search.noResults

search.searching

dataCollection.invalidEmail
note.createNoteMessage

search.noResults

search.searching

orderForm.title

orderForm.productCode
orderForm.description
orderForm.quantity
orderForm.itemPrice
orderForm.price
orderForm.totalPrice
orderForm.deliveryDetails.billingAddress
orderForm.deliveryDetails.deliveryAddress
orderForm.noItems
HEALTH AND WELL-BEING


animal kingdom.’


Heart disease While reduced or poor-quality sleep has been associated with an increased risk of heart disease, little is known about how sleep protects cardiovascular health. Now a US team at Massachusetts General Hospital and Harvard Medical School has suggested some answers. The team led by Filip Swirski


investigated the effects of disrupting sleep in mice genetically modified to be prone to atherosclerosis or plaque build-up in the arteries, which is a common cause of heart disease. They found that the sleep-deprived mice developed larger arterial plaques and had higher levels of monocytes and neutrophils—inflammatory cells that contribute to atherosclerosis—in their blood vessels than animals from the same strain allowed to sleep normally. And there were no changes in weight, cholesterol levels or glucose tolerance.6 What’s more, they also found


that levels of the hormone hypocretin, which is produced in the hypothalamus and involved in sleep regulation, were significantly reduced in the sleep-deprived mice. Hypocretin is normally produced at high levels when animals are awake. They report that the hormone had an unexpected role in controlling white blood cell production; sleep-deprived mice produced almost double the number of stem cells that give rise to white blood cells in the bone marrow. Experiments with mice lacking the gene for hypocretin revealed that sleep-deprived animals with lower levels of hypocretin experienced increased monocyte production and accelerated atherosclerosis. ‘This is a direct demonstration


that hypocretin is also an important inflammatory mediator,’ says Swirski. ‘We now need to study this pathway in humans, explore additional mechanisms by which proper sleep maintains vascular health and further explore this newly identified neuro- immune axis.’


Brain health Brain health is another good reason to get a good night’s sleep. By studying Alzheimer’s disease (AD) patients, US researchers have suggested that poor-quality sleep in later life could be a red flag for


deteriorating brain health. Researchers at Washington


University School of Medicine in St. Louis have found that older people who have less slow-wave sleep – the deep sleep needed to consolidate memories and wake up feeling refreshed – have higher levels of the brain protein tau. This protein appears at increased levels in AD patients and has been linked to brain damage and cognitive decline. In people with AD, clumps of tau (tangles) accumulate in parts of the brain important for memory (the hippocampus and entorhinal cortex) and then move into other brain regions. As tau tangles spread, people increasingly struggle to think clearly. Brendan Lucey, director of the


Washington University Sleep Medicine Center, and colleagues studied 119 people aged 60 or older.7


Around


80% were ‘cognitively normal’, and the remainder were very mildly impaired. The participants’ sleep was monitored at home for a week and they kept sleep diaries. The researchers also measured levels of tau and amyloid beta – another protein that forms plaques in the brain in AD patients – in the brain and in the cerebrospinal fluid. After controlling for other factors, the researchers found that decreased slow-wave sleep coincided with higher levels of tau in the brain and a higher tau-to-amyloid ratio in the cerebrospinal fluid. ‘The key is that it wasn’t the total amount of sleep that was linked to tau, it was the slow-wave sleep, which reflects quality of sleep,’ Lucey said. ‘The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren’t getting as good quality sleep….What’s interesting is that we saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired, meaning that reduced slow-wave activity may be a marker for the transition between normal and impaired.’ Lucey suggests that measuring


how people sleep may be a non- invasive way to screen for AD before, or just as, people begin to develop problems with memory and thinking. ‘I don’t expect sleep monitoring to replace brain scans or cerebrospinal


fluid analysis, but it could supplement them. It’s something that could be easily followed over time, and if someone’s sleep habits start changing, that could be a sign for doctors to take a closer look at what might be going on in their brains.’ In a separate study, Washington


University researchers showed that sleep disruption causes tau to increase rapidly and spread over time. Senior author David Holtzman, head of the Department of Neurology, and colleagues measured tau levels in mice, which are nocturnal, and people with normal and disrupted sleep.8


Older people who have less slow-wave sleep - the deep sleep needed to consolidate memories and wake up feeling refreshed - have higher levels of the brain protein tau. This protein appears at increased levels in AD patients and has been linked to brain damage and cognitive decline.


Adrenaline and prostaglandin levels dip during sleep. Researchers in Germany compared T cells taken from healthy volunteers while they slept or were awake all night. Sleep improves the potential ability of T cells to attach to their targets and is good for the immune system, they found, while chronic stress is not.


The researchers found that tau


levels in the fluid surrounding brain cells in mice were roughly twice as high at night when the animals were awake and active, than during the day when the mice dozed frequently. Disturbing the mice’s rest during the day caused daytime tau levels to double. When Lucey analysed cerebrospinal fluid from eight people after a normal night of sleep and again after they were kept awake all night, he found that tau levels rose by about half following the sleepless night.


The findings suggest that tau


is released during waking hours, and then reined back during sleep allowing it to be cleared away. The team suggests that sleep deprivation interrupts this cycle, so tau starts to build up. To study whether sleep affects the


References 1 Sleep; doi: 10.1093/sleep/ zsy182


2 Why We Sleep, 2017, Allen Lane, ISBN-13: 978- 0241269060


3 Journal of Neuroscience; doi: 10.1523/ JNEUROSCI.2408-18.2018


4 Science; doi: 10.1126/science. aat1650


5 Nature Communications; doi: 10.1038/s41467-019-08806-w


6 Nature, 2019, 566, 383 7 Science Translational Medicine, doi: 10.1126/ scitranslmed.aau6550


8 Science; doi: 10.1126/science. aav2546


spread of tau tangles, the researchers seeded the hippocampi of mice with tiny clumps of tau and then prevented the mice from sleeping for long periods. Another group was injected with tau clumps but allowed to sleep whenever they liked. After four weeks, tau tangles had spread further in the sleep-deprived mice. Significantly, the new tangles appeared in the same areas of the brain affected in people with AD. ‘The interesting thing about this study is that it suggests that real-life factors such as sleep might affect how fast Alzheimer’s spreads through the brain,’ says Holtzman. ‘We don’t know yet whether getting adequate sleep as people age will protect against Alzheimer’s. But it can’t hurt, and this and other data suggest that it may even help delay and slow down the disease process if it has begun.’


06 | 2019 29


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52