Young children often display similar eating behaviour as their parents, with a parent’s own eating style influencing how they feed their children, research at Aston University has shown.
The work, published in the journal Appetite, suggests that parents can help to shape healthy eating behaviour in their children both by how they themselves eat, as well as how they feed their children.
A team led by Professor Jacqueline Blissett at Aston University, asked parents to assess their own eating behaviour and looked for associations between those behaviours and those of their children.
The team grouped parents into four eating styles – ‘typical eating’, ‘avid eating’, ‘emotional eating’ and ‘avoidant eating’. Typical eaters, who made up 41.4% of the sample, have no extreme behaviours. Avid eaters (37.3%) have high food approach traits such as eating in response to food cues in the environment and their emotions, rather than hunger signals. Emotional eaters (15.7%) also eat in response to emotion but do not enjoy food as much as avid eaters. Avoidant eaters (5.6%) are extremely selective about food and have a low enjoyment of eating.
The direct links between child and parent behaviour were particularly clear in parents with avid or avoidant eating behaviours, whose children tended to have similar eating behaviour. Parents who had avid or emotional eating styles were more likely to use food to soothe or comfort a child, who then in turn displayed avid or emotional eating traits. Where parents with avid or emotional eating traits provided a balanced and varied range of foods, the child was less likely to display the same behaviour.
The research follows on from previous work by the team, which identified the four main types of eating behaviour in children and linked parental feeding practices to those traits.
“Parents are a key influence in children’s eating behaviour but equally, parents have the perfect opportunity to encourage a balanced diet and healthy eating from a young age in their children. Therefore, it is important to establish how a parent’s eating style is associated with their children’s eating style and what factors could be modified to encourage healthy relationships with food.”
She and the team will now look at developing an intervention to support parents to use other ways to regulate emotions, model healthy eating, and create a healthy home food environment. This could help to prevent less favourable eating behaviours being passed down the generations from parent to child.
Scientists have discovered that ‘turning off’ the cytokine IL-11 can significantly increase the healthy lifespan of mice by almost 25%.
The scientists, at the Medical Research Council Laboratory of Medical Science (MRC LMS), Imperial College London and Duke-NUS Medical School in Singapore, tested the effects of IL-11 by creating mice with the gene for IL-11 (interleukin 11) deleted. This extended the lives of the mice by over 20% on average. The cytokine has for years been misidentified as an anti-inflammatory and anti-fibrotic.
They also treated 75-week-old mice, equivalent to the age of about 55 years in humans, with an injection of an anti-IL-11 antibody, a drug that stops the effects of the IL-11 in the body.
Median lifespan extended
The results, published in Nature, were dramatic, with mice given the anti-IL-11 drug from 75 weeks of age until death having their median lifespan extended by 22.4% in males and 25% in females. The mice lived for an average of 155 weeks, compared with 120 weeks in untreated mice.
The treatment largely reduced deaths from cancer in the animals, as well as reducing the many diseases caused by fibrosis, chronic inflammation and poor metabolism, which are hallmarks of ageing. There were very few side effects observed.
Fewer cancers and free from the usual signs of ageing and frailty
Professor Stuart Cook, who was co-corresponding author, from MRC LMS, Imperial College London and Duke-NUS Medical School in Singapore, said:
These findings are very exciting. The treated mice had fewer cancers, and were free from the usual signs of ageing and frailty, but we also saw reduced muscle wasting and improvement in muscle strength. In other words, the old mice receiving anti-IL11 were healthier.
Previously proposed life-extending drugs and treatments have either had poor side-effect profiles, or don’t work in both sexes, or could extend life, but not healthy life, however this does not appear to be the case for IL-11.
While these findings are only in mice, it raises the tantalising possibility that the drugs could have a similar effect in elderly humans. Anti-IL-11 treatments are currently in human clinical trials for other conditions, potentially providing exciting opportunities to study its effects in ageing humans in the future.
This project started back in 2017 when a collaborator of ours sent us some tissue samples for another project. Out of curiosity, I ran some experiments to check for IL-11 levels. From the readings, we could clearly see that the levels of IL-11 increased with age and that’s when we got really excited!
We found these rising levels contribute to negative effects in the body, such as inflammation and preventing organs from healing and regenerating after injury. Although our work was done in mice, we hope that these findings will be highly relevant to human health, given that we have seen similar effects in studies of human cells and tissues.
This research is an important step toward better understanding ageing and we have demonstrated, in mice, a therapy that could potentially extend healthy ageing, by reducing frailty and the physiological manifestations of ageing.
Previously, scientists have posited that IL-11 is an evolutionary hangover in humans, as while it is vital for limb regeneration in some animal species, it is thought to be largely redundant in humans.
IL-11 linked to chronic inflammation and frailty
However, after about the age of 55 in humans, more IL-11 is produced and past research has linked this to chronic inflammation, fibrosis in organs, disorders of metabolism, muscle wasting (sarcopaenia), frailty, and cardiac fibrosis. These conditions are many of the signs we associate with ageing.
