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Winter is here, which means the season of sickness too is here. While viruses and sickness run throughout, winter is when the chilly weather further makes it worse for those prone to sickness. Especially, if they are kids, as their immunity is not fully developed.
Anytime a child is exposed to another child, they will fall sick. This is because germs are transferred in the air or by touch, and children, being curious, always touch things, including their own faces, mouths and easily pick up germs and spread them. While prevention is impossible, there are steps that can be taken to reduce this.
Experts and medical professionals recommend to follow the vaccine schedule by the Centers for Disease Control (CDC) and American Academy of Pediatrics (AAP). Vaccines have be proven to protect people, children, and infants from serious and deadly infections.
While sicknesses like a common cold do not have a vaccine, good hygiene can help prevent the spread of germs. Teaching your kids to wash hands after touching toys, or any other surface and other people is a great way to start it.
Is there really any truth in the statement? When we encounter infections, our immune system creates antibodies that either prevent future infections or help the body fight them off more effectively, often leading to milder illness. The "hygiene hypothesis" proposes that living in an overly clean environment might hinder the immune system's development, potentially increasing the risk of allergic conditions like asthma.
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Although research has explored this idea, many immunologists (experts in the immune system) have raised concerns and expressed disagreement with the hypothesis.
In reality, most children don’t grow up in sterile environments. They are naturally exposed to a variety of germs, providing ample opportunities for their immune systems to strengthen and adapt.
It is a good practice to regularly disinfect your children's toys and anything they share with others or take to school.
It is important to know the difference between cleaning, sanitizing, and disinfecting. While cleaning removes visible dirt, sanitizing decreases the number of germs on the surface, whereas disinfecting kills germs.
Also make sure to read the labels correctly and prevent any toxic toys to make its way to your kids, so it cannot be inhaled or ingested.
You can start by cleaning all the toys that has come in contact with your child's hands and mouth with soap and water. Then, use a sanitizer to clean everyday items, things that remain in your child's environment. Then use disinfectant, especially if your child is sick or if someone sick has touched your child's toys.
If you are wondering which sanitizers to go for, the Environmental Protection Agency (EPA) website has come up with a list of approved sanitizers and disinfectants that are effective.
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Rare infections transmitted from a pregnant woman to her baby may be linked to a higher risk of autism and intellectual disability, according to a large new study.
Researchers at the Karolinska Institutet in Sweden found that children with congenital TORCH infections had about three times the risk of autism compared with children without these infections.
TORCH refers to infections that can be transmitted from mother to foetus during pregnancy, including:
These infections can cross the placenta and infect the developing fetus.
“It is important to emphasize that it is unusual for these infections to be transmitted from mother to child. They account for a very small proportion of all cases of autism in the population, but for those children who are actually affected, we see a clearly elevated risk of both autism and intellectual disability,” said Reneé Gardner, a researcher at the Department of Global Public Health at Karolinska Institutet.
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Published in JAMA Pediatrics, the study analysed data from 3.7 million people born in Sweden between 1987 and 2021. Of these, 975 had a diagnosed congenital TORCH infection. The participants were followed for up to three decades.
Compared with children without a congenital TORCH infection, those with one were:
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The researchers also compared children with TORCH infections with their unaffected siblings to assess whether shared family factors could explain the findings.
The results were similar, suggesting that the associations were not explained solely by factors shared within families.
No clear association was found between TORCH infections and ADHD or obsessive-compulsive disorder. However, children with the infections had poorer academic performance on average, even when they did not have an autism or intellectual disability diagnosis.
“Although these congenital infections are rare, some of them can be prevented, which makes them important from a public health perspective,” Gardner said.
The researchers also noted that rubella has virtually disappeared in Sweden following the introduction of national vaccination program. The prevention also depends on the infection:
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We may now have a clearer explanation behind ‘mommy brain’ or ‘momnesia’. Walking into a room and forgetting why you went there or losing track of a conversation is not simply a side effect of becoming a mother.
A new study has discerned a possible explanation for the phenomenon commonly known as “momnesia,” “pregnancy brain” or “mommy brain”. The findings were published in Science Bulletin.
According to the study, persistent high levels of estrogen during pregnancy may disrupt a particular brain circuit involved in memory.
Researchers found that high estrogen affected communication between the hypothalamus and hippocampus, two brain regions involved in regulating different aspects of brain function, including memory.
Pregnancy-related forgetfulness is generally considered to be temporary changes in memory and cognition during pregnancy.
Researchers say forgetfulness can become noticeable in late pregnancy stage and may continue well into the postpartum period before improving.
Women may have trouble recalling names or words, keeping track of events or completing everyday tasks.
