Wednesday, December 18, 2019
Obesity, but not poor diet and inactivity, linked to higher risk of dementia
A large study that followed more than one million women for nearly two decades has found that obesity in midlife is linked to a greater risk of dementia later in life; however, poor diet and lack of exercise are not. The study is published in the December 18, 2019, online issue of Neurology®, the medical journal of the American Academy of Neurology.
"Some previous studies have suggested poor diet or a lack of exercise may increase a person's risk of dementia," said study author Sarah Floud, PhD, of the Nuffield Department of Population Health at the University of Oxford in the United Kingdom. "However, our study found these factors are not linked to the long-term risk of dementia. Short-term associations between these factors and dementia risk are likely to reflect changes in behavior, such as eating poorly and being inactive, due to early symptoms of dementia."
The study involved one of every four women born in the United Kingdom between 1935 to 1950, or nearly 1,137,000 women. They had an average age of 56 and did not have dementia at the start of the study. Participants were asked about their height, weight, diet and exercise at the start of the study.
BMI is a measure of a person's body size based on their height and weight. For the study, a BMI between 20 and 25 was considered desirable, and a BMI of 30 or higher was considered obese. Women who reported exercising less than once per week were considered inactive. Those who exercised more often were considered active. Women's reported usual diet was used to calculate their calorie intake.
Researchers then followed the women for an average of 18 years. After 15 years from the start of the study, 18,695 women were diagnosed with dementia.
Researchers adjusted for age, education, smoking and many other factors. They found that women who were obese at the start of the study had, in the long-term, a 21-percent greater risk of dementia compared to women with a desirable BMI. Among the obese women, 2.1 percent, or 3,948 of 177,991 women, were diagnosed with dementia. This is compared to 1.6 percent of women with desirable BMI, or 7,248 of 434,923 women, who were diagnosed with the disease.
However, while low calorie intake and inactivity were associated with a higher risk of dementia during the first 10 years of the study, these associations weakened substantially, and after 15 years, neither was strongly linked to dementia risk.
"Other studies have shown that people become inactive and lose weight up to a decade before they are diagnosed with dementia," said Floud. "The short-term links between dementia, inactivity and low calorie intake are likely to be the result of the earliest signs of the disease, before symptoms start to show."
Floud continued, "On the other hand, obesity in midlife was linked with dementia 15 or more years later. Obesity is a well-established risk factor for cerebrovascular disease. Cerebrovascular disease contributes to dementia later in life."
A limitation of the study was that it looked at women only, so the results may not be the same for men.
Early-life exposure to dogs may lessen risk of developing schizophrenia
Ever since humans domesticated the dog, the faithful, obedient and protective animal has provided its owner with companionship and emotional well-being. Now, a study from Johns Hopkins Medicine suggests that being around "man's best friend" from an early age may have a health benefit as well -- lessening the chance of developing schizophrenia as an adult.
And while Fido may help prevent that condition, the jury is still out on whether or not there's any link, positive or negative, between being raised with Fluffy the cat and later developing either schizophrenia or bipolar disorder.
"Serious psychiatric disorders have been associated with alterations in the immune system linked to environmental exposures in early life, and since household pets are often among the first things with which children have close contact, it was logical for us to explore the possibilities of a connection between the two," says Robert Yolken, M.D., chair of the Stanley Division of Pediatric Neurovirology and professor of neurovirology in pediatrics at the Johns Hopkins Children's Center, and lead author of a research paper recently posted online in the journal PLOS One.
In the study, Yolken and colleagues at Sheppard Pratt Health System in Baltimore investigated the relationship between exposure to a household pet cat or dog during the first 12 years of life and a later diagnosis of schizophrenia or bipolar disorder. For schizophrenia, the researchers were surprised to see a statistically significant decrease in the risk of a person developing the disorder if exposed to a dog early in life. Across the entire age range studied, there was no significant link between dogs and bipolar disorder, or between cats and either psychiatric disorder.
The researchers caution that more studies are needed to confirm these findings, to search for the factors behind any strongly supported links, and to more precisely define the actual risks of developing psychiatric disorders from exposing infants and children under age 13 to pet cats and dogs.
