshire, extra support for care home residents means they go to A&E nearly a third less often and are almost a quarter less likely to need admission. In Dudley, West Midlands, doctors, nurses and others have worked together to reduce time spent in hospital by the equivalent of 9,600 bed days.

This year NHS bodies in eight places will come together with local councils and other organisations to work as complete care systems, with the needs of patients, not those of institutions, driving decision-making. Local councils can support the NHS through disease prevention via education, housing and transport policies, and social services can help keep people out of hospital. Rather than being the Trojan horse for privatisation that some critics may fear, this is a bold attempt to unite a fractured system and stop people being pushed from pillar to post.

Scientific progress means that soon we will be able to partially predict the future health risk of each child, and hence of the population at large. This science ratifies the wisdom of the founding principles of our NHS, where we share the burden of those risks and pool our money through taxation in order to treat each patient fairly. Our task now as a nation is to enable the NHS to properly adapt to medical advances and public expectations.

This is a challenge. The good news is that, as it heads into its 70th birthday year, we can say that the future of the health service is already in sight in parts of the country, but just not everywhere.

 Bruce Keogh is medical director of the National Health Service in England

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How Britain plans to lead the global science race to treat dementia

It has struck nearly a million people in the UK, yet even its cause is still unclear

CT scans of a brain showing the progress of Alzheimer’s disease. Atrophy is shown by enlarged ventricles (white areas at the centre).
CT scans of a brain showing the progress of Alzheimer’s disease. Atrophy is shown by enlarged ventricles (white areas at the centre). 

Early next year, Professor Bart De Strooper will sit down in an empty office in University College London and start to plan a project that aims to revolutionise our understanding and treatment of dementia. Dozens of leading researchers will be appointed to his £250m project which has been set up to create a national network of dementia research centres – with UCL at its hub.

The establishment of the UK Dementia Research Institute – which was announced last week – follows the pledge, made in 2012 by former prime minister David Cameron, to tackle the disease at a national level and comes as evidence points to its increasing impact on the nation. Earlier this year, it was disclosed that dementia is now the leading cause of death in England and Wales. At the same time, pharmaceutical companies have reported poor results from trials of drugs designed to slow down the progress of Alzheimer’s disease, the most common form of dementia.

“Humans have truly wonderful brains that can cope with terrible diseases like Alzheimer’s for decades and can find all sorts of ways to get around defects that are growing inside,” said De Strooper, who is currently based at the University of Leuven in Belgium. “Eventually individuals succumb to the condition and start to display memory loss and other symptoms – but usually only after decades have passed and their brains have gone through considerable changes. This makes it very difficult to treat the disease. That is the challenge that we need to tackle.”

Current understanding of Alzheimer’s suggests the disease is triggered when beta amyloid, a protein in nerve cell membranes, starts to clump together. Slowly the brain undergoes metabolic changes as amyloid clumping continues. In particular, a protein known as tau, which is involved in memory storage, is affected. It starts to form tangles inside the brain’s neurons and these die off. Eventually, symptoms – such as severe memory loss – manifest themselves.

To date, most attempts at drug interventions have focused on medicines that could prevent beta amyloid from forming clumps, the most recent being Solanezumab, developed by the pharmaceutical company Eli Lilly. However, results of clinical trials of the drug – revealed last month – indicated that it had no significant effect on the thinking abilities of people with mild Alzheimer’s. Solanezumab had also failed in people with more advanced versions of the disease in earlier trials.

This double failure has led some scientists to argue that amyloid clumping is not a cause of the disease but is merely a symptom. By targeting it, scientists are wasting time, it is argued. Professor John Hardy, a geneticist based at UCL – who has played a key role in setting up the college’s Dementia Research Institute – does not agree. “All the evidence we have from families affected by early onset dementia indicates that the disease begins with the deposition of amyloid plaques in the brain,” he said. “The trouble is that this buildup starts 15 to 20 years before dementia’s symptoms appear. The drugs we have developed so far offer treatments that are, in effect, too little and too late.”