According to the author of the study Dr Zheng Sun of Baylor College of Medicine, about 80% of pregnant women report these changes. The researchers say that this condition does not appear to be a decline in intelligence or cognitive ability.
According to Reuters, Dr Yanlin He, another study leader, said, “The important point is that pregnancy does not simply make someone ‘less intelligent.’ The effects appear to be more subtle and specific to certain cognitive tasks.”
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During pregnancy, estrogen levels increase drastically and reach its peak during the third trimester.
The researchers focused on estrogen receptor alpha in neurons located in the lateral hypothalamus. In experiments based on mice who were exposed to high estrogen level conditions like in pregnancy, these neurons became more active.
Those neurons send signals to the hippocampus, a brain region crucial for memory formation. The researchers found that increased activity in this region suppressed hippocampal activity and impaired performance on memory tests.
When researchers switched off the hypothalamus-to-hippocampus pathway, the memory problems in the mice were prevented. Activating the pathway, meanwhile, impaired memory even without elevated estrogen.
Removing estrogen receptors from the hypothalamic neurons also reversed the estrogen-related memory problems in the mice.
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The researchers also assessed memory in 70 women, including women at different stages of pregnancy and women who were not pregnant.
Memory problems surfaced during late pregnancy stages and were linked with higher circulating estrogen levels. The researchers reported changes across several memory-related tasks.
But it is important to note that the researchers did not directly measure or manipulate this specific brain circuit in pregnant women. That means the human findings support the mechanism observed in mice, but do not prove that exactly the same circuit causes memory changes during human pregnancy.
The study has cemented evidence that many pregnant women experience forgetfulness, but it does not mean pregnancy causes permanent memory loss. For most women, pregnancy-related forgetfulness generally improves after childbirth.
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The gut microbiome may influence how type 1 diabetes develops in children at high genetic risk, a new study suggests.
Researchers found that children whose gut microbiome stopped developing early had about three times the risk of developing type 1 diabetes or the immune attack that precedes it, compared with those whose microbiomes continued to mature.
The findings, published in Nature Metabolism, also showed that genetics influenced how strongly some microbiome patterns were associated with disease risk.
Type 1 diabetes affects more than 9 million people worldwide, including 1.8 million children and adolescents.
"Understanding the role of microbiome development in diabetes progression could lead to early prediction and prevention strategies, giving us more options to delay or even prevent the clinical manifestation of this disease," said co-corresponding author Daniel Wang, associate scientist with the Channing Division of Network Medicine in the Mass General Brigham Department of Medicine.
The longitudinal observational TEDDY Study followed 887 children at high genetic risk of type 1 diabetes and analyzed more than 12,000 stool samples collected during their first six years.
Participants came from Finland, Germany, Sweden and the United States.
Because the immune system can attack insulin-producing cells years before symptoms appear, researchers counted both the first detection of this immune attack and a clinical diagnosis as disease-related outcomes.
They identified three microbiome development patterns: early-matured, late-matured and early-plateaued.
Children with early-matured microbiomes developed greater bacterial diversity during their first year. Those with late-matured microbiomes started more slowly but eventually caught up.
The early-plateaued group showed slow development that failed to catch up, with low bacterial diversity persisting through the first three years.
Children with an early-plateaued microbiome had about three times the risk of developing type 1 diabetes or its preceding immune attack.
The association was also seen when the researchers analyzed the immune stage and clinical diagnosis separately.
The finding emerged from repeated stool sampling over time, suggesting a single microbiome snapshot could have missed the association.
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The bacterial differences also reflected how the children's microbiomes adapted as their diets changed.
In the early-matured group, bacteria shifted sooner from milk-adapted species such as Bifidobacterium toward bacteria that break down dietary fiber.
In the early-plateaued group, the microbiome remained more focused on digesting milk sugars even after solid foods were introduced and relied on a narrower range of bacterial species.
Lead author Danyue Dong, a postdoctoral research fellow in the Channing Division of Network Medicine at Mass General Brigham shared that "genetic background" can also influence the risk. Dong noted that combining microbiome and genetic information gives a more accurate picture.
"By analyzing interactions between the microbiome and host genetics, we found genetic variants, particularly those involved in antimicrobial and antiviral immune responses, that shaped how strongly the late-matured pattern was related to disease risk. The early-plateaued pattern, by contrast, carried higher risk regardless of genetic background," the expert said.
The study was observational, so it cannot establish that microbiome changes cause type 1 diabetes. Clinical trials are needed to determine whether modifying the microbiome can reduce disease risk.
The findings also came from children already at high genetic risk, meaning they may not apply to the general population.
Researchers say future pediatric care could potentially include microbiome testing during the first years of life. However, approaches such as dietary supplements would need to prove effective in clinical trials before being used for prevention.
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