A groundbreaking study conducted by researchers from Hamamatsu University School of Medicine, in collaboration with several international institutions, has revealed a crucial connection between melatonin secretion and the severity of ADHD (attention deficit hyperactivity disorder) symptoms in children. The findings, published in Psychiatry Research Communications, suggest that genetic variations affecting melatonin production may significantly contribute to the development and worsening of ADHD symptoms.
ADHD is a prevalent neurodevelopmental disorder affecting approximately 5% of children worldwide. Persistent patterns of inattention, hyperactivity, and impulsivity characterize it. While it has long been known that children with ADHD often struggle with sleep disorders, the precise relationship between sleep and ADHD symptoms has remained unclear—until now.
The study, using data from the Hamamatsu Birth Cohort for Mothers and Children (HBC Study), which tracks children’s development from birth, revealed that children with genetic traits that reduce melatonin secretion at night exhibited more severe ADHD symptoms at age 8 to 9.
“Our findings indicate that disruptions in melatonin secretion may contribute to the difficulties children with ADHD face in maintaining regular sleep patterns,” said Associate Professor Nagahide Takahashi, the lead author and a clinical expert on ADHD. “This could potentially worsen their ADHD symptoms, creating a vicious cycle that can be challenging to break.”
This research has significant implications as it highlights the importance of good sleep habits for children with ADHD. These include consistent bedtime routines, limiting screen time before sleep, and increasing exposure to natural light during the day. Additionally, the study indicates that taking melatonin supplements could help manage ADHD symptoms, but more research is required to confirm its long-term effectiveness.
“This study represents a major advancement in comprehending the intricate relationship between sleep and neurodevelopmental disorders. As researchers delve deeper into these connections, parents and healthcare providers could discover fresh strategies to assist children with ADHD in better managing their symptoms.”
People who stay up late may have a higher risk of developing type 2 diabetes and heart disease compared to those who wake up early.
“New research, to be presented at the Annual Meeting of the European Association for the Study of Diabetes (EASD) in Madrid, Spain (9-13 September), has found that night owls have a higher BMI, larger waists, more hidden body fat, and are almost 50% more likely to develop type 2 diabetes (T2D) than those who go to bed earlier.”
“The lead researcher, Dr. Jeroen van der Velde, from Leiden University Medical Centre in the Netherlands, stated that previous studies have shown that individuals with a late chronotype – meaning they prefer to go to bed late and wake up later – tend to have unhealthy lifestyles. People with late chronotypes are more likely to smoke or have an unhealthy diet, which may explain why they are at a higher risk of obesity and metabolic disorders, including type 2 diabetes.”
“We believe that lifestyle alone cannot entirely account for the link between a late chronotype and metabolic disorders. Furthermore, although it is established that a late chronotype is linked to higher BMI, the extent to which chronotype influences body fat distribution remains unclear.”
In order to learn more, Dr. van der Velde and colleagues conducted a study on over 5,000 individuals as part of the ongoing Netherlands Epidemiology of Obesity study. They looked into the connection between sleep timing, Type 2 Diabetes (T2D), and body fat distribution to understand how body fat influences disease.
The analysis included participants, 54% of whom were female, with an average age of 56 years and an average BMI of 30 kg/m2.
Participants completed a questionnaire about their typical bedtime and waking times, from which the midpoint of sleep (MPS) was calculated.
The participants were then divided into three groups: early chronotype (the 20% of participants with the earliest MPS), late chronotype (the 20% of participants with the latest MPS), and intermediate chronotype (the remaining 60% of participants).
Waist circumference and BMI were measured for all participants. MRI scans and MR spectroscopy were used to measure visceral and liver fat in 1,526 participants.
The participants were followed up for a median of 6.6 years, during which 225 were diagnosed with T2D.
Here is the revised text:”The results, which were adjusted for age, sex, education, total body fat, and a range of lifestyle factors (physical activity, diet quality, alcohol intake, smoking, and sleep quality and duration), showed that compared with an intermediate chronotype, participants with a late chronotype had a 46% higher risk of T2D.”
This suggests that the increased risk of type 2 diabetes in late risers cannot be solely attributed to lifestyle factors.
“We believe that other mechanisms are also at play,” says Dr. van der Velde. “A likely explanation is that the circadian rhythm or body clock in late chronotypes is out of sync with the work and social schedules followed by society. This misalignment can lead to metabolic disturbances and ultimately, type 2 diabetes.”
