‘Journal of Neurology, Neurosurgery & Psychiatry” (July 10, 2020):
We tested the hypothesis that apathy, but not depression, is associated with dementia in patients with SVD. We found that higher baseline apathy, as well as increasing apathy over time, were associated with an increased dementia risk. In contrast, neither baseline depression or change in depression was associated with dementia. The relationship between apathy and dementia remained after controlling for other well-established risk factors including age, education and cognition. Finally, adding apathy to models predicting dementia improved model fit. These results suggest that apathy may be a prodromal symptom of dementia in patients with SVD.
Cerebral small vessel disease (SVD) is the leading vascular cause of dementia and plays a major role in cognitive decline and mortality.1 2 SVD affects the small vessels of the brain, leading to damage in the subcortical grey and white matter.1 The resulting clinical presentation includes cognitive and neuropsychiatric symptoms.1
Apathy is a reduction in goal-directed behaviour, which is a common neuropsychiatric symptom in SVD.3 Importantly, apathy is dissociable from depression,3 4 another symptom in SVD for which low mood is a predominant manifestation.5 Although there is some symptomatic overlap between the two,6 research using diffusion imaging reported that apathy, but not depression, was associated with white matter network damage in SVD.3 Many of the white matter pathways underlying apathy overlap with those related to cognitive impairment, and accordingly apathy, rather than depression, has been associated with cognitive deficits in SVD.7 These results suggest that apathy and cognitive impairment are symptomatic of prodromal dementia in SVD.
“Numerous studies have linked insufficient sleep with significant health consequences. Yet, many people ignore the signs of sleep problems or don’t allow enough time to get adequate sleep,” said lead researcher Eileen Leary. She is a senior manager of clinical research at Stanford University in Palo Alto, Calif.
“REM sleep appears to be a reliable predictor of mortality and may have other predictive health values,” Leary said. “Strategies to preserve REM may influence clinical therapies and reduce mortality risk, particularly for adults with less than 15% of REM sleep.”
REM (rapid eye movement) sleep is when dreams occur and the body repairs itself from the ravages of the day. For every 5% reduction in REM sleep, mortality rates increase 13% to 17% among older and middle-aged adults, researchers report.
For the study, Leary and her colleagues included more than 2,600 men, average age 76, who were followed for a median of 12 years. They also collected data on nearly 1,400 men and women, average age 52, who were part of another study and were followed for a median of 21 years.
Poor REM sleep was tied to early death from any cause as well as death from cardiovascular and other diseases, the researchers found.
…the beneficial effects of TRE are dose dependent, with greater reductions in body weight, fat mass, and improvement in glucose tolerance when a 9-h protocol was implemented versus 12 and 15 h. The optimal TRE time frame to recommend for people has not been tested. Clear improvements have been noted after 6-, 8-, 9-, and 10-h protocols. It is likely that the greater time restriction would result in greater weight losses, which may maximize the metabolic benefits.
Eating out of phase with daily circadian rhythms induces metabolic desynchrony in peripheral metabolic organs and may increase chronic disease risk. Time-restricted eating (TRE) is a dietary approach that consolidates all calorie intake to 6- to 10-h periods during the active phase of the day, without necessarily altering diet quality and quantity.
TRE reduces body weight, improves glucose tolerance, protects from hepatosteatosis, increases metabolic flexibility, reduces atherogenic lipids and blood pressure, and improves gut function and cardiometabolic health in preclinical studies. This review discusses the importance of meal timing on the circadian system, the metabolic health benefits of TRE in preclinical models and humans, the possible mechanisms of action, the challenges we face in implementing TRE in humans, and the possible consequences of delaying initiation of TRE.
“On a high-sugar diet, we find that the fruit flies’ dopaminergic neurons are less active, because the high sugar intake decreases the intensity of the sweetness signal that comes from the mouth,” Dus said. “Animals use this feedback from dopamine to make predictions about how rewarding or filling a food will be. In the high-sugar diet flies, this process is broken—they get less dopamine neuron activation and so end up eating more than they need, which over time makes them gain weight.”
It is well known that consuming food and drink high in sugar is not great for us, but scientists are continuing to unravel the intricacies of how the sweet stuff drives negative health outcomes. The latest finding comes from researchers at the University of Michigan, who through studies in fruit flies have found that excess amounts of sugar can shut down crucial neural circuits linked to regulating satiety, possibly leading to overeating in humans.
“We’ve discovered that fragmented sleep is associated with a unique pathway — chronic circulating inflammation throughout the blood stream — which, in turn, is linked to higher amounts of plaques in coronary arteries,” said study senior author Matthew Walker, a UC Berkeley professor of psychology and neuroscience.
Disrupted nightly sleep and clogged arteries tend to sneak up on us as we age. And while both disorders may seem unrelated, a new UC Berkeley study helps explain why they are, in fact, pathologically intertwined.
Some tips to improve sleep quality
Maintain a regular sleep routine, going to bed and waking up at the same time each day.
As part of a nightly wind-down routine, avoid viewing computer, smartphone and TV screens in the last hour before bedtime, and keep phones and other digital devices out of the bedroom.
Engage in some form of physical exercise during the day.
Get exposure to natural daylight, especially in the first half of the day.
Avoid stimulants, like caffeine, and sedatives, like alcohol, later in the day.
UC Berkeley sleep scientists have begun to reveal what it is about fragmented nightly sleep that leads to the fatty arterial plaque buildup known as atherosclerosis that can result in fatal heart disease.
