Facebook Founder and CEO Mark Zuckerberg delivers the commencement address at Harvard's 366th commencement exercises on May 25, 2017 in Cambridge, Massachusetts
Finding your purpose can seem daunting, but Facebook founder and CEO Mark Zuckerberg says it's also not enough.
"Today I want to talk about purpose. But I'm not here to give you the standard commencement about finding your purpose. We're millennials. We'll try to do that instinctively," says Zuckerberg.
"Instead, I'm here to tell you finding your purpose isn't enough. The challenge for our generation is creating a world where everyone has a sense of purpose," he says.
"As I've traveled around, I've sat with children in juvenile detention and opioid addicts, who told me their lives could have turned out differently if they just had something to do, an after school program or somewhere to go. I've met factory workers who know their old jobs aren't coming back and are trying to find their place," he says.
"To keep our society moving forward, we have a generational challenge — to not only create new jobs, but create a renewed sense of purpose."
Zuckerberg lays out three ways that the next generation should go about building a world where everyone has the opportunity to have purpose.
1. Take on "big, meaningful" projects
Previous generations rallied together to put a man on the moon, build the Hoover Dam and immunize children against polio, he says. These monumental efforts give entire communities a sense of purpose.
Tackling the largest problems in society today can be overwhelming, but he advises young people not to be intimidated if they don't know exactly what they are doing or how to fix the problem.
"I know, you're probably thinking: I don't know how to build a dam, or get a million people involved in anything. But let me tell you a secret: no one does when they begin. Ideas don't come out fully formed. They only become clear as you work on them. You just have to get started," he explains.
"If I had to understand everything about connecting people before I began, I never would have started Facebook."
According to Zuckerberg, large problems young people could tackle include fixing climate change, improving health care and modernizing the voting process.
2. Fix inequality so that everyone can chase their dreams
Zuckerberg says part of the reason he was able to build Facebook is that support from his family meant he was not scared of trying things. His father was a dentist and they were financially secure.
"The greatest successes come from having the freedom to fail," and he had that, he says.
"If I had to support my family growing up instead of having time to code, if I didn't know I'd be fine if Facebook didn't work out, I wouldn't be standing here today," he explains.
"We should explore ideas like universal basic income to give everyone a cushion to try new things. We're going to change jobs many times, so we need affordable childcare to get to work and healthcare that aren't tied to one company," he says.
"We're all going to make mistakes, so we need a society that focuses less on locking us up or stigmatizing us. And as technology keeps changing, we need to focus more on continuous education throughout our lives."
3. Build a global community
At a time when President Donald Trump was elected on a nationalist platform and the United Kingdom elected to remove itself from the European Union, Zuckerberg argues for building global communities.
"We have grown up connected," says Zuckerberg. "In a survey asking millennials around the world what defines our identity, the most popular answer wasn't nationality, religion or ethnicity; it was 'citizen of the world.' That's a big deal. Every generation expands the circle of people we consider 'one of us.' For us, it now encompasses the entire world."
Building communities, even global ones, though, starts on a local level, he says.
"Change starts local. Even global changes start small — with people like us. In our generation, the struggle of whether we connect more, whether we achieve our biggest opportunities, comes down to this — your ability to build communities and create a world where every single person has a sense of purpose."
Equipment: pancake griddle, or non-stick frying pan
1. In a mixing bowl, sieve together the dry ingredients: flour, bicarbonate of soda, cream of tartar and sugar. Add to this the milk and egg and whisk to a smooth batter, finally adding the warm melted butter. Pass through a sieve to get rid of any lumps and if necessary thin with more milk. The batter should have a dropping consistency, but remain thick enough to retain its shape on the griddle.
2. Heat the griddle (or frying pan) over a medium heat and grease with clarified butter. Using a dessert spoon or small ladle, carefully pour spoonfuls of the batter on to the griddle. After one side has cooked, flip the scones with a palette knife to cook the other. Once you feel more confident you can cook a few scones at a time, being careful not to let them over-cook on either side.
3. Serve warm with butter and home-made preserves.
Flaked Salmon, Broad Bean and Tarragon Quiche
Serves 4–6.
For the pastry: 125g (1 cup) plain flour a pinch of salt 25g (1/8 cup) cold butter, diced 25g (1/8 cup) lard 2 tablespoons milk (Or use 1 × 250g block of ready-made shortcrust pastry)
For the filling: 75ml (1/3 cup) milk 75ml (1/3 cup) double cream 2 medium free-range eggs 1 tablespoon fresh tarragon, chopped salt and pepper 50g (½ cup) cheddar cheese, grated 100g (¾ cup) poached salmon, flaked 60g (1/3 cup) cooked and shelled broad beans or soya beans
Equipment: 20 cm/8″ flan tin
1. Preheat the oven to 190°C (375°F, gas mark 5).
2. To make the pastry, sieve the flour and salt into a bowl, add the fats and rub the mixture through your fingertips until you get a sandy, breadcrumb-like texture. Add the milk a little at a time and bring the ingredients together into a dough. Cover and allow to rest in the fridge for 30–45 minutes.