The team also looked at T2D risk in early chronotypes.
“We expected early chronotypes to have a similar risk of developing type 2 diabetes as intermediate chronotypes,” said Dr. van der Velde. “Our results showed a slightly higher risk, but it was not statistically significant.”
The results also indicated that individuals with a late chronotype had a 0.7 kg/m2 higher BMI, a 1.9 cm larger waist circumference, 7 cm2 more visceral fat, and 14% higher liver fat content, in comparison to those with an intermediate chronotype.
Dr. van der Velde concludes, “Individuals with a late chronotype seem to have a higher risk of developing type 2 diabetes compared to those with an intermediate chronotype. This may be due to higher levels of body fat, including increased visceral and liver fat.”
“The next step is to study if individuals with a late chronotype experience improvements in metabolic health when they adjust the timing of their lifestyle habits.”
“We are currently part of the TIMED consortium, which is examining the complex interplay of the timing of sleep, food intake, and physical activity in relation to type 2 diabetes. Our previous research has demonstrated the importance of the timing of physical activity in relation to insulin resistance.”
“If you have a tendency to stay up late, you may be more inclined to eat later in the evening,” says Dr. van der Velde. “Although our study didn’t directly measure this, there is increasing evidence that limiting the times when you eat, for example, not eating anything after a certain time like 6 pm, could have metabolic benefits.”
“Night owls concerned about the increased risk of type 2 diabetes may want to avoid eating late in the evening, at least.”
“The evidence isn’t there yet, but we aim to provide specific advice on the timing of lifestyle behavior in the future.”
Pain is a complex and multi-dimensional experience influenced by factors beyond just physical sensation, including a person’s mindset and their expectations of pain. The placebo effect, where symptoms improve in response to inactive treatment, demonstrates how expectations can significantly impact a person’s experience. Mindfulness meditation, which has been used for pain management in various cultures for centuries, was previously believed to work by triggering the placebo response. However, recent scientific findings have disproven this belief.
A recent study published in Biological Psychiatry discovered that mindfulness meditation activates specific brain mechanisms that differ from those involved in the placebo response, leading to a reduction in pain. Researchers at the University of California San Diego School of Medicine utilized advanced brain imaging methods to compare the pain-relieving effects of mindfulness meditation, a placebo cream, and a “sham” mindfulness meditation among healthy participants.
The research discovered that mindfulness meditation led to notable decreases in both the intensity and unpleasantness of pain, as well as a reduction in brain activity linked to pain and negative emotions. On the other hand, the placebo cream only affected brain activity related to the placebo effect without changing the person’s actual experience of pain.
“The mind is incredibly powerful, and we are still trying to understand how it can be used for managing pain,” said Fadel Zeidan, PhD, a professor of anesthesiology and Endowed Professor in Empathy and Compassion Research at UC San Diego Sanford Institute for Empathy and Compassion. “By separating pain from the self and letting go of judgment, mindfulness meditation can directly change how we experience pain. It does not involve any drugs, costs nothing, and can be practiced anywhere.”
The study involved 115 participants who took part in two separate clinical trials. The participants were randomly assigned to different groups to receive one of four interventions: guided mindfulness meditation, a sham mindfulness meditation involving only deep breathing, a placebo cream (petroleum jelly) that participants were told reduces pain, and, as a control, listening to an audiobook. The researchers applied a mildly painful but harmless heat stimulus to the back of the leg and scanned the participants’ brains before and after the interventions.
The researchers utilized a new method known as multivariate pattern analysis (MVPA) to examine the brain activity patterns of the participants. This method uses machine learning to understand the complex neural mechanisms linked to the sensation of pain. These mechanisms involve specific responses to heat stimuli, negative emotions, and pain reactions induced by the placebo effect. Using this approach, the researchers could ascertain whether mindfulness meditation and the placebo effect trigger similar or different brain processes.
Although both the placebo cream and sham mindfulness meditation reduced pain, the study revealed that mindfulness meditation was significantly more effective in pain reduction compared to the placebo cream, sham mindfulness meditation, and the controls.