When two or more such conditions occur in an individual, it is known as multimorbidity, which encompasses a range of conditions including lung disease, cardiovascular disease, diabetes, vision and hearing decline and a host of other conditions.
Professor Cook said:
The IL-11 gene activity increases in all tissues in the mouse with age. When it gets turned on it causes multimorbidity, which is diseases of ageing and loss of function across the whole body, ranging from eyesight to hearing, from muscle to hair, and from the pump function of the heart to the kidneys.
Multimorbidity among biggest global healthcare challenges
Multimorbidity and frailty are acknowledged to be among the biggest global healthcare challenges of the 21st century, according to many leading health bodies, including the NHS and the World Health Organization.
Currently, no treatment for multimorbidity is available, other than to try to treat the separate multiple underlying causes individually.
The scientists caution that the results in this study were in mice and the safety and effectiveness of these treatments in humans need further establishing in clinical trials before people consider using anti-IL-11 drugs for this purpose.
Radiation is a powerful tool for treating cancer, but prolonged exposure can damage the skin. Radiation-induced skin injuries are painful and increase a person’s chances of infection and long-term inflammation. Now, researchers in ACS Biomaterials Science & Engineering report an aspirin-containing hydrogel that mimics the nutrient-rich fluid between cells and accelerates healing of skin damaged by radiation in animals. With further development, the new salve could provide effective and rapid wound healing for humans.
Most people undergoing radiotherapy for cancer will experience radiation-induced skin injury that can include redness, pain, ulcers, necrosis and infection. There are few treatments for these wounds, with the most common methods being debridement and hyperbaric oxygenation. Wound dressings made from hydrogels are gaining popularity because they are easy to apply and provide a wet environment for healing that is similar to the inside of the body. Glycopeptide-based hydrogels are especially promising: In laboratory and animal studies, the nanofibre structures have promoted cellular growth and regulated cell adhesion and migration. A research team led by Jiamin Zhang, Wei Wang, Yumin Zhang and Jianfeng Liu proposed loading aspirin, a common anti-inflammatory drug, into a glycopeptide-based hydrogel to create a multifunctional wound dressing for radiation-induced skin injuries.
In lab tests with cultured cells, the researchers found that the aspirin-contained hydrogel scavenged reactive oxygen species, repaired DNA double-strand breaks and inhibited inflammation caused by radiation exposure without affecting cellular growth. In mouse models of radiation-induced skin injury, the researchers found that dressing wounds for three weeks with the salve reduced acute injuries and accelerated healing – results that the team says point to its potential as an easy-to-administer, on-demand treatment option for reducing radiation damage and promoting healing in humans.
Skin cell (keratinocyte)
This normal human skin cell was treated with a growth factor that triggered the formation of specialised protein structures that enable the cell to move. We depend on cell movement for such basic functions as wound healing and launching an immune response. Credit: Torsten Wittmann, University of California, San Francisco
Fingerprints are one of the best-recognised examples of pattern formation by epithelial cells. The primary cells in the epithelium are the keratinocytes, and they are known to form patterns at the microscopic and macroscopic levels. While factors affecting this pattern formation have been reported, the exact mechanisms underlying the process are still not fully understood.
A team of researchers, led by Associate Professor Ken Natsuga at the Faculty of Medicine, Hokkaido University, have revealed that cell-cell adhesion governs pattern formation in keratinocytes. Their findings were published in the journal Life Science Alliance.
“In this study, we used an immortalised keratinocyte cell line, called HaCaT, which retains all the properties of normal keratinocytes,” Natsuga explained. “In order to ensure that our findings were accurate, we established single-cell cultures from this cell line.”
The team observed pattern formation in both the original heterogeneous cell line, as well as in single-cell-derived cultures. During culturing, the keratinocytes moved randomly and spontaneously formed high- and low-density regions, leading to pattern formation.
The pattern formation was markedly influenced by starvation. When the culture medium was renewed, patterns were obscured, but reappeared as the nutrients in the culture medium were consumed by the keratinocytes.
The team then examined the gene expression in the keratinocytes, which revealed that cell adhesion proteins and keratinocyte differentiation proteins were upregulated in high-density regions. “As cell adhesion is necessary for the development of high-cell-density regions, we specifically investigated the expression of adherens junction (AJ) molecules such as E-cadherin and actin,” Natsuga elaborated. “We found that these molecules were localised at the intercellular junctions of high-density regions.”
The authors then used a mathematical model to confirm that, under spatially uniform density and stress, strong cell adhesion leads to the formation of density patterns. They were also able to demonstrate that the keratinocyte patterns influenced cell proliferation and differentiation, and that serum starvation influences epidermal stratification (a type of differentiation) in skin cells from mice.
“Our study presents a novel and robust model of cell–cell adhesion-induced patterning (CAIP),” concludes Natsuga. “We have deepened our mechanistic insight into cellular organization and its consequences for cell fate decisions and epithelial stratification.” The team demonstrated that epithelial cell–cell adhesion is essential and sufficient for patterning. Future work will focus on adding more variables to the model to understand other processes that occur concurrently during development.