According to the American Pet Products Association's most recent National Pet Owners Survey, there are 94 million pet cats and 90 million pet dogs in the United States. Previous studies have identified early life exposures to pet cats and dogs as environmental factors that may alter the immune system through various means, including allergic responses, contact with zoonotic (animal) bacteria and viruses, changes in a home's microbiome, and pet-induced stress reduction effects on human brain chemistry.
Some investigators, Yolken notes, suspect that this "immune modulation" may alter the risk of developing psychiatric disorders to which a person is genetically or otherwise predisposed.
In their current study, Yolken and colleagues looked at a population of 1,371 men and women between the ages of 18 and 65 that consisted of 396 people with schizophrenia, 381 with bipolar disorder and 594 controls. Information documented about each person included age, gender, race/ethnicity, place of birth and highest level of parental education (as a measure of socioeconomic status). Patients with schizophrenia and bipolar disorder were recruited from inpatient, day hospital and rehabilitation programs of Sheppard Pratt Health System. Control group members were recruited from the Baltimore area and were screened to rule out any current or past psychiatric disorders.
All study participants were asked if they had a household pet cat or dog or both during their first 12 years of life. Those who reported that a pet cat or dog was in their house when they were born were considered to be exposed to that animal since birth.
The relationship between the age of first household pet exposure and psychiatric diagnosis was defined using a statistical model that produces a hazard ratio -- a measure over time of how often specific events (in this case, exposure to a household pet and development of a psychiatric disorder) happen in a study group compared to their frequency in a control group. A hazard ratio of 1 suggests no difference between groups, while a ratio greater than 1 indicates an increased likelihood of developing schizophrenia or bipolar disorder. Likewise, a ratio less than 1 shows a decreased chance.
Analyses were conducted for four age ranges: birth to 3, 4 to 5, 6 to 8 and 9 to 12.
Surprisingly, Yolken says, the findings suggests that people who are exposed to a pet dog before their 13th birthday are significantly less likely -- as much as 24% -- to be diagnosed later with schizophrenia.
"The largest apparent protective effect was found for children who had a household pet dog at birth or were first exposed after birth but before age 3," he says.
Yolken adds that if it is assumed that the hazard ratio is an accurate reflection of relative risk, then some 840,000 cases of schizophrenia (24% of the 3.5 million people diagnosed with the disorder in the United States) might be prevented by pet dog exposure or other factors associated with pet dog exposure.
"There are several plausible explanations for this possible 'protective' effect from contact with dogs -- perhaps something in the canine microbiome that gets passed to humans and bolsters the immune system against or subdues a genetic predisposition to schizophrenia," Yolken says.
For bipolar disorder, the study results suggest there is no risk association, either positive or negative, with being around dogs as an infant or young child.
Overall for all ages examined, early exposure to pet cats was neutral as the study could not link felines with either an increased or decreased risk of developing schizophrenia or bipolar disorder.
"However, we did find a slightly increased risk of developing both disorders for those who were first in contact with cats between the ages of 9 and 12," Yolken says. "This indicates that the time of exposure may be critical to whether or not it alters the risk."
One example of a suspected pet-borne trigger for schizophrenia is the disease toxoplasmosis, a condition in which cats are the primary hosts of a parasite transmitted to humans via the animals' feces. Pregnant women have been advised for years not to change cat litter boxes to eliminate the risk of the illness passing through the placenta to their fetuses and causing a miscarriage, stillbirth, or potentially, psychiatric disorders in a child born with the infection.
In a 2003 review paper, Yolken and colleague E. Fuller Torrey, M.D., associate director of research at the Stanley Medical Research Institute in Bethesda, Maryland, provided evidence from multiple epidemiological studies conducted since 1953 that showed there also is a statistical connection between a person exposed to the parasite that causes toxoplasmosis and an increased risk of developing schizophrenia. The researchers found that a large number of people in those studies who were diagnosed with serious psychiatric disorders, including schizophrenia, also had high levels of antibodies to the toxoplasmosis parasite.
Because of this finding and others like it, most research has focused on investigating a potential link between early exposure to cats and psychiatric disorder development. Yolken says the most recent study is among the first to consider contact with dogs as well.