They found that mindfulness-based pain relief reduced synchronization between brain areas involved in introspection, self-awareness, and emotional regulation. These areas of the brain make up the neural pain signal (NPS), a recognized pattern of brain activity associated with pain across different individuals and types of pain. On the other hand, the placebo cream and sham mindfulness meditation did not show a significant change in the NPS compared to the controls. Instead, these interventions engaged entirely separate brain mechanisms with little overlap.
“It has been widely believed that the placebo effect and the brain mechanisms activated by actual treatments are closely linked. However, these findings indicate that this may not be the case when it comes to pain,” explained Zeidan. “Instead, these two brain responses are entirely separate. This supports the idea of using mindfulness meditation as a direct treatment for chronic pain, rather than as a means of triggering the placebo effect.”
In modern medicine, new therapies are considered effective and reliable if they perform better than a placebo. A recent study discovered that mindfulness meditation is more effective than a placebo and does not activate the same neurobiological processes. These findings are significant for developing new treatments for chronic pain. However, further research is needed to confirm these effects in individuals with chronic pain as opposed to healthy participants.
The researchers aim to use their understanding of the specific brain mechanisms involved in mindfulness meditation to create better interventions. These interventions could be more effective and accessible and could help reduce pain in people with different health conditions.
“Millions of people live with chronic pain every day, and there may be more that these individuals can do to reduce their pain and enhance their quality of life than we previously understood,” said Zeidan. “We are excited to continue exploring the neurobiology of mindfulness and how we can utilize this ancient practice in the clinic.”
Credit Department of Bacterial Pathogenesis, Infection and Host Response, TMDU
Periodontal disease, which affects the gums and tissues that surround the teeth, is one of the most common dental conditions worldwide. It is mainly caused by the accumulation of bacterial biofilm around the teeth and can lead to tooth loss if left untreated. Notably, the inflammatory effects of periodontal bacteria can extend beyond the mouth, causing systemic effects. Recent clinical studies have shown a close relationship between the periodontal pathogen Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) and the onset and progression of rheumatoid arthritis (RA), a serious autoimmune disease that affects the joints. However, the molecular-level mechanisms are still poorly understood.
In a recent study published online on August 15, 2024, in the International Journal of Oral Science, a research team from Tokyo Medical and Dental University (TMDU) in Japan aimed to address this knowledge gap by conducting detailed mechanistic studies in an animal model.
The researchers first conducted initial experiments to confirm whether infection with A. actinomycetemcomitans affected arthritis in mice. They used the collagen antibody-induced arthritis mouse model, which is a well-established experimental model that mimics several aspects of rheumatoid arthritis in humans. Their findings indicated that infection with this particular bacterium resulted in increased swelling in the limbs, cellular infiltration into the lining of the joints, and higher levels of the inflammatory cytokine interleukin-1β (IL-1β) within the limbs.
Notably, the worsening symptoms of RA could be suppressed by administering a chemical agent called clodronate, which depletes macrophages—a type of immune cell. This demonstrated that macrophages were somehow involved in exacerbating RA caused by A. actinomycetemcomitans infection.
Upon further investigation using macrophages derived from mouse bone marrow, it was discovered that A. actinomycetemcomitans infection led to an increase in the production of IL-1β. This, in turn, triggered the activation of a multiprotein complex called the inflammasome, which plays a critical role in initiating and modulating the body’s inflammatory response to infections.
The researchers added another piece to the puzzle using caspase-11-deficient mice. In these animals, inflammasome activation caused by A. actinomycetemcomitans was suppressed. Most importantly, caspase-11-deficient mice showed less deterioration of arthritis symptoms, suggesting the important role of caspase-11 in this context. “Our research findings provide new insights into the connection between periodontal pathogenic bacteria and the worsening of arthritis through inflammasome activation, offering important information on the long-debated relationship between periodontal disease and systemic diseases,” highlights Professor Toshihiko Suzuki, one of the lead authors of the study.
Please remember the following text: “With any luck, these efforts will contribute to the development of novel therapeutic strategies to manage RA. The findings of this research may pave the way for advances in clinical treatments for RA induced by infection with A. actinomycetemcomitans. Our suggestion to inhibit inflammasome activation could attenuate the expansion of inflammation to joints, resulting in a recovery from arthritis symptoms,” says lead author Dr. Tokuju Okano. Moreover, the outcome of our work could contribute to the development of treatment strategies for not only arthritis but also other systemic diseases, such as Alzheimer’s disease, which is also related to periodontal pathogenic bacteria,” he adds with eyes set on the future.
