Researchers from Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, have found new evidence that vitamin D may be metabolized differently in people with an elevated body mass index (BMI). The study, appearing in JAMA Network Open, is a new analysis of data from the VITAL trial, a large nationwide clinical trial led by Brigham researchers that investigated whether taking vitamin D or marine omega-3 supplements could reduce the risk of developing cancer, heart disease, or stroke.
“The analysis of the original VITAL data found that vitamin D supplementation correlated with positive effects on several health outcomes, but only among people with a BMI under 25,” said first author Deirdre K. Tobias, ScD, an associate epidemiologist in Brigham’s Division of Preventive Medicine. “There seems to be something different happening with vitamin D metabolism at higher body weights, and this study may help explain diminished outcomes of supplementation for individuals with an elevated BMI.”
Vitamin D is an essential nutrient involved in many biological processes, most notably helping our body absorb minerals, such as calcium and magnesium. While some of the vitamin D we need is made in the body from sunlight, vitamin D deficiencies are often treated with supplementation. Evidence from laboratory studies, epidemiologic research and clinical research has also suggested that vitamin D may play a role in the incidence and progression of cancer and cardiovascular disease, and it was this evidence that prompted the original VITAL trial.
The VITAL trial was a randomized, double-blind, placebo-controlled trial in 25,871 U.S. participants, which included men over the age of 50 and women over the age of 55. All participants were free of cancer and cardiovascular disease at the time of enrollment. While the trial found little benefit of vitamin D supplementation for preventing cancer, heart attack, or stroke in the overall cohort, there was a statistical correlation between BMI and cancer incidence, cancer mortality, and autoimmune disease incidence. Other studies suggest similar results for type 2 diabetes.
The new study aimed to investigate this correlation. The researchers analyzed data from 16,515 participants from the original trial who provided blood samples at baseline (before randomization to vitamin D), as well as 2,742 with a follow-up blood sample taken after two years. The researchers measured the levels of total and free vitamin D, as well as many other novel biomarkers for vitamin D, such as its metabolites, calcium, and parathyroid hormone, which helps the body utilize vitamin D.
“Most studies like this focus on the total vitamin D blood level,” said senior author JoAnn E. Manson, MD, DrPH, chief of the Division of Preventive Medicine at the Brigham and principal investigator of VITAL. “The fact that we were able to look at this expanded profile of vitamin D metabolites and novel biomarkers gave us unique insights into vitamin D availability and activity, and whether vitamin D metabolism might be disrupted in some people but not in others.”
The researchers found that vitamin D supplementation increased most of the biomarkers associated with vitamin D metabolism in people, regardless of their weight. However, these increases were significantly smaller in people with elevated BMIs.
“We observed striking differences after two years, indicating a blunted response to vitamin D supplementation with higher BMI,” Tobias said. “This may have implications clinically and potentially explain some of the observed differences in the effectiveness of vitamin D supplementation by obesity status.”
“This study sheds light on why we’re seeing 30-40 percent reductions in cancer deaths, autoimmune diseases, and other outcomes with vitamin D supplementation among those with lower BMIs but minimal benefit in those with higher BMIs, suggesting it may be possible to achieve benefits across the population with more personalized dosing of vitamin D,” said Manson. “These nuances make it clear that there’s more to the vitamin D story.”
The authors conclude that the VITAL findings are a call to action for the research community to continue exploring the potential benefits of vitamin D supplementation for preventing cancer and other diseases and to take BMI into account when evaluating the supplement’s health impacts.
IMAGE: A SIMPLE NASAL SPRAY SIGNIFICANTLY REDUCED SNORING AND BREATHING DIFFICULTIES IN CHILDREN AND HALVED THE NUMBER NEEDING TO HAVE THEIR TONSILS REMOVED, ACCORDING TO A NEW STUDY.view more
CREDIT: NENAD STOJKOVIC
A simple nasal spray significantly reduced snoring and breathing difficulties in children and halved the number needing to have their tonsils removed, according to a new study.