3. Lightly flour the work surface and roll out the pastry to make a circle a little larger than the top of your flan tin and approximately 0.5 cm thick. Line the tin with the pastry, taking care not to make any holes in it or the filling will leak. Cover and rest for a further 30 minutes in the fridge.
4. Line the pastry case with baking paper, add baking beans and bake blind for 15 minutes. Remove from the oven and take out the baking paper and beans.
5. Reduce the oven temperature to 150°C/300°F/gas mark 2.
6. Beat together the milk, cream, eggs, herbs and seasoning. Scatter half of the grated cheese in the blind-baked pastry case, top with the flaked salmon and beans, and then pour over the milk-and-egg mix. If required, give the filling a gentle stir to ensure it is is evenly dispersed, but again be careful not to damage the pastry case. Sprinkle over the remaining cheese. Place into the oven and bake for 20–25 minutes until set and lightly golden.
Carrot Cake
Ingredients: 2 small free-range eggs 105g (½ cup) dark brown sugar 105g (½ cup) soft brown sugar 150g (11/8 cups) wholemeal flour ¼ teaspoon salt ½ teaspoon bicarbonate of soda ½ teaspoon ground nutmeg 1 teaspoon ground cinnamon 35g (1/8 cup) sour cream 105g (3/8 cup) sunflower oil 180g (3 cups) carrots, grated 45g (½ cup) desiccated coconut For the cream cheese topping: 110g (½ cup) full-fat soft cream cheese 50g (¼ cup) unsalted butter 50g (1/3 cup) icing sugar juice of ½ lemon
Equipment: 18 cm/7″ cake tin
1. Preheat the oven to 170ºC (325ºF, gas mark 3).
2. Prepare the cake tin by greasing with butter and lining the bottom and sides with baking paper. Place the lined tin on to a flat, heavy-duty baking tray and leave to one side until required.
3. Whisk together the eggs, sugars and sunflower oil in a bowl until thoroughly mixed. In a separate bowl, sift together the flour, salt, bicarbonate of soda and spices. Fold the dry ingredients into the egg mix until all ingredients are combined evenly. Finally, fold through the grated carrots and sour cream.
4. Pour the carrot cake mix into the lined cake tin. Place on the middle shelf of the preheated oven and bake for approximately 35 minutes, or until the cake springs back when touched. Once baked, remove from the oven and allow to cool on a wire rack.
For the cream cheese topping: 5. Sift the icing sugar into a bowl and add the softened butter. Beat well until light and fluffy. Add the cream cheese and continue beating until a smooth consistency is achieved. Finally, slowly add the lemon juice whilst still mixing.
To assemble the carrot cake: 6. Once completely cool, remove the carrot cake from the cake tin and place on your desired serving plate or cake stand. Using a palette knife, carefully smooth the cream cheese topping evenly across the top of the cake.
Victoria Sponge
For the Victoria sponge: 3 free-range eggs 150g (¾ cup) unrefined caster sugar 150g (2/3 cup) unsalted butter, softened 150g (1¼ cups) self-raising flour, sieved ½ teaspoon of vanilla essence
For the vanilla buttercream: 150g (2/3 cup) unsalted butter, softened 220g (1¾ cups) icing sugar, sieved 1/3 split vanilla pod
And strawberry jam
Equipment: 2 × 20 cm/8″ Victoria sponge cake tins
1. Preheat the oven to 180ºC (350ºF, gas mark 4).
2. Prepare the cake tins by greasing with butter and lining the bottom with a circular piece of baking paper. Leave to one side until required.
3. Cream together the caster sugar, vanilla essence and softened butter in a bowl until light and fluffy. Gradually add the beaten eggs, a little at a time to avoid the mixture curdling. Finally, fold through the sieved flour until all the ingredients are perfectly combined.
4. Divide the cake mix evenly between the two prepared cake tins and carefully smooth the mix to create two level layers. Place on the middle shelf of the preheated oven and bake for approximately 20 minutes or until the cake appears golden brown and an inserted skewer comes out clean. Once baked, remove from the oven and allow to cool slightly before turning the cakes out on to a wire rack.
To make the buttercream: 5. Cream the softened butter with the sieved icing sugar and the seeds from the split vanilla pod. The buttercream will become pale and fluffy with little flecks of vanilla seeds throughout.
To assemble the Victoria sponge: 6. Once the cakes have completely cooled, carefully and evenly spread a layer of buttercream on to the top of the first cake. Next add a thick layer of your home-made jam, before carefully placing the second cake on top of the jam and very gently pressing down. Finally, dust the top of the cake with icing sugar.
EquipmentElectric mixer or bowl and whisk Disposable piping bag (optional) Mini muffin tray
1. Preheat the oven to 170C. Beat together the egg whites, ground almonds and sugar until thick and smooth. Stir in the almond extract.
2. Set aside for five minutes to rest, before pouring into a piping bag. Rest in the fridge for half an hour.
3. I like my macaroons really chewy. In order to achieve this, the batter needs to be quite runny - too runny to effectively shape into biscuits. You can add an additional 50g of almonds, if you wish to roll the biscuits out, but I find that baking the macaroons in a mini muffin tray means your batter can be very loose.