"A better understanding of the mechanisms underlying the associations between pet exposure and psychiatric disorders would allow us to develop appropriate prevention and treatment strategies," Yolken says.
Good sleep patterns offset genetic susceptibility to heart disease and stroke
Getting a good night's sleep could be beneficial for long-term
health. A pioneering new study led by Dr. Lu Qi, director of the Tulane
University Obesity Research Center, found that even if people had a high
genetic risk of heart disease or stroke, healthy sleep patterns could
help offset that risk. The study is published in the European Heart Journal.
The researchers looked at genetic variations known as SNPs (single nucleotide polymorphisms) that were already known to be linked to the development of heart disease and stroke. They analysed the SNPs from blood samples taken from more than 385,000 healthy participants in the UK Biobank project and used them to create a genetic risk score to determine whether the participants were at high, intermediate or low risk of cardiovascular problems.
The researchers followed the participants for an average of 8.5 years, during which time there were 7,280 cases of heart disease or stroke.
"We found that compared to those with an unhealthy sleep pattern, participants with good sleeping habits had a 35% reduced risk of cardiovascular disease and a 34% reduced risk of both heart disease and stroke," Qi says. Researchers say those with the healthiest sleep patterns slept 7 to 8 hours a night, without insomnia, snoring or daytime drowsiness.
When the researchers looked at the combined effect of sleep habits and genetic susceptibility on cardiovascular disease, they found that participants with both a high genetic risk and a poor sleep pattern had a more than 2.5-fold greater risk of heart disease and a 1.5-fold greater risk of stroke compared to those with a low genetic risk and a healthy sleep pattern. This meant that there were 11 more cases of heart disease and five more cases of stroke per 1000 people a year among poor sleepers with a high genetic risk compared to good sleepers with a low genetic risk. However, a healthy sleep pattern compensated slightly for a high genetic risk, with just over a two-fold increased risk for these people.
A person with a high genetic risk but a healthy sleep pattern had a 2.1-fold greater risk of heart disease and a 1.3-fold greater risk of stroke compared to someone with a low genetic risk and a good sleep pattern. While someone with a low genetic risk, but an unhealthy sleep pattern had 1.7-fold greater risk of heart disease and a 1.6-fold greater risk of stroke.
"As with other findings from observational studies, our results indicate an association, not a causal relation," Qi says. "However, these findings may motivate other investigations and, at least, suggest that it is essential to consider overall sleep behaviors when considering a person's risk of heart disease or stroke."
The researchers looked at genetic variations known as SNPs (single nucleotide polymorphisms) that were already known to be linked to the development of heart disease and stroke. They analysed the SNPs from blood samples taken from more than 385,000 healthy participants in the UK Biobank project and used them to create a genetic risk score to determine whether the participants were at high, intermediate or low risk of cardiovascular problems.
The researchers followed the participants for an average of 8.5 years, during which time there were 7,280 cases of heart disease or stroke.
"We found that compared to those with an unhealthy sleep pattern, participants with good sleeping habits had a 35% reduced risk of cardiovascular disease and a 34% reduced risk of both heart disease and stroke," Qi says. Researchers say those with the healthiest sleep patterns slept 7 to 8 hours a night, without insomnia, snoring or daytime drowsiness.
When the researchers looked at the combined effect of sleep habits and genetic susceptibility on cardiovascular disease, they found that participants with both a high genetic risk and a poor sleep pattern had a more than 2.5-fold greater risk of heart disease and a 1.5-fold greater risk of stroke compared to those with a low genetic risk and a healthy sleep pattern. This meant that there were 11 more cases of heart disease and five more cases of stroke per 1000 people a year among poor sleepers with a high genetic risk compared to good sleepers with a low genetic risk. However, a healthy sleep pattern compensated slightly for a high genetic risk, with just over a two-fold increased risk for these people.
A person with a high genetic risk but a healthy sleep pattern had a 2.1-fold greater risk of heart disease and a 1.3-fold greater risk of stroke compared to someone with a low genetic risk and a good sleep pattern. While someone with a low genetic risk, but an unhealthy sleep pattern had 1.7-fold greater risk of heart disease and a 1.6-fold greater risk of stroke.