Hardy drew a parallel between cholesterol buildup in blood vessels that eventually leads to cardiac disease and the buildup of amyloid plaques in the brain and the onset of Alzheimer’s. “Unfortunately, we have no equivalent of a cholesterol test to assess how much amyloid is clumping in a person’s brain,” he added. “However, that could change in the near future.”

Research suggests between 20 and 30 genes are involved in predisposing people to Alzheimer’s.
Research suggests between 20 and 30 genes are involved in predisposing people to Alzheimer’s. 

Recent research has pinpointed a group of around 20 to 30 genes that are involved in predisposing individuals to Alzheimer’s. These genes come in different variants. Some variants of a gene predispose individuals to dementia more than other variants of that gene. If a person inherits a package of genes made up of variants that particularly predispose to dementia, they are very likely to develop Alzheimer’s.

“We are now within five years of developing a chip that will be able to tell – from a blood test – whether a person is likely to have amyloid plaques forming inside their brains in middle age,” added Hardy. “This would then be followed up by a brain scan to confirm if this is true or not.”

This would be dementia’s equivalent of a cholesterol test. The problem is that there is, as yet, no equivalent of drugs which would halt this amyloid buildup in a way that parallels the use of statins to block buildups of cholesterol, once detected, and so head off cardiac illness. For their part, researchers argue that the use of drugs like Solanezumab – although seemingly ineffective on patients in whom amyloid plaques have become established – could be far more effective in the early stage of the condition.

Many other issues complicate our understanding of dementia, however. “A good example is provided by the immune system,” said David Reynolds, chief scientific officer of Alzheimer’s Research UK. “There is a lot of evidence now that the immune system is involved in the development of Alzheimer’s after beta amyloid clumps appear.”

However, the nature of that immune response is still not fully understood. “We do not know whether the immune system tends to overreact – as with conditions like rheumatoid arthritis in which the body’s own tissue is attacked by its own immune defences – or react weakly and allow amyloid clumps to develop when they could be stopped,” added Reynolds. “Certainly it would be unwise to wade in with drugs until we know exactly what it is we want to achieve.”

And this is where the distributed nature of the Dementia Research Institute network could prove important. Based in different university cities (Edinburgh, Oxford and Cambridge are all candidates for units), these outlying centres will focus on different aspects of the disease: environmental factors, care of dementia patients – and immunology. “The creation and direction of these centres will depend on existing expertise at that university,” added Reynolds. “A centre that focuses on immunology and dementia would be particularly useful in finding new ways to tackle the condition.”

The Dementia Research Institute network is to be supported, over the next 10 years, by £150m funding from the Medical Research Council – with further inputs of £50m each being made by Alzheimer’s Research UK and by the Alzheimer’s Society. This commitment marks a significant increase in dementia research in the UK, which had already raised its annual funding from £50m in 2008 to £90m in 2012 and is now a world leader in the field.

“It is good news but we need to put it in perspective,” said James Pickett, of the Alzheimer’s Society. “In 2012 we spent more than £500m on cancer research; there are five times more researchers working on cancer in the UK; while the number of clinical trials of dementia drugs is less than 1% of those of cancer drugs.”

At the same time, the need for some form of treatment to tackle dementia is becoming increasingly urgent. More and more people are living to their 80s and 90s when their chances of getting dementia increase markedly. There are currently 850,000 people with dementia in the UK, a figure that will rise to one million by 2025 and two million by 2051.

“We are going to have to be very nuanced in understanding all the risk factors involved in dementia – and in appreciating why factors like education and general health provide some protection against its onset,” said Professor Carol Brayne, of Cambridge. “That is going to be the strength of the institute. It offers us the opportunity, for the first time, to follow so many different avenues and approaches to dealing with and understanding the dementia.”


Dementia overtook heart disease as the leading cause of death in England and Wales last year. More than 61,000 people died of the condition in 2015, 11.6% of all recorded deaths.