The research, led by the Murdoch Children’s Research Institute and published in JAMA Pediatrics, found a saline (salt water) nasal spray was just as effective as an anti-inflammatory steroid nasal spray at easing sleep disordered breathing in children after six weeks of treatment.
The findings stated both nasal sprays cleared symptoms while asleep in about 40 per cent of cases and thoseassessed by a surgeon as needing their tonsils and/or adenoids removed was reduced by half. The randomised-controlled “MIST” trial of the sprays involved 276 children, aged 3-12 years, and was carried outat The Royal Children's Hospital and Monash Children's Hospital.
Tonsillectomy is the most common paediatric elective surgery for children in Australia with more than 40,000 performed each year. Commonly used to treat children’s snoring, the procedure is costly, painful and a significant burden on hospital resources.
Murdoch Children’s Dr Alice Baker said Victorian children typically waited more than a year in the public system for surgery to remove tonsils and adenoids, prompting a need to look for an alternative treatment for sleep disordered breathing. Some children may also be having their tonsils and adenoids out unnecessarily, she said.
“Nasal sprays work by cleaning the nose and/or reducing inflammation not just in the nose but all the way down the back of the throat to the adenoids and tonsillar tissue to alleviate the symptoms,” Dr Baker said.
Snoring and breathing difficulties during sleep affect about 12 per cent of children and can cause significant long-term issues impacting cognitive function, behaviour and cardiovascular health.
Murdoch Children’s Associate Professor Kirsten Perrett said the study found a substantial number of children with sleep disordered breathing could initially be managed by their GP and may not require referral to specialist services as currently recommended.
“A large proportion of children who snore and have breathing difficulties could be managed successfully by their primary care physician, using six weeks of an intranasal saline spray as a first-line treatment,” she said.
“Using this cheaper and readily available treatment would increase the quality of life of these children, reduce the burden on specialist services, decrease surgery waiting times and reduce hospital costs.”
Stephen Graham and Emily Tuner-Graham said their son, Thomas, 7, had stopped snoring and no longer needed his tonsils removed since taking part in the trial.
“From three years of age Thomas started snoring and we were concerned that he would eventually need surgery,” they said.
“Prior to joining the trial, a specialist recommended having his tonsils out. It’s a such huge relief that by just using a nasal spray his breathing difficulties have cleared.”
IMAGE: CHOLINE IS A VITAL NUTRIENT FOR BRAIN AND BODY HEALTH. WHILE IT IS AVAILABLE IN A VARIETY OF FOODS, MOST AMERICANS DO NOT MEET THE REQUIRED AMOUNT FOR PROPER HEALTH. A NEW STUDY SUGGESTS THAT INSUFFICIENT CHOLINE CAN LEAD TO PATHOLOGIES IN THE HEART AND LIVER AND IS ASSOCIATED WITH THE DEVELOPMENT TWO HALLMARKS OF ALZHEIMER'S DISEASE: AMYLOID PLAQUES AND TAO TANGLES.view more
CREDIT: GRAPHIC BY SHIREEN DOOLING
Choline, an essential nutrient produced in small amounts in the liver and found in foods including eggs, broccoli, beans, meat and poultry, is a vital ingredient for human health. A new study explores deficiency in dietary choline adversely affects the body and may be a missing piece in the puzzle of Alzheimer’s disease.
It’s estimated that more than 90% of Americans are not meeting the recommended daily intake of choline. The current research, conducted in mice, suggests that dietary choline deficiency can have profound negative effects on the heart, liver and other organs.
Lack of adequate choline is also linked with profound changes in the brain associated with Alzheimer’s disease. These include pathologies implicated in the development of two classic hallmarks of the illness, amyloid plaques, which aggregate in the intercellular spaces between neurons, and tau tangles, which condense within the bodies of neurons.