We observed that increased adherence to the MedDiet modulates specific components of the gut microbiota that were associated with a reduction in risk of frailty, improved cognitive function and reduced inflammatory status.
Dr Philip Smith, Digital and Education Editor of Gut and Consultant Gastroenterologist at the Royal Liverpool Hospital interviews Professor Paul O’Toole; who is Professor of Microbial Genomics, Head of School of Microbiology and Principal Investigator in APC Microbiome Ireland, an SFI funded centre at University College Cork, Ireland, on “Mediterranean diet intervention alters the gut microbiome in older people reducing frailty and improving health status: the NU-AGE 1-year dietary intervention across 5 European countries” published in paper copy in Gut in July 2020.
“We took an unbiased approach and searched throughout the body for indicators of damage from sleep deprivation. We were surprised to find it was the gut that plays a key role in causing death,” said senior study author Dragana Rogulja, assistant professor of neurobiology in the Blavatnik Institute at HMS.
The first signs of insufficient sleep are universally familiar. There’s tiredness and fatigue, difficulty concentrating, perhaps irritability or even tired giggles. Far fewer people have experienced the effects of prolonged sleep deprivation, including disorientation, paranoia, and hallucinations.
Total, prolonged sleep deprivation, however, can be fatal. While it has been reported in humans only anecdotally, a widely cited study in rats conducted by Chicago-based researchers in 1989 showed that a total lack of sleep inevitably leads to death. Yet, despite decades of study, a central question has remained unsolved: Why do animals die when they don’t sleep?
Now, Harvard Medical School (HMS) neuroscientists have identified an unexpected, causal link between sleep deprivation and premature death.
From The Lancet Diabetes & Endocrinology (June 2020):
Our findings show that the intensive lifestyle intervention led to significant weight loss at 12 months, and was associated with diabetes remission in over 60% of participants and normoglycaemia in over 30% of participants. The provision of this lifestyle intervention could allow a large proportion of young individuals with early diabetes to achieve improvements in key cardiometabolic outcomes, with potential long-term benefits for health and wellbeing.
Type 2 diabetes is affecting people at an increasingly younger age, particularly in the Middle East and in north Africa. We aimed to assess whether an intensive lifestyle intervention would lead to significant weight loss and improved glycaemia in young individuals with early diabetes.
Between July 16, 2017, and Sept 30, 2018, we enrolled and randomly assigned 158 participants (n=79 in each group) to the study. 147 participants (70 in the intervention group and 77 in the control group) were included in the final intention-to-treat analysis population. Between baseline and 12 months, the mean bodyweight of participants in the intervention group reduced by 11·98 kg (95% CI 9·72 to 14·23) compared with 3·98 kg (2·78 to 5·18) in the control group (adjusted mean difference −6·08 kg [95% CI −8·37 to −3·79], p<0·0001). In the intervention group, 21% of participants achieved more than 15% weight loss between baseline and 12 months compared with 1% of participants in the control group (p<0·0001). Diabetes remission occurred in 61% of participants in the intervention group compared with 12% of those in the control group (odds ratio [OR] 12·03 [95% CI 5·17 to 28·03], p<0·0001). 33% of participants in the intervention group had normoglycaemia compared with 4% of participants in the control group (OR 12·07 [3·43 to 42·45], p<0·0001).
From the American Journal of Clinical Nutrition (April 22, 2020):
Our findings imply that higher long-term dietary intakes of flavonoids are associated with lower risks of ADRD and AD in US adults.
Our findings provide new evidence that diets higher in flavonols, anthocyanins, and flavonoid polymers are associated with a lower risk of developing ADRD. These associations were sustained after accounting for a variety of potential confounders including key nutrients related to ADRD risk and overall diet quality. Similar findings were seen with AD risk for flavonols and anthocyanins but the association with flavonoid polymers was no longer statistically significant.
Along with improvements in healthcare and medical technology, the aging of the baby boom generation will result in an unprecedented rise in the number of older Americans (1, 2). Currently, there are >50 million Americans aged ≥65 y, and that is projected to more than double by 2060 (3). A consequence of this increase in older adults is the escalation of age-related diseases (4, 5). Alzheimer disease (AD) and related dementias (ADRD), a group of symptoms in which there is progressive deterioration in cognitive function severe enough to interfere with a person’s daily living activities, are regarded as among the most significant public health challenges largely affecting adults aged >65 y (6). AD is the most common form of dementia, making up ∼60–80% of dementia cases. Currently, 5.8 million Americans are living with AD, and by 2050 that is projected to escalate to 14 million (7).
…ultra-processed foods are generally the foods available to nurses working nightshifts, firefighters returning to their department after a call, police officers patrolling neighborhoods, or military soldiers during field-exercises. Thus, time-restricted eating removes the added stress of what to eat, and serves as a practical intervention conducive to the schedules of many people.
Time-restricted eating has been shown to lower circulating insulin, blood pressure, body fat and overall body weight, inflammation, and oxidative stress.
Time-restricted eating is a nutrition intervention which alternates between a period of fasting (12 – 16 hours) followed by a period of eating (8 – 12 hours). Unlike other diets, which focus on the caloric content of a meal or which foods you should eat, time-restricted eating focuses exclusively on when you eat by compressing and standardizing the feeding window each day. In turn, people following this type of eating pattern naturally enter a state of caloric deficit.