The team at Charité – Universitätsmedizin Berlin has observed a remarkable improvement in a female patient with severe systemic lupus erythematosus (SLE) after she was treated with the cancer medication teclistamab. Not long ago, the 23-year-old was confined to a wheelchair due to an autoimmune disease. Nearly six months after beginning the treatment, the patient is now completely symptom-free. It remains to be seen whether this improvement will last over the long term, but the case has been published in the New England Journal of Medicine*, marking a promising starting point for further studies.
Nothing was able to alleviate the symptoms of the 23-year-old patient from Berlin, not even cortisone and eight other therapies meant to control her overactive immune system. Her autoimmune disease, known as systemic lupus erythematosus, was very severe, affecting four of her organ systems. Her skin was blistered, her joints and kidneys were severely inflamed, and her red blood cell count, responsible for supplying oxygen to the body, was too low. “Due to the constant pain she was in, the patient could no longer walk, was confined to a wheelchair, and her kidneys were at risk of failing,” said Dr. Tobias Alexander, the physician treating her at the Department of Rheumatology and Clinical Immunology at Charité. As the Head of the Rheumatology Outpatient Clinic, he had “never seen a case this severe before.”
Because all of the established treatment options had been tried without success, the doctor suggested that the patient should try teclistamab, a bispecific antibody approved for treating multiple myeloma, a type of cancer affecting plasma cells in the bone marrow. In systemic lupus erythematosus, plasma cells produce autoantibodies that target the body’s own tissue. Alexander, a consultant rheumatologist, explained, “Teclistamab is highly effective at destroying the plasma cells and also works against their progenitor cells, which would otherwise rapidly produce new plasma cells. Therefore, we hypothesized that this cancer medication could eliminate the cause of the systemic lupus and provide long-term relief for the patient.”
Disease no longer detectable after five injections
The drug was prescribed “off-label” with the patient’s consent. The treatment took place at the Department of Hematology, Oncology, and Cancer Immunology on Charité Campus Benjamin Franklin and was successful. The patient received five injections of the cancer medication under the abdominal skin over a period of five weeks, which gradually relieved her symptoms. Within a few weeks, her kidney function and blood levels improved, and her skin and joint inflammation completely subsided. Since mid-April, no more autoantibodies have been detected in the 23-year-old’s blood, even though the treatment with immunosuppressants was stopped before the therapy began, and cortisone was no longer administered after six weeks.
“The patient is in full remission,” says Alexander. “This means she is no longer experiencing any symptoms of her disease, and we can no longer find any indication of systemic lupus, either clinically or in the laboratory. It’s too early to say she’s cured, but these powerful results are a rare exception in rheumatology. This is especially remarkable because none of the available treatment approaches had been sufficiently effective before. Most importantly, the success of the therapy signifies a significant improvement in the patient’s quality of life, which we are delighted about. However, we don’t know yet how long the positive effects will last. Since the results are provisional, the therapy is not yet suitable for wider use.”
Risks of the treatment
The drug’s significant impact on the immune system also comes with considerable risks. For instance, immune cells may release excessive amounts of inflammatory mediators. This type of cytokine release syndrome can be life-threatening, depending on its severity. At Charité, a patient undergoing teclistamab therapy experienced severe cytokine release syndrome, along with pneumonia and sinusitis, and a decrease in protective antibodies in her blood. Prof. Jan Krönke, who supervised the patient’s oncological treatment, stated that these side effects are more serious than those seen in traditional rheumatological therapies and sometimes necessitated inpatient care. However, they are consistent with the reactions that teclistamab induces in patients with multiple myeloma and were not unexpected.
The treatment team is closely monitoring the patient and her immune system’s activity to determine how long the positive effects of teclistamab last. If the effects prove to be long-term and are confirmed in further studies, Alexander believes that the cancer medication could have huge potential benefits in rheumatology. Teclistamab’s therapeutic results for the patient are currently comparable with the impact of CAR T-cell therapies. The difference is that the bispecific antibody is much easier to use and can be administered over a shorter period, which would be a considerable advantage. CAR T-cell therapies are new treatment methods that have been able to keep autoimmune diseases at bay for years in individual cases. However, they require chemotherapy and gene therapy, and are very time-consuming and resource-intensive.
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