4. Squeeze a tablespoon of the batter into each muffin hole. Sprinkle the top of each macaroon with chopped almonds. Bake for around 20 minutes, until lightly golden, and set on top.
Cool completely before serving with tea or coffee.
A eulogy to the NHS: What happened to the world my generation built?
In 1926, Harry Leslie Smith's sister died of TB in a workhouse infirmary, too poor for proper medical care. In 1948, the creation of the NHS put a stop to all that. In an extract from his new book, Harry's Last Stand, he describes his despair at the coalition's dismantling of the welfare state
Harry Leslie Smith: 'The creation of the NHS made us understand that we were our brother’s keeper.' Photograph: Sarah Lee for the Guardian
Amidwife with a penchant for gin delivered me into the arms of my exhausted mother on a cold, blustery day in February 1923. I slept that night in my new crib, a dresser drawer beside her bed, unaware of the troubles that surrounded me. Because my dad was a coal miner, we lived rough and ready in the hardscrabble Yorkshire town of Barnsley. Money and happiness didn't come easily for the likes of us.
Considering the hunger, the turmoil and the squalor in Britain during the early years of the 20th century, it was miraculous that I lived to see my third birthday. That I survived colic, flu, infection, scrapes and bangs without the benefits of modern sanitation, hygiene or health care, I must give thanks to my sturdy peasant genes. As a baby, I was ignorant of the great sorrow that enveloped England and Europe like a damp, grey fog. The nation was still in mourning for her dead from the world's first Great War. It had ended only five short years before my arrival. Nearly a million British soldiers had been killed in that conflict. It had begun in farce in 1914 and ended in bloody tragedy in 1918. In four years, that war killed more than 37 million men, women and children around the world.
Even when the guns across the battlefields were made dumb by peace, the killing didn't stop. Death refused to take a holiday and a pestilence stormed across the globe. It was called the Spanish flu. The pandemic lasted until 1921 and erased 100 million people from the ledger book of the living.
Like most people in Barnsley, my family occupied a terraced house. They were built back-to-back and in a row of 10 units. There was little space, privacy or comfort for us or any of the other occupants. It was just a place to rest your head after spending 10 hours hacking coal from the side of a rock face hundreds of feet below ground. Three walls out of four were connected to another household.
Barnsley covered in snow, 1930. Photograph: Fox Photos
The floors were made of hard slate rock and were sparsely covered with old rags that had been hand-woven into coarse mats. The interior walls were comprised of wet limestone coated in a gruel-thin whitewash that never seemed to look clean.
In summer our home was hot, in autumn damp, and in winter bitterly cold, while spring was as wet as autumn again. The house had no electricity and only the parlour and scullery possessed a gaslight fixture. After sunset, it sputtered and hissed a gloomy yellow light that illuminated our poverty. I shared a room with my older sister, Alberta. We slept together on a straw mattress that was host to many insects and reeked of time and other people's piss. Its covering was made from a rough material that was as uncomfortable to me as the occasions when my father tickled my face with his moustache. Depending on the season, I slept in my undershirt or remained fully clothed. During the cold months, Alberta and I nestled together and shared our body heat to stave off the chilling frost beating against the windowpane. Our parlour had no furniture except a stool and an upright piano that had come as part of my dad's legacy from his father. But it stood mute against the wall because the room was occupied by my infirm and dying eldest sister, Marion.
At the age of four she had contracted tuberculosis, which was a common disease among our class. Her ailment was caused because my parents were compelled to live in a disease-ridden mining slum at the end of the Great War. Eventually my parents were able to leave the slum but by then the damage had already been done to my sister's health, and the TB spread into her spine. It left her a paraplegic with a hunchback. For the last 12 months of her life, Marion was totally dependent on my mother to be fed, bathed and clothed. In those days, there was no national health service; you either had the dosh to pay for your medicine or you did without. Your only hope for some medical care was the council poorhouse that accepted indigent patients.
Miners leaving a Yorkshire pit after an explosion, 1930. Photograph: Associated Newspapers/Rex
As a young lad, I was encouraged by my parents to spend time with my ailing sister. I think it was because they knew that she was dying and they wanted me to remember her for the rest of my life. I didn't comprehend illness or death because I was only three, so I contented myself with playing near her sick bed. On some occasions, I told her nonsense stories, but my sister couldn't respond to my kindness because the disease had destroyed her vocal cords.
Even though she was in extreme pain while the TB ate away at her spine and invaded her vital organs, she was silent. My sister always seemed to be looking past me with her large expressive eyes. Perhaps she was waiting for death, or perhaps she found the gaslight casting shadows on the opposite wall an appealing distraction from the monotony of the pain that consumed her 10-year-old body.
TB was known in the 19th century as the poet's disease, but I saw no lyricism in the way it killed Marion. As the autumn days grew shorter in 1926, so did the time my sister had to live. Her last weeks were unbearable but she still fought death. She thrashed her arms about in defiance against the coming end to her life. My parents tried to calm her by stroking her hair or singing to her, but she wasn't pacified. Instead, Marion wept silent tears and continued to struggle with so much ferocity that in the end my dad reluctantly restrained her to her bed with a rope.