The Office for National Statistics said the increase had occurred because people were living for longer while deaths from other causes, including heart disease, had gone down. In addition, doctors are now better at diagnosing dementia, and it is appearing more often on death certificates.

The bulk of dementia deaths last year were among women: 41,283, compared to 20,403 in men.

According to the Alzheimer’s Society, dementia is the only one of the top 10 causes of death that we cannot prevent or even slow down.

The leading cause of dementia is Alzheimer’s disease, which accounts for 62% of all cases in the UK: 520,000 of the 850,000 people living with dementia in the UK today. Other forms of the disease include vascular dementia and Lewy Body dementia.

Dementia costs the UK economy approximately £26bn per year, according to the Alzheimer’s Society.

If a drug could be found to slow cognitive decline in dementia, that would delay the need for paid care and reduce the financial burden on families, the NHS and social care.

PressTV – UK food poverty turns into ‘health emergency’.

Food poverty in Britain has currently reached the levels of a “public health emergency,” a group of doctors and academics warn.

“This (food poverty) has all the signs of a public health emergency that could go unrecognized until it is too late to take preventive action,” health experts said in a letter to the British Medical Journal (BMJ).

Experts also raised concerns over the increase in the use of food banks and the number of malnourished cases, linking the problem to the rising cost of living and the UK government’s changes to the country’s welfare system.

They cited that the government statistics show the number of malnutrition-related admissions to hospitals across England has more than doubled since 2008-09.

Moreover, public health professionals draw attention to a recent report from the Institute for Fiscal Studies (IFS) which found a decrease in the amount of calories consumed by British families.

Chris Mould, chief executive of the Trussell Trust, Britain’s largest organizer of food banks, urged the government to set up an inquiry into food poverty.

“These alarming developments point towards serious trouble for the nation in the years ahead unless urgent action is taken now,” Mould said.

Earlier in November, a survey showed that more than a quarter of adults in Britain have experienced food poverty during the last 12 months.

According to the poll, conducted by the Trussell Trust, store giant Tesco and food redistribution charity FareShare, some 27 percent of British adults said they found it harder to feed their family than a year ago.

British forests under threat.

Ash dieback

A year after the first case of ash dieback in wild trees in Britain, the disease has now spread across much of England, Wales and Scotland. The public is being asked to be the “eyes and ears” of the countryside amid concern about new global threats that could spell disaster for forests.

Six most unwanted tree pests

Oak processionary moth
  • Oak processionary moth (pictured): first detected in Ealing and Richmond in 2006, then outbreaks in south London, west London and Berkshire – it defoliates and weakens trees, making them susceptible to pests and diseases
  • Asian longhorn beetle: wood-boring insect that can cause damage to a range of trees – a major 2012 outbreak in Kent was traced to wood packaging imported from the Far East
  • Citrus longhorn beetle: a few have arrived on trees imported from China, Japan and South Korea, but have so far been intercepted
  • Chalara dieback of ash: fungal disease of ash trees, now established in the UK, which causes crown death and wilting and dieback of branches
  • Pine processionary moth: insect moving north through France and now breeding near Paris – 1995 outbreak in Scotland was contained
  • Emerald Ash borer: beetle that damages ash trees – a native of Asia, it’s arrived in the US in imported wooden packing material

Source: The OPAL Tree Health Survey

In a London park, forester Simon Levey is checking a moth trap strung high in the canopy of an oak tree.

He is searching for signs of the oak processionary moth, which is present in parts of the capital and Berkshire.

When the moth’s caterpillars emerge from their nests, they can strip oak trees bare and harm human health.

“What we’re looking for in these oak trees we see around us is their nests,” says Mr Levey.

“They’re like a grey wart on the side of a tree that can range from the size of a golf ball, if not smaller, to things that are almost a couple of foot in size.”

It is the moth’s caterpillars – with their thousands of tiny hairs – that are the hazard. Touching the caterpillars or their nests can cause skin rashes or, in extreme cases, sore throats, breathing difficulties and eye problems.