The new research, led by scientists at Arizona State University, describes pathologies in normal mice deprived of dietary choline as well as choline deficient transgenic mice, which already exhibit symptoms associated with the disease. In both cases, dietary choline deficiency results in liver damage, enlargement of the heart and neurologic alterations in the AD mice typically accompanying Alzheimer’s disease, including increased levels of plaque-forming amyloid-beta protein and disease-linked alterations in tau protein.
Further, the study illustrates that choline deficiency in mice causes significant weight gain, and alterations in glucose metabolism, (which are tied to conditions such as diabetes), and deficits in motor skills.
In the case of humans, “it's a twofold problem,” according to Ramon Velazquez, senior author of the study and Assistant professor with the ASU-Banner Neurodegenerative Disease Research Center. “First, people don't reach the adequate daily intake of choline established by the Institute of Medicine in 1998. And secondly, there is vast literature showing that the recommended daily intake amounts are not optimal for brain-related functions.”
Ramon Velazquez led the new study on the importance of dietary choline for the brain and other organs. He is a researcher in the ASU-Banner Neurodegereative Disease Research Center.
The research highlights a constellation of physical and neurological changes linked to choline deficiency. Sufficient choline in the diet reduces levels of the amino acid homocysteine, which has been recognized as a neurotoxin contributing to neurodegeneration and is important for mediating functions such as learning and memory, through the production of acetylcholine.
The growing awareness of choline’s importance should encourage all adults to ensure proper choline intake. This is particularly true for those on plant-based diets, which may be low in naturally occurring choline, given that foods high in choline are eggs, meats, and poultry.
Plant-based, choline-rich foods, including soybeans, Brussel sprouts and toast can help boost choline in these cases. Further, inexpensive, over-the-counter choline supplements are encouraged to ensure system-wide health and guard the brain from the effects of neurodegeneration.
Brain-boosting nutrient
Choline is needed to produce acetylcholine, a neurotransmitter that plays an essential role in memory, muscle control and mood. Choline also builds cell membranes and helps regulate gene expression. The established recommendations set forth by the Institute of Medicine were based on evidence preventing fatty liver disease in men. New lines of evidence imply that the established recommended daily intake of dietary choline for adult women (425mg/day) and adult men (550mg/day) may not be optimal for proper brain health and cognition. Additionally, ~90% of Americans are not meeting the recommendation levels and may not even be aware that dietary choline is required on a daily basis.
Despite decades of research and billions of dollars invested since the discovery of the devastating ailment over a century ago, there remains no therapy capable of slowing the advance of the illness. Yet, new research findings suggest that environmental and lifestyle changes, including adequate choline, may help protect the brain from Alzheimer’s disease as well as improving overall health.
Velazquez is joined on the study by co-lead authors Nikhil Dave and Jessica Judd. The work is highly interdisciplinary, including researchers from the ASU Biosciences Mass spectrometry facility, and the Translational Cardiovascular Research Center at the University of Arizona College of Medicine in Phoenix, AZ.
“This collaborative work, spanning multiple institutions and surveying the molecular processes of aging at the systems level, adds to the body of evidence produced around the importance of dietary choline in healthy aging,” said Nikhil Dave.
“What I found particularly compelling about this project was that multiple organs, whose malfunction can have implications for brain health, were negatively impacted by a choline deficient diet", said Jessica Judd.
The research appears in the current issue of the journal Aging Cell.
A prolific and mysterious killer
Alzheimer’s disease is the leading cause of dementia and the fifth leading cause of death among Americans aged 65 and older. Today, Alzheimer’s affects 6.5 million in the U.S. alone and is projected to strike close to 14 million Americans by 2060. By this time, the costs of managing Alzheimer’s are expected to exceed a $20 trillion, threatening the healthcare infrastructure while causing immense suffering.