My parents decided that there was nothing more that could be done for Marion in their care, so they arranged for her to be placed in our local workhouse infirmary. It was the last stop for many people who were too poor to pay for a doctor or proper hospital care. The workhouse in our community was a forbidding building that had been constructed during the age of Dickens. In the century before I was born it was used to imprison debtors, house orphans and provide primitive health care to the indigent. By the time Marion was sent there, it was no longer used as a prison. However, orphans, the sick and those with communicable diseases were still incarcerated behind its thick, towering black walls.
On one of the last days in September my mother pawned her best dress and my father's Sunday suit and hired a man with an old dray horse and cart to come to our house and collect Marion. When he arrived, my dad carried Marion outside and carefully placed her into the delivery carriage where my mother was waiting
Alberta and I stood on the side of the street and waved goodbye to Marion. I asked my dad where my sister was going and he mournfully replied: "She's going to a better place than here." Afterwards, he put his arms around me and Alberta and we watched the horse-drawn carriage slowly plod down our road towards the workhouse infirmary.
That was the last time I saw my sister alive.
Marion died a month later in the arms of my mother. There was no wake, no funeral service and even much later there was no headstone erected to mark her brief passage in life. My family, like the rest of our community, was just too poor to afford the accoutrements of mourning. We relied on my dad's minuscule salary just to keep us with a roof over our heads and dry in the perpetual hard luck rain of Yorkshire. Even my dead sister's landau was quickly dispatched to the pawnbroker's shop where it was swapped for a few coins to help feed her hungry living siblings.
My sister's body was committed to a pauper's pit and interred in an unmarked grave along with a dozen other forgotten victims of penury. My parents didn't even have a picture to remember their daughter's life. To the outside world, it was as if she was never there, but for our family her life and her end profoundly affected us. My father never mentioned Marion's name again. It wasn't out of callousness or disrespect, but because her death festered in his soul like a wound that never healed. For the rest of his life my dad carried with him an unwarranted guilt that he was responsible for Marion's tuberculosis, and it cut him deep. As for my mother, she often talked about Marion. As my family stumbled from misery to calamity, through the pitch dark of the Great Depression, my mother invoked my dead sister's name as a warning that the workhouse awaited each of us, unless the world and our circumstances changed.
It would be almost 20 years before, in 1948, the NHS was formed, and for the first time in my civilian life I went to a doctor's surgery and was treated for bronchitis with antibiotics that assured me a speedy and safe recovery. The cost to me was nothing, and I was grateful because I was skint, having just started back in the civilian working world.
An NHS immunization van in the 50s. Photograph: Popperfoto
As I convalesced, I was gobsmacked at the great consequences of free health care and the potential it offered to improve our society. It was a transformational shift in how we as a country viewed our fellow citizens. The creation of the NHS made us understand that we were in truth our brother's keeper, and that taxation benefits everyone through maintaining not just our roads and sewers but the health of our children, workers and elderly.
To me, the introduction of free health care was the first brick laid on the road to the social welfare state. So it has always been difficult for me to listen to politicians, proud possessors of health insurance and shares in private health care companies, when they talk about how the health service that we fought so hard to build must change. The coalition government's Health and Social Care Act will create a two-tier health care system. This act will see the NHS stripped down like a derelict house is by criminals for copper wiring.
Ukip has even proposed that A&E patients should have the right to buy their way to the front of the queue, while in Merseyside a private for-profit cancer clinic has set up shop under the NHS umbrella. Where will all of this end? What will be given the greatest priority in a new health care system that sends every service, from blood work to chemotherapy, out to the lowest bid tender?
It ends where I began my life – in a Britain that believed health care depended on your social status. So if you were rich and insured you received timely medical treatment, while the rest of the country got the drippings. One-fifth of the lords who voted in the controversial act – which provides a gateway to privatise our health care system – were found to have connections to private health care companies. If that doesn't make you angry, nothing will.
Sometimes I try to think how I might explain to Marion how we built these beautiful structures in our society – which protected the poor, which kept them safe at work, healthy in their lives, supported them when they were down on their luck – only to watch them be destroyed within a few short generations. But I cannot find the words.
Harry's Last Stand by Harry Leslie Smith is published by Icon Books at £12.99. To order a copy for £9.99, visit theguardian.com/bookshop or call 0330 333 6846.'
Around the corner I have a friend, In this great city that has no end; Yet the days go by, and weeks rush on, And before I know it a year is gone, And I never see my old friend's face, For Life is a swift and terrible race. He knows I like him just as well, As in the days when I rang his bell, And he rang mine. We were younger then, And now we are busy, tired men: Tired with playing a foolish game, Tired with trying to make a name. "To-morrow," I say, "I will call on Jim "Just to show that I'm thinking of him." But to-morrow comes -- and to-morrow goes, And distance between us grows and grows.