"As with other findings from observational studies, our results indicate an association, not a causal relation," Qi says. "However, these findings may motivate other investigations and, at least, suggest that it is essential to consider overall sleep behaviors when considering a person's risk of heart disease or stroke."
Tuesday, December 17, 2019
Large study links sustained weight loss to reduced breast cancer risk
Results show that higher breast cancer risk from excess body weight can be reversed with weight loss
American Cancer Society
In the United States, more than two in three adult women are overweight or obese. And while high body mass index (BMI) is an established risk factor for postmenopausal breast cancer, there has not been adequate evidence to determine if that risk is reversible by losing excess weight.
To learn more, investigators from the American Cancer Society, Harvard T.H. Chan School of Public Health, and others used the Pooling Project of Prospective Studies of Diet and Cancer (DCPP) to estimate the association of sustained weight loss in middle or later adulthood on subsequent breast cancer risk. Their analysis included more than 180,000 women aged 50 and older from ten prospective studies. The new analysis is the first with a large enough sample size to examine the important question of whether sustained weight loss can impact breast cancer risk with statistical precision. Weight was assessed three times over approximately 10 years: at study enrollment; after about five years; then again about four years later.
The results showed women with sustained weight loss had a lower risk of breast cancer than women whose weight remained stable, and the larger the amount of sustained weight loss, the lower was the risk of breast cancer. Women who lost 2 to 4.5 kg (about 4.4 to 10 lbs.) had a 13% lower risk (HR= 0.87, 95% CI: 0.77-0.99) than women with stable weight. Women who lost 4.5 to 9 kg (10- 20 lbs.) had a 16% lower risk (HR=0.84, 95% CI: 0.73-0.96). Women who lost 9 kg or more (20+ lbs.) had a 26% lower risk (HR=0.74, 95% CI: 0.58-0.94).
In addition, women who lost 9 kg or more and gained some (but not all) of the weight back had a lower risk of breast cancer compared with those whose weight remained stable (HR=0.77, 95% CI: 0.62-0.97).
"Our results suggest that even a modest amount of sustained weight loss is associated with lower breast cancer risk for women over 50," said Lauren Teras, PhD, lead author of the study. "These findings may be a strong motivator for the two-thirds of American women who are overweight to lose some of that weight. Even if you gain weight after age 50, it is not too late to lower your risk of breast cancer."
The highest costs associated with cardiometabolic disease may be attributable to suboptimal consumption of foods such as nuts and seeds, and seafood-derived omega-3 fats
Approximately $50 billion dollars of the annual healthcare cost of cardiometabolic disease in the US population could be associated with poor diet, according to a research article published this week in the open access journal PLOS Medicine. The results of the study, conducted by Renata Micha and Thomas Gaziano of Tufts University and the Brigham and Women's Hospital, Boston, United States and colleagues, suggest that the highest costs associated with cardiometabolic disease may be attributable to suboptimal consumption of foods such as nuts and seeds, and seafood-derived omega-3 fats.
While unhealthy diet contributes to the risk of developing diseases such as type 2 diabetes, stroke, and coronary heart disease, the related healthcare costs are unknown. In the new study, which was part of the National Institutes of Health- funded Food-PRICE (Policy Review and Intervention Cost Effectiveness) Project to improve diet-related health in the US population, Micha, Gaziano and colleagues used a microsimulation modeling approach to estimate cardiometabolic disease costs associated with suboptimal consumption of ten food groups in US adults between 35 and 85 years of age. In their model, the authors incorporated dietary intake and cardiovascular disease risk factor data from the 2009-2012 National Health and Nutrition Examination Survey (NHANES), a program of studies assessing health and nutrition in the US.
The study estimated that the annual cardiometabolic disease cost associated with suboptimal diet is $301 per person, and $50.4 billion for the US population, corresponding to 18.2% of the total cardiometabolic disease cost. Further, the results suggest that the largest estimated annual costs per person are associated with lower than recommended consumption of foods such as nuts and seeds ($81), and omega-3 fats derived from seafood ($76). It is important to note that the study diet data are derived from individuals' recollections of recent food consumption, and could be subject to recall errors, or may not reflect an individual's long-term dietary habits.