The accumulation of sticky protein fragments outside neurons, (which form amyloid-beta plaques), and the buildup of an abnormal form of the protein tau within the bodies of neurons (tau tangles) have long been recognized signposts of Alzheimer’s disease. These brain alterations are typically followed by neurodegeneration, involving the damage and destruction of neurons. Plaques are believed to damage cell-to-cell communications in the brain while tangles block the transport of vital nutrients essential for proper cell function and survival.
In addition to amyloid-beta plaques and neurofibrillary tangles, the disease causes cell death in the brain and increasing cognitive impairment. The current work also found dysregulation of proteins in the hippocampus, a key structure affected in Alzheimer’s disease, tied to learning and memory. Both normal and AD mice showed dysregulated proteins in the hippocampus with a choline deficient diet, with the AD model showing severe effects.
Gathering storm
The recent, dramatic increase in Alzheimer’s disease incidence is of grave concern. Although deaths from stroke, heart disease and HIV decreased between 2000 and 2019, deaths from Alzheimer’s increased more than 145%. In addition to the toll on patients caused by the disease, Alzheimer’s has placed an immense burden on those caring for the sick. In 2021 alone, 16 billion hours of care were provided by over 11 million family members and other unpaid caregivers.
The first outward symptoms of the disease are usually related to language, memory, and thinking problems, as brain regions associated with these tasks tend to be among the first affected. Yet researchers now know that by the time the disease causes observable symptoms, it has been quietly ravaging the brain for 20 years or more.
Many factors contribute to the development of Alzheimer’s disease, from genetic predisposition to age, lifestyle and environmental influences. For reasons that remain murky, females face an increased risk of developing the disease.
Recent studies have identified diet as a significant factor associated with preventing cognitive decline. In earlier research, Velazquez and his colleagues demonstrated that when mice were fed a high choline diet, their offspring showed improvements in spatial memory, compared with a normal choline regimen in the womb. Intriguingly, the beneficial effects of choline supplementation are transgenerational, not only protecting mice receiving choline supplementation during gestation and lactation, but also the subsequent offspring of these mice, suggesting inherited modifications in their genes.
Subsequent studies in the Velazquez lab showed that choline administered to female mice throughout life yielded improvements in spatial memory, compared with those receiving a normal choline regimen.
Multifaceted effects
The new study examines mice at 3-12 months or early to late adulthood, (roughly equivalent to 20-60 years of age for humans). In the case of both normal and transgenic mice displaying symptoms of Alzheimer’s, those exposed to a deficient choline diet exhibited weight gain and adverse effects to their metabolism. Damage to the liver was observed through tissue analysis, as well as enlargement of the heart. Elevated soluble, oligomeric and insoluble amyloid-beta protein were detected as well as modifications to tau protein characteristic of those leading to neurofibrillary tangles in the brain.
Further, choline deficient mice performed poorly in a test of motor skills, when compared with mice receiving adequate choline in their diet. These adverse effects were heightened in the transgenic mice. Translating these findings to humans, this implies that people who are predisposed to Alzheimer’s disease or in the throes of the illness should ensure they are getting enough choline.
The study also involved a detailed exploration of proteins in the hippocampus, an area of the brain acutely affected by Alzheimer’s disease, as well as proteins detected in blood. Dietary choline deficiency altered important hippocampal networks. These pathologies include disruption of pathways associated with microtubule function and postsynaptic membrane regulation—both essential for proper brain function. In blood, proteins produced in the liver that play a role in metabolic function were particularly dysregulated with the choline deficient diet.
“Our work provides further support that dietary choline should be consumed on a daily basis given the need throughout the body,” Velazquez says.
Ultimately, controlled human clinical trials will be essential for establishing the effectiveness and appropriate dosages of choline, before encouraging lifelong choline supplementation. Nevertheless, the powerful new findings offer hope that choline may be one tool in the arsenal needed to defend the brain from neurodegeneration and age-related cognitive decline.