Around the corner -- yet miles away,... "Here's a telegram sir,..." "Jim died today." And that's what we get, and deserve in the end: Around the corner, a vanished friend. _A WORLD OF WINDOWS AND OTHER POEMS_, p66 by Charles Hanson Towne George H. Doran Company, New York, 1919. https://www.classe.cornell.edu/~seb/around_the_corner.html
It’s time for doctors to apologise to their ME patients
For too long the medical community has dismissed 'Chronic Fatigue Syndrome' as a mental illness which can be cured with therapy and exercise
By Dr Charles Shepherd
9:35AM GMT 07 Dec 2015
Back in 1955, a mysterious polio-like illness affected 262 doctors and nurses at London’s Royal Free Hospital. The hospital had to close for just over three months.
The outbreak was written up in The Lancet and a new neurological disease entered medical language: myalgic encephalomyelitis, or ME, as it still remains in the WHO Classification of Diseases. "Myalgic" referred to the muscle symptoms; "encephalomyelitis" referred to the various neurological symptoms.
Others were not convinced that ME was a neurological disease, and two decades later two psychiatrists, without interviewing any of the patients, wrote a paper for the British Medical Journal where they concluded that the Royal Free outbreak was due to mass hysteria.
The mud from the BMJ stuck. Like most doctors at the time, I left medical school believing that ME was not a real disease and I would probably never see a case. I was wrong.
Ignored or dismissed by doctors, people with ME went undiagnosed or misdiagnosed for long periods of time, often combined with harmful management advice – as is still the case. I can confirm this after developing classic ME following chickenpox, caught from one of my hospital patients. Some developed severe ME, becoming housebound or bed-bound with no medical help. Some never recovered.
During the 1980s, ME was redefined and given a dreadful new name: chronic fatigue syndrome (CFS). The term CFS trivialised a serious medical condition – the equivalent of trivialising dementia by calling it a chronic forgetfulness syndrome – and shifted the focus from a "disease" to a single symptom, "chronic fatigue".
CFS also brought in a much wider group of people suffering from chronic undiagnosed fatigue. A powerful body of psychiatric opinion convinced the medical profession that CFS was basically a mental health problem whereby people became trapped in a vicious circle of abnormal illness beliefs and behaviours, inactivity and deconditioning. In other words, there was no "disease" present.
The CFS model of causation resulted in two controversial forms of behavioural management – cognitive behaviour therapy (CBT) and graded exercise therapy (GET) – being recommended by NICE as the main form of treatment.
Now we have the PACE trial – the largest and most recent assessment of CBT and GET, which has cost the taxpayer almost £5 million. At long term follow-up, and contrary to what was reported in the press, the PACE trial found no significant difference between CBT, GET, adaptive pacing and specialised medical care.
Public reaction to the spin that has been put on the PACE trial results for CBT and GET has resulted in over 10,000 people signing a petition calling for claims relating to so-called recovery to be retracted and six academic researchers calling for an independent review of the study.
By contrast, in evidence collected from 1,428 people with ME by the ME Association, for which I am medical adviser, 73 per cent reported that CBT had no effect on symptoms while 74 per cent said reported that GET had made their condition worse. The MEA has therefore recommended that NICE withdraws their advice relating to GET.
On the progressive side of this medical divide are physicians and researchers who, like the patient community, believe that ME is a serious multi-system disease, often triggered by infection, but maintained by abnormalities involving, neurology, muscle, and the immune system.
In the UK, a research collaborative with a strong emphasis on the biomedical research has been established. And a major report from the prestigious US Institute of Medicine has recently concluded that ME is a "serious, chronic, complex, systemic disease that can profoundly affect the lives of patients". ME is not a psychological problem.
Biomedical research into ME is revealing abnormalities in the way that muscle creates energy, along with evidence of an ongoing overactive immune system response. New types of brain imaging are demonstrating low-level inflammation in several specific parts of the brain.
The argument here is not with mental illness, which is just as real and horrible as physical illness. As with any long-term illness, some people will develop mental health problems where talking therapies can clearly be of help.
The argument is with a simplistic and seriously flawed model of causation that patients know is wrong and which has seriously delayed progress in understanding the underlying cause of ME and developing effective forms of treatment.
Opening the 2015 research collaborative section of neuropathology, Jose Montoya, professor of medicine at the University of Stanford, said: “I have a wish and a dream that medical and scientific societies will apologise to their ME patients."
I agree – the time has come for doctors and scientists to apologise for the very neglectful way in which ME has been researched and treated over the past 60 years. Doctors need to start listening to their patients and there must now be increased investment in biomedical research to gain a better understanding of the disease process and to develop treatments that these patients desperately need.
Dr Charles Shepherd is medical adviser to the ME Association
When patients are recovering from traumatic injuries and confined to bed rest, the main goal is to get them up and moving as quickly as possible. Sooner is better than later.
With patients in intensive care, each day immobilized in bed can increase the chances of additional complications involving various body systems, from musculoskeletal issues to pulmonary problems. Clinicians should focus on the following areas.
Musculoskeletal difficulties.