In Croydon, inspections are being carried out for the moth around a 2km zone as part of a rigorous programme of control and monitoring. Infected areas are sprayed with a bacteriological agent to destroy nests and caterpillars.

The traps – which contain a sex hormone that attracts male moths – are set outside from July to September, when adult moths are in flight, to see how far they have spread.

“We’ve actually created a ring of traps for these moths round the infected area just to see if the moths are flying beyond where we would expect them to be,” says Mr Levey.

The trap
Traps contain a sex hormone to attract the oak processionary moth

Dr Nigel Straw from the Centre for Forestry and Climate Change at the Forestry Commission says monitoring is key to organising a control programme – including surveys from the ground and pheromone trapping.

Oak processionary moth caterpillars

Any moths captured are sent to the Forestry Commission’s research station in Hampshire for analysis.

“We will look at how many moths have been caught and at which locations and this will tell us where we are likely to have trees with eggs which will lead to infestations next year,” says Dr Straw.

Officials hope the outbreak in Croydon can be contained. But they accept the battle is lost in west and south-west London – where the moth is here to stay.

Britain should expect “many hundreds” more pests and pathogens to arrive in the coming years, say scientists at Exeter University.

The rise in global trade means pests that damage crops such as fungi, beetle and moths are now moving into new territories faster than other wildlife, aided by climate change, they report in the journal Nature Climate Change.

Hundreds of pests and pathogens have shifted their ranges towards the poles by an average of about 3km a year since 1960.

Insects are moving even faster, expanding their range by tens of kilometres a year, says Dr Daniel Bebber.

“We know things are spreading and part of that spread is due to climate change. It’s just one more impact that climate change is having on us. Things are being introduced all the time to different places. Climate change can help things to establish.”

In Croydon, Simon Levey is concerned about a decline if not a “potentially catastrophic loss” of some of Britain’s dominant tree species, including the oak.

Close-up of layers of bark with the disease
Bark from a tree with symptoms of acute oak decline in Surrey

He says acute oak decline is present in the area, but it is difficult to identify.

“There’s huge pressure on resources in terms of actually getting out there and identifying them,” he says, “I suspect that if things progress as they do, we might face a real problem with our oak trees – a significant change in our landscape similar to the landscape changes when Dutch elm disease had its heyday in the ’70s.”

With only limited government resources to monitor for new pests, some of that job may fall to the public.

This is not unprecedented. In the past, the citrus longhorn beetle, which can arrive on deliveries from Asia of tree and shrub plants, and goods in wooden crates and packaging, has been spotted by vigilant members of the public. In July, Martin Ward, the UK government‘s chief plant health officer, asked for help from the public to spot Asian longhorn and citrus longhorn beetles.

“Government plant health services cannot do this work alone, and we need the public to act as our eyes and ears in gardens, parks, woodlands and workplaces to help us spot threats quickly before they become a serious problem,” he said.

“The public can really help us at this time of year by looking out for these two potentially serious beetle pests. They thrive in climates similar to ours, and their establishment could result in losses of trees from a wide range of species.”

Spraying pesticide in New York, 2005
Spraying pesticide in Central Park to kill Asian long-horned beetles

The Woodland Trust is currently training volunteers to look out for signs of tree diseases, while a citizen science project, known as Opal (Open Air Laboratories), is harnessing people-power to build a national picture of tree health. In the long term, however, there are big questions about the future shape and role of Britain’s treescape.

“What protects trees in the long term is diversity both in species and genetics,” says Dr Bebber.

“We don’t have a very diverse tree flora – both in genetics and species diversity. We lost our elms in large because they were so genetically uniform.

“We can learn from the science of ecology and evolution and look at the natural world and see that diversity is the protection. We certainly don’t want to see the oak disappearing, the ash disappearing – it would be a sadder Britain.”

Woodland Trust worker disinfects his boots at Pound Farm Woodland
Ash dieback threatens the UK’s population of 80 million ash trees