COVID-19 is changing household behaviors related to how we are exposed to various household chemicals linked to poor health outcomes. People surveyed earlier in the pandemic were using less personal care products but more household cleaners, eating less fast food and restaurant food but more ultra-processed food. These changes which occurred since the pandemic onset are also linked to pandemic-related traumatic stress, which itself may worsen health outcomes.
Researchers at Columbia University Mailman School of Public Health along with partners from Dartmouth College, as part of the Environmental influences on Child Health Outcomes (ECHO) consortium, analyzed responses to a survey from 1,535 adults in six states. Results are published in the journal PLOS ONE.
Personal care products. Overall, participants reported using fewer personal care products, including hair products (perms or relaxers, hair dye, hair sprays, hair gels) and makeup/body products (nail polish, make-up, perfume, lotion) since the start of the pandemic. Participants who experienced more pandemic-related traumatic stress were more likely to report using fewer hair products and cosmetics. Approximately half of all respondents reported using more liquid soaps (52%) and antibacterial soaps (48%) and 81 percent of respondents reported using more hand sanitizer gels. The use of all three products was associated with pandemic-related traumatic stress symptoms.
Household cleansers. Two-thirds of respondents reported using more antibacterial cleaners and 54 percent reported using more bleach-containing cleaning products—changes made more likely among those experiencing more pandemic-related traumatic stress.
Food-related behaviors. Nearly half (49%) of respondents said they eat more home-cooked meals because of the pandemic. One-third (34%) of respondents reported eating less fast food since the start of the pandemic. Both of these behavior changes were more common among those with more symptoms of pandemic-related traumatic stress. In all, 12 percent reported eating more ultra-processed foods, and 24 percent reported eating less processed foods, with the latter more likely among those with symptoms of pandemic-related traumatic stress.
The Upshot
While the study did not include measurements of environmental exposures, the researchers say that the scientific literature suggests that these behavior changes likely reflect changes in their exposures to environmental chemicals. They also likely reflect changes—both good and bad—to health outcomes linked to these chemicals.
“We can infer that some behaviors like less consumption of fast foods and less use of personal care products might lower exposures to some phthalates and phenols, while greater use of personal and household cleansers may be associated with higher exposure to quaternary ammonium compounds and glycol ethers; and more frequent consumption of ultra-processed food could increase exposure to phthalates and phenols,” says lead author Julie Herbstman, PhD, director of the Columbia Center for Children’s Environmental Health (CCCEH) and professor of environmental health sciences.
Phthalates are linked asthma, attention-deficit hyperactivity disorder, breast cancer, obesity and type II diabetes and neurodevelopmental and behavioral issues. Phenols like BPA are linked to reproductive dysfunction, reduced birth size, cognitive and/or behavior outcomes, asthma, and obesity. Quaternary ammonium compounds are skin irritants and can also lead to asthma exacerbations. Exposure to glycol ethers may also irritate skin, eyes, nose, and throat and may also lead to anemia and/or adverse reproductive outcomes like birth defects.
A Roadmap to Interventions
The study identifies several factors that make some of these behavior changes more likely, including symptoms of pandemic-related traumatic stress and living in a household where someone tested positive for COVID-19, as well as race/ethnicity. Going forward, the researchers plan to repeat their analysis, adding a biological measure of chemical exposures to assess whether the trends in pandemic-related behavior change reported here do, in fact, result in shifts in exposures measured through biomarkers of internal dose. They also say it is important to continue to monitor pandemic-related behavior change as pandemic severity waxes and wanes.
The researchers say their study could lead to an intervention to reduce exposure to harmful environmental chemicals.
“Interventions and campaigns targeting the reduction of environmental exposures, pandemic-related traumatic stress, as well as those that facilitate behavior change can help improve health outcomes that are indirectly related to the pandemic,” says Herbstman.