Excessive bed rest can lead to contractures, muscle weakness and a loss of skeletal mass.
Contractures. Contractures may be in the muscles (myogenic) or joints (arthrogenic). Loss of ankle dorsiflexion and external shoulder rotation are the most common locations for contractors, and both affect a patient’s ability to function. Myogenic contractures have indistinct, soft endpoints; arthrogenic contractures have solid, firm endpoints.
Myogenic contractures are due to intrinsic or extrinsic factors. Intrinsic factors include muscle damage due to hemorrhaging, edema, inflammation, ischemia or myopathy. Extrinsic factors, such as spasticity, paralysis or immobilization from shortened posture, act on normal muscles and cause them to lose normal elasticity.
Contractures form with changes to type III and type I collagen. Type III collagen is loose and coiled, and surrounds muscles and tendons, while type I is dense and located in ligaments. In five to seven days, type III collagen begins to shorten. In about three weeks of muscle immobilization, type I replaces type III and muscles become densely contracted.
Capillaries shorten and straighten in muscle held in shortened posture, such as lying down, for six to eight weeks. These capillary changes may explain why contracted muscles hemorrhage when stretched too quickly. After a few months of bed rest, muscles start to lose sarcomeres—the contractile structural elements of striated muscle fibers.
Lack of motion can also cause arthrogenic contractures. Capsular fibrosis can occur during simple immobilization, but fibrosis is worse when cartilage is damaged by infection, trauma or inflammation. Early remobilization appears to slightly increase synovitis, although it may help preserve articular cartilage in the long run.
A slight period of rest, followed by remobilization, seems to be the best recipe for traumatically injured muscles and joints. Injured muscles that are mobilized too rapidly have dense scars with minimal muscle fiber penetration; muscles mobilized at a later point have better muscle fiber penetration into scars. However, damaged joints that are mobilized too soon can have exacerbated synovitis, while those mobilized too late have excessive loss of articular cartilage.
Strength deficiencies. Muscles that aren’t actively contracted lose strength at a rate of 10 percent to 15 percent per week. After four weeks, a patient may only have 50 percent to 60 percent of his total strength left. The 50 percent figure is more accurate in the presence of various contributing conditions, such as acidosis, infection, neoplasm, uncontrolled diabetes, renal failure, burns and trauma.
These conditions accelerate protein loss through the ubiquitin-proteasome pathway. This pathway is activated during these states and, as a result, protein conjugates with ubiquitin and marks it for degradation. Antigravity muscles (quadriceps, trunk extensors) are typically more severely affected than other muscles.
Remember that it takes time to regain strength after a period of immobility. A good rule of thumb: It takes twice the length of the period of immobility in a relatively healthy patient, and even longer in a clinically sick patient. Much of the strength improvement in the first one to two weeks after remobilization is due to central neurological “resynchronization.” After that, strength increases are primarily due to muscle hypertrophy.
Skeletal mass loss. Bones and tendons need the pull of gravity to maintain mass. Bed rest inhibits osteoblasts and activates osteoclasts, which lead to a breakdown of bone. Urinary calcium excretion increases by the second or third day of bed rest; maximum loss occurs after one month. The return to normal bone density is slow and often takes three to six months. Paralysis and premorbid osteoporosis in.crease the risk of significant bone loss.
Patients who’ve been immobile for at least several weeks won’t regain premorbid bone density for several months. During this recovery period, they’re at increased risk for fractures if they fall.
In addition, patients can experience an increase in disc fluid, since these structures rely on movement for nourishment. Discs imbibe and swell with bed rest.
Patients with discogenic low back pain often experience increased stiffness and pain in the morning when injured discs swell, which then puts pressure on sensitive annular and vertebral endplate structures. Negative outcomes for treating low back pain with bed rest may be due to the disc’s need for movement.
Urologic problems
Bed rest can in.crease the risk of kidney stones. Kidneys are retroperitoneal and posterior. The course of urine moving through the bladder and urethra is inferior and anterior, which works fine when a patient is sitting or standing upright. However, bedridden patients are basically urinating uphill when they’re lying down. When patients also have weakened abdominal and pelvic floor musculature, incomplete emptying and urinary statis can occur. This can lead to renal and bladder stones.
To prevent stones from forming and to ensure adequate bladder emptying, encourage patients to get up to urinate if possible, instead of allowing them to rely on a bedpan.
Gastrointestinal issues
Two primary gastrointestinal issues are negative nitrogen balance and constipation.
Negative nitrogen balance. Excessive bed rest can cause atrophy of intestinal mucosa and glands, while decreasing the rate of nutrient absorption. These changes can contribute to increased muscle catabolism, which leads to a negative nitrogen balance. This starts by the fifth day of bed rest and peaks during the second week. Nitrogen balance usually returns after a patient’s been up for the same amount of time that he’s been down for bed rest.
Constipation. The combination of de.creased peristalsis, decreased plasma volume, pharmaceutical interventions, loss of abdominal strength to generate intra-abdominal pressure and biomechanically disadvantageous positioning for defecation can lead to constipation.