These results suggest that improvements in diet may help to reduce the cost burden associated with cardiometabolic diseases in the US. The authors explain that the high costs attributable to specific dietary groups in this study, such as nuts and seeds, are in part related to the fact that individual consumption of these food components is relatively low, noting that "...from the economic perspective, intervention policies focused not just on the benefit or harm of dietary factors, but also focused on how far the population is from achieving ideal consumption are more likely to have economic benefit."
Artificial sweeteners may be doing more harm than good

Credit: Creative Commons
A recently published review led by UniSA Professor Peter Clifton reveals that people who use low-calorie sweeteners (LCS) are more likely to gain weight, the exact opposite of what consumers expect.
This is despite controlled clinical trials showing that artificial sweeteners do lead to weight loss.
There has been a 200 per cent increase in LCS usage among children and a 54 per cent increase among adults in the past 20 years, Prof Clifton says.
Low calorie sweeteners are used in place of sucrose, glucose and fructose. They have an intense sweet flavour without the calories, but recent studies have highlighted potential adverse health effects.
Prof Clifton says a US study of 5158 adults over a seven-year period found that those who consumed large quantities of artificial sweeteners gained more weight than non-users.
"Consumers of artificial sweeteners do not reduce their overall intake of sugar. They use both sugar and low-calorie sweeteners and may psychologically feel they can indulge in their favourite foods.
"Artificial sweeteners also change the gut bacteria which may lead to weight gain and risk of type 2 diabetes," he says.
Artificially sweetened beverages (ASB) are also linked with increased risks of death and cardiovascular disease, and strokes and dementia among older people, but it is not clear why.
Prof Clifton cites 13 studies which investigated the effects of ASB intake on the risk of type 2 diabetes, all of which found either no link or a positive one. One study found that substituting ASB for sugar-sweetened beverages or fruit juices was associated with a 5-7 per cent lower risk of type 2 diabetes.
"A better option than low-calorie sweeteners is to stick to a healthy diet, which includes plenty of whole grains, dairy, seafood, legumes, vegetables and fruits and plain water," Prof Clifton says.
Good aerobic fitness doesn't protect children against type 2 diabetes, staying active does

Credit: Eero Haapala
Good aerobic fitness does not protect against insulin resistance
It is a generally accepted idea that good aerobic fitness reduces the risk of type 2 diabetes, and it has also been thought to protect against other obesity-induced adverse changes in the glucose metabolism. However, this idea is based on studies whose methodology does not allow a distinction between the roles of aerobic fitness and body fat percentage as risk factors of insulin resistance and type 2 diabetes.
"Our study clearly shows that aerobic fitness is not associated with insulin resistance when body composition is taken into consideration properly. Moreover, good aerobic fitness doesn't seem to protect against obesity-induced insulin resistance. It seems that the role of poor aerobic fitness as a risk factor of type 2 diabetes has been grossly exaggerated," says Researcher Eero Haapala, PhD, from the Faculty of Sport and Health Sciences at the University of Jyväskylä. Dr Haapala is also an Adjunct Professor of Paediatric Exercise Physiology at the University of Eastern Finland.
Development of insulin resistance can be prevented
The researchers found that more brisk physical activity and less sedentary time were associated with reduced insulin resistance regardless of the level of aerobic fitness and body fat percentage. Getting more physical activity and less sedentary time also protected obese children against the development of insulin resistance.
"A key take-home message from our study is that more physical activity and less sedentary time play key roles in the prevention of type 2 diabetes already in childhood. For obese children, these seem to be especially important," Dr Haapala notes.
The study analysed 452 children between 6 and 8 years of age, exploring associations between their aerobic fitness, body fat percentage, physical activity, sedentary time and insulin resistance. Aerobic fitness was assessed using a maximal exercise test on a cycle ergometer, and body fat percentage by DXA measurement. Physical activity and sedentary time were measured using a combined movement and heart rate sensor, and insulin resistance was assessed by measuring glucose and insulin levels from blood samples.
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