Nitrites and nitrates occur naturally in water and soil and are commonly ingested from drinking water and dietary sources. They are also used as food additives to increase shelf life. A study publishing January 17th in the open access journal PLOS Medicine by Bernard Srour of the Nutritional Epidemiology Research Team (EREN-CRESS) of Inserm, INRAE, Cnam, and Sorbonne Paris Nord University, Bobigny, France and colleagues suggests an association between dietary exposure to nitrites and risk of type 2 diabetes.
According to the authors, “These results provide a new piece of evidence in the context of current discussions regarding the need for a reduction of nitrite additives’ use in processed meats by the food industry, and could support the need for better regulation of soil contamination by fertilizers. In the meantime, several public health authorities worldwide already recommend citizens to limit their consumption of foods containing controversial additives, including sodium nitrite”.
Srour and Touvier add, “This is the first largescale cohort study to suggest a direct association between additives-originated nitrites and type-2 diabetes risk. It also corroborates previously suggested associations between total dietary nitrites and T2D risk.”
Six minutes of high-intensity exercise could extend the lifespan of a healthy brain and delay the onset of neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. New research published in The Journal of Physiology shows that a short but intense bout of cycling increases the production of a specialised protein that is essential for brain formation, learning and memory, and could protect the brain from age-related cognitive decline. This insight on exercise is part of the drive to develop accessible, equitable and affordable non-pharmacological approaches that anyone can adopt to promote healthy ageing.
The specialised protein named brain-derived neurotrophic factor (BDNF) promotes neuroplasticity (the ability of the brain to form new connections and pathways) and the survival of neurons. Animal studies have shown that increasing the availability of BDNF encourages the formation and storage of memories, enhances learning and overall boosts cognitive performance. These key roles and its apparent neuroprotective qualities have led to the interest in BDNF for ageing research.
Lead author Travis Gibbons from University of Otago, New Zealand said,
“BDNF has shown great promise in animal models, but pharmaceutical interventions have thus far failed to safely harness the protective power of BDNF in humans. We saw the need to explore non-pharmacological approaches that can preserve the brain’s capacity which humans can use to naturally increase BDNF to help with healthy ageing.”
To tease apart the influence of fasting and exercise on BDNF production the researchers, from the University of Otago, New Zealand,compared the following factors to study the isolated and interactive effects:
Fasting for 20 hours,
Light exercise (90-minute low intensity cycling),
High-intensity exercise (six-minute bout of vigorous cycling),
Combined fasting and exercise.
They found thatbrief but vigorous exercise was the most efficient way to increase BDNF compared to one day of fasting with or without a lengthy session of light exercise.BDNF increased by four to five-fold (396 pg L-1 to 1170 pg L-1) more compared to fasting (no change in BDNF concentration) or prolonged activity (slight increase in BDNF concentration, 336 pg L-1 to 390 pg L-1).
The cause for these differences is not yet known and more research is needed to understand the mechanisms involved. One hypothesis is related to the cerebral substrate switch and glucose metabolism, the brain’s primary fuel source. The cerebral substrate switch is when the brain switches its favoured fuel source for another to ensure the body’s energy demands are met, for example metabolising lactate rather than glucose during exercise. The brain’s transition from consuming glucose to lactate initiates pathways that result in elevated levels of BDNF in the blood.
The observed increase in BDNF during exercise could be due to the increased number of platelets (the smallest blood cell) which store large amounts of BDNF. The concentration of platelets circulating in the blood is more heavily influenced by exercise than fasting and increases by 20%.
12 physically active participants (six males, six females aged between 18 and 56 years) took part in the study. The balanced ratio of male and female participants was to provide a better representation of the population rather than indicate sex differences.
Further research is underway to delve deeper into the effects of calorie restriction and exercise to distinguish the influence on BDNF and the cognitive benefits.
Travis Gibbons said,
“We are now studying how fasting for longer durations, for example up to three days, influences BDNF. We are curious whether exercising hard at the start of a fast accelerates the beneficial effects of fasting. Fasting and exercise are rarely studied together. We think fasting and exercise can be used in conjunction to optimise BDNF production in the human brain.”