Constipation can cause malaise, anorexia, pain, intractable hiccups, mental anguish, nausea and vomiting in patients who are trying to recover from illness or trauma. Consider using prevention techniques, such as stool softeners, fiber and fluids, before constipation sets in.
In addition, it’s important to have an accurate clinical record of bowel evacuation available, says Gary Goldberg, MD, director of brain injury rehabilitation at the University of Pittsburgh Medical Center Health System and professor in the University of Pittsburgh department of physical medicine and rehabilitation.
Pulmonary problems
As with other joints and muscles, those responsible for respiration (neck and trunk muscles) deteriorate with bed rest.
Weakness and tightness. Costovertebral and costochondral range of motion decrease. Weakness of the diaphragm, intercostals and accessory muscles of respiration develop. The rate of decline for respiratory muscles is similar to that of other muscles. Therefore, negative inspiratory force may be about one-half of what they were initially after four weeks of bed rest.
In the presence of central or peripheral neurological conditions associated with muscle paralysis, a patient has less physiologic reserve, says Dr. Goldberg. And during bed rest, the rate at which inspiratory force deteriorates is greater.
Alterated ventilation/perfusion. When patients are in the supine position, posterior lung fields are overperfused, and anterior lung fields are underperfused. The posterior lung fields become atelectactic—due to inspiratory weakness, decreased colloidal osmotic pressure and hydrostatic pressure—and the anterior becomes dry. Mucociliary action is less effective, coughing is weak and pneumonia or lung infection may develop. Posterior lung fields are poorly ventilated and overperfused, which leads to shunting and deterioration of arterial blood gases.
Optimizing mechanical factors are equally important as an antibiotic choice with respect to successfully clearing a nosocomial pulmonary infection. For instance, you should help the patient turn, sit up (so the lungs can dangle) and mobilize.
Endocrine system
The endocrine system can fall victim to decreased carbohydrate tolerance and generalized hyporesponsiveness.
Decreased carbohydrate tolerance. Insulin-binding sites decrease with carbohydrate intolerance, and hyperglycemia can develop. The severity of this problem is directly related to the length of bed rest. And if the patient is taking steroids, it only exacerbates the situation.
Carbohydrate metabolism seems to return to normal rapidly with isotonic—not isometric—exercise. There’s also evidence that even one exercise session can increase the insulin sensitivity for insulin-resistant patients.
Generalized hyporesponsiveness. Bed rest may reduce androgen levels. It also may decrease growth hormone release in response to hypoglycemia, ACTH levels and the amount of catecholamine released from the adrenal medulla.
Watch carefully for rapidly decreasing insulin requirements and hypoglycemic episodes as a patient is simultaneously mobilized and tapered off steroids.
Cardiovascular system
You must pay attention to cardiovascular issues, such as postural hypotension, decreased cardiac function, volume redistribution and deep vein thrombosis/pulmonary embolus.
Postural hypotension. When patients are moving from supine to upright, roughly 700ccs of blood move from the chest into the lower extremities. The sympathetic nervous system maintains blood pressure, which leads to the release of catecholamines. In turn, venous tone and venous return to the heart increase, along with a rise in heart rate and arterial performance.
After three weeks of bed rest, however, this mechanism is completely blunted for reasons that aren’t clear. But return of postural reflexes occurs between three and 10 weeks. Patients who are elderly, more severely traumatized, ill or have other predisposing tendencies toward postural hypotension, such as autonomic dysfunction in patients with diabetes, may need more time to recover. Patients are also at higher risk for falls due to cerebral hypoperfusion associated with postural hypotension, Dr. Goldberg says.
Those with coronary or cerebrovascular disease are at risk for strokeand myocardial infarction with remobilization. Remember that coronary arteries fill during diastole and that diuretics and antihypertensives may derail postural pressure control. Lower extremity compressive stockings and abdominal binders can help these high-risk patients.
Decreased cardiac function. After two weeks, stroke volume decreases by about 15 percent and a resting heart rate increases by 0.5 beats per minute per day of bed rest. After three weeks, VO2 max decreases by 25 percent.
Return of exercise tolerance after three weeks of bed rest mirrors the return of postural reflexes, which takes about three to 10 weeks of activity.
Volume redistribution. With recumbancy, 700ccs of blood flows to the thoracic veins and right atrium. Cardiac output temporarily increases and the kidneys may believe that there’s too much intravascular volume.
Renin and ADH release are suppressed and “extra” sodium and water are excreted; plasma volume decreases by 12 percent by the fourth day. As a result, the effective circulating blood volume decreases and blood viscosity increases. Isotonic exercises can prevent this volume redistribution.
Deep vein thrombosis/pulmonary embolus. Clinicians have observed a direct relationship between frequency of deep vein thrombosis (DVT) and length of bed rest. Venous stasis and mild hyper-coaguability from increased blood viscosity are associated with bed rest.
However, a little ambulation seems to help a lot. For example, in stroke patients, DVT is five times more common for people who can’t ambulate, compared to those who can walk at least 50 feet.
