«Saturated fat intake may influence a person's expression of
genetic obesity risk.»
Not exact matches
The Mayo Clinic states common
risk factors as changes in female hormones, older age,
obesity, and inherited
genetic conditions — not sugar or beverage consumption.
Results were similar in analyses of sleep patterns; among participants with some
genetic risk of
obesity, those who woke up frequently or slept more restlessly had higher BMIs than those who slept more efficiently.
«Physical inactivity and restless sleep exacerbate
genetic risk of
obesity: Findings reported at ASHG 2017 Annual Meeting.»
Low levels of physical activity and inefficient sleep patterns intensify the effects of
genetic risk factors for
obesity, according to results of a large - scale study presented at the American Society of Human Genetics (ASHG) 2017 Annual Meeting in Orlando, Fla..
«We wanted to find out if
obesity - related genes and activity level have an interactive effect on
obesity risk — if there is a «double whammy» effect of being both at
genetic risk and physically inactive, beyond the additive effect of these factors,» said Dr. Wood.
The researchers computed a
genetic risk score for each participant based on 76 common variants known to be associated with elevated
risk of
obesity, and analyzed this score in the context of accelerometer data and participants» BMIs.
Genetic risk score could be useful in identifying people who are predisposed to
obesity and could ultimately lead to personalized dietary recommendations.
Genetic risk factors may make some individuals more susceptible to these changes in the environment, and thus more prone to
obesity.
Although several environmental and
genetic factors have been shown to contribute to the
risk of T2D (e.g.,
obesity, inactivity, and aging), the origin of this disease is still not completely understood (Stumvoll et al., 2005).
Check out Diane's other recent publication «
Genetic risk for
obesity predicts nucleus accumbens size and responsivity to real - world food cues»
This
genetic risk factor is independent of other
risk factors, such as cholesterol,
obesity and smoking, and therefore provides an additional method for identifying individuals who may derive benefit from earlier and more aggressive prevention efforts.
Angela C Estampador, 1,2 Paul W Franks1, 3,4 1Department of Clinical Sciences,
Genetic and Molecular Epidemiology Unit, Lund University, Skåne University Hospital Malmö, Malmö, Sweden; 2Department of Endocrinology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark; 3Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden; 4Department of Nutrition, Harvard School of Public Health, Boston, MA, USA Abstract: Evidence has emerged across the past few decades that the lifetime
risk of developing morbidities like type 2 diabetes,
obesity, and cardiovascular disease may be influenced by exposures that occur in utero and in childhood.
The genes were identified through population - and genome - wide linkage scans and association analyses of at -
risk haplotypes utilizing
genetic and clinical data from the 17,000 participants in deCODE's
obesity program in Iceland.
ASHG 2017: Physical Inactivity and Restless Sleep Exacerbate
Genetic Risk of
Obesity ASHG Press Release — October 20, 2017
And, we'll tie together the previous levels by connecting how inflammation related to the previous system discussions - poor digestion, immune dysfunction, hormonal dysregulation,
genetic snps, and environmental toxin exposures (including emotional toxins)- contribute to an increased
risk of chronic rehab challenges, including chronic joint pain, poor surgical or injury recovery,
obesity, memory loss or dementia, diabetes, or even poor sports performance.
The researchers measured the participants»
genetic risk by identifying how many of the 32 known variants of the so - called
obesity gene each person had.
Regarding the child, the importance of the intrauterine and early postnatal environments for metabolic programming and modifications of the epigenome is increasingly recognised, 12 — 14 particularly for metabolic diseases such as
obesity and diabetes.15 Thus, GDM is related to macrosomia at birth (> 4 kg), to excess body fat and (central)
obesity and to insulin secretion in infants and children, the
obesity being in part mediated by maternal body mass index (BMI) or birth weight.16 — 23 Intrauterine exposure to GDM also doubles the
risk for subsequent type 2 diabetes in offspring compared with offspring of mothers with a high
genetic predisposition for type 2 diabetes, but with normal glucose tolerance during the index pregnancy.24 Maternal prepregnancy overweight and excessive gestational weight gain also predict high birth weight and adiposity during infancy.12 25 This is highly relevant, as up to 60 % — 70 % of women with GDM are overweight or obese before pregnancy.26 Finally, maternal lifestyle behaviour such as a high fat diet or lack of physical activity during pregnancy can influence offspring adiposity independent of maternal
obesity.12 27
A
genetic risk score combining 32 SNPs is associated with body mass index and improves
obesity prediction in people with major depressive disorder.
We are exploring new insights into the
genetic roots of autism; finding pediatric bio-behavioral markers of bipolar disorder; creating effective therapies for OCD; devising effective prevention strategies for adolescent sexual
risk behaviors and
obesity; and much more.