Mounting evidence suggests that prolonged sitting—a staple of modern-day life—is hazardous to your health, even if you exercise regularly. Based on these findings, doctors advise all adults to sit less and move more.
But how often do we need to get up from our chairs? And for how long?
Few studies have compared multiple options to come up with the answer most office workers want: What is the least amount of activity needed to counteract the health impact of a workday filled with sitting?
Now a study by Columbia University exercise physiologists has an answer: just five minutes of walking every half hour during periods of prolonged sitting can offset some of the most harmful effects.
The study, led by Keith Diaz, PhD, associate professor of behavioral medicine at Columbia University Vagelos College of Physicians and Surgeons, was published online in Medicine & Science in Sports & Exercise, the journal of the American College of Sports Medicine.
Unlike other studies that test one or two activity options, Diaz’s study tested five different exercise “snacks”: one minute of walking after every 30 minutes of sitting, one minute after 60 minutes; five minutes every 30; five minutes every 60; and no walking.
“If we hadn’t compared multiple options and varied the frequency and duration of the exercise, we would have only been able to provide people with our best guesses of the optimal routine,” Diaz says.
Each of the 11 adults who participated in the study came to Diaz’s laboratory, where participants sat in an ergonomic chair for eight hours, rising only for their prescribed exercise snack of treadmill walking or a bathroom break. Researchers kept an eye on each participant to ensure they did not over- or under-exercise and periodically measured the participants’ blood pressure and blood sugar (key indicators of cardiovascular health). Participants were allowed to work on a laptop, read, and use their phones during the sessions and were provided standardized meals.
The optimal amount of movement, the researchers found, was five minutes of walking every 30 minutes. This was the only amount that significantly lowered both blood sugar and blood pressure. In addition, this walking regimen had a dramatic effect on how the participants responded to large meals, reducing blood sugar spikes by 58% compared with sitting all day.
Taking a walking break every 30 minutes for one minute also provided modest benefits for blood sugar levels throughout the day, while walking every 60 minutes (either for one minute or five minutes) provided no benefit.
All amounts of walking significantly reduced blood pressure by 4 to 5 mmHg compared with sitting all day. “This is a sizeable decrease, comparable to the reduction you would expect from exercising daily for six months,” says Diaz.
The researchers also periodically measured participants’ levels of mood, fatigue, and cognitive performance during the testing. All walking regimens, except walking one minute every hour, led to significant decreases in fatigue and significant improvements in mood. None of the walking regimens influenced cognition.
“The effects on mood and fatigue are important,” Diaz says. “People tend to repeat behaviors that make them feel good and that are enjoyable.”
The Columbia researchers are currently testing 25 different doses of walking on health outcomes and testing a wider variety of people: Participants in the current study were in their 40s, 50s, and 60s, and most did not have diabetes or high blood pressure.
“What we know now is that for optimal health, you need to move regularly at work, in addition to a daily exercise routine,” says Diaz. “While that may sound impractical, our findings show that even small amounts of walking spread through the work day can significantly lower your risk of heart disease and other chronic illnesses.”
More information
Keith Diaz, PhD, is the Florence Irving Associate Professor of Behavioral Medicine in the Department of Medicine at Columbia University Vagelos College of Physicians and Surgeons and director of the Exercise Testing Laboratory in the Center for Behavioral Cardiovascular Health.
The study is titled “Breaking Up Prolonged Sitting to Improve Cardiometabolic Risk: Dose-Response Analysis of a Randomized Cross-Over Trial.”
The other contributors are Andrea T. Duran(Columbia), Ciaran P. Friel (Feinstein Institutes of Medical Research, Northwell Health), Maria A. Serafini (Columbia), Ipek Ensari(Columbia), and Ying Kuen Cheung(Columbia).