Neurologic Changes
Bed rest can tax the neurological system. For example, after several days of bed rest, patients may experience decreased concentration, orientation and intellectual skills. Behavioral and emotional changes may cause anxiety, depression, irritability and less tolerance to pain. Sensory deprivation and central nervous system changes in neurochemistry may play a role in these alterations. Research has shown changes in the levels of brain amines and behavior in rat models undergoing bed rest, which correlates to increased anxiety and depression.
Compressive mononeuropathies, particularly of the peroneal nerve at the fibular head and ulnar at the elbow, are common as well. Moreover, axillary and sciatic mononeuropathies from injections may develop. The risk factors for falls and fractures, such as weakness, ataxia, decreased bone density, postural hypotension, peripheral nerve dysfunction and confusion, add up after prolonged bed rest.
Bed rest does have obvious benefits and is necessary during initial phases of recovery from critical illness or surgery, says Dr. Goldberg. But it doesn’t have to be detrimental to a patient’s healthy outcome if you recognize potential risks, implement prevention and get patients up and moving as soon as it’s safe.
This article was adapted from a presentation at the American Academy of Physical Medicine and Rehabilitation by James K. Richardson, MD, associate professor at the University of Michigan Medical Center in Ann Arbor. Information is attributed to Dr. Richardson, unless otherwise noted.
Returning to exercise after being bedridden for a longer time should happen progressively, so as to allow the body to adapt to the new routine after days of immobility.
Although resting for several days may sound like a gentle thing, being bedridden actually leads to deconditioning, which can impact your health in negative ways. For this reason it is usually recommended for people to start moving and doing recovery exercises as soon as possible after being hospitalized.
The human body was designed to move in the upright position, against gravity, and the interaction with the gravitational force benefits the entire organism, from bones and muscles to the circulatory system. When you spend several days in horizontal position, as happens when bedridden, the weight-bearing muscles like the ones in the neck, back, abdomen or legs may lose their tone and become weaker, thus “deconditioned”.
The wasting of muscles can happen faster or slower, depending on one’s fitness level and lifestyle. One week of complete bed rest can lead to a decrease of 20-30% in muscle strength, and can cause structural changes to muscles, bones, nerves and blood vessels, affecting not only one’s physical appearance and muscle tone, but also their balance, coordination and even walking ability.
The joints are also affected by physical inactivity, as the cartilage begins to deteriorate. After spending several days in bed, blood can start to pool in the lower body and this can lead to swollen and painful feet as well as to dizziness and weakness when finally getting out of bed. The blood pressure is affected by prolonged bed rest, the density of blood increases and the amount of oxygen transported to cells and tissues decreases.
One becomes more prone to falls and fractures after spending several days in bed, so it’s important for them to start an exercise program as soon as their body is recovered. Although it may take more time to regain the muscle strength and tone, the benefits of returning to an active lifestyle are usually experienced from the first training sessions.
Types of exercise that are safe after prolonged bed rest
One of the safest forms of exercise for people who were bedridden for several days is represented by mobilization exercises, which can be passive or active. These movements improve the range of motion in joints and stimulate circulation, target the ankles, knees, hips, shoulders and elbows.
To perform these exercises, one may need help from a caretaker or another person, whose role is to move the patient’s joints if he or she cannot move the limbs. As unpleasant as it may sound, it’s actually common for bedridden patients to lose their ability to move the joints and to require help from a caregiver when first returning to exercise.
The passive mobilization exercises usually consist in simple movements that involve bending the joints, pushing the limbs and doing flexion and extension exercises for the various body areas, in order to stretch the muscles and stimulate the blood flow and production of synovial fluid in joints. Active mobilization exercises are similar to passive ones but this time the patient performs the exercises himself.
Although less demanding than muscle strengthening exercises, active mobilization movements still require strength and coordination from the patient, and involve not only the major joints but also smaller ones, like the wrist for example. The purpose of these exercises is for the patient to gain back control of their musculoskeletal system and to progressively expose the organism to gravity, for regaining muscle strength, flexibility, coordination and agility.
Another type of exercise that should be added to one’s routine as muscles get stronger and joints regain their flexibility is strengthening movements, done without resistance at the beginning and with light weights after a couple of weeks. Muscle strengthening exercises reverse the negative effects of prolong bed rest, stimulating circulation and preventing muscle atrophy.
After passive and active mobilization exercises, one should do some stretching movements to lengthen the muscles, then start walking and do simple movements like marching with the knees up, bending the waist, arms and legs, kicking with the legs or arms, lunging to the front and side and so on. Squeezing together the arms, knees and thighs while using a soft ball as resistance also helps in strengthening the muscles. To add more resistance you can use elastic bands, and then as your body gets stronger, you can add light dumbbells.
Besides these exercises you should also start incorporating cardio activities into your daily program, for reversing the effects of bed rest on the circulatory system. Walking and cycling on a recumbent bike are safe and low-impact activities which can speed up rehabilitation and improve endurance. You can increase the intensity by walking on a treadmill and exercising on a cross trainer, or you can simply take the stairs when you feel prepared for this activity, as it will improve both your endurance and muscle strength.
