Are you struggling to sleep at night, feeling restless and unfocused during the day? Do you find it hard to concentrate on tasks or activities that normally bring you joy? You’re not alone. Research suggests that adults with Attention Deficit Hyperactivity Disorder (ADHD) traits are more likely to experience insomnia, which can exacerbate their symptoms.

A recent study published in BMJ Mental Health found a strong link between ADHD traits, insomnia severity, and reduced life satisfaction. The researchers analyzed data from over 1,300 adult participants who completed an online survey about ADHD traits, sleep disturbances, circadian factors, depression, and quality of life. Their findings revealed that:

* Adults with higher ADHD traits reported worse depression, more severe insomnia, lower sleep quality, and a preference for going to bed and waking up later.
* Insomnia severity predicted a lower quality of life, suggesting that it may be a key factor in the vicious cycle between ADHD and reduced well-being.

The study’s lead author, Dr. Sarah L. Chellappa, notes that “sleep disruption can impact neurobehavioral and cognitive systems, including attention and emotional regulation.” This underscores the importance of addressing insomnia in individuals with ADHD traits.

Professor Samuele Cortese, a co-author on the paper, emphasizes the need for further research to understand this complex interplay between ADHD and insomnia. He suggests that targeting insomnia complaints through therapies like Cognitive Behavioral Therapy for Insomnia (CBT-I) or Sleep Restriction therapy may help improve the quality of life for individuals with higher ADHD traits.

While the study’s findings are promising, it’s essential to remember that every individual is unique, and addressing insomnia requires a personalized approach. By acknowledging the intersection of ADHD and insomnia, we can begin to break this vicious cycle and work towards improving overall well-being.

If you or someone you know struggles with ADHD and insomnia, consider consulting a healthcare professional for guidance on managing symptoms and improving quality of life.

The relationship between exercise and mental health has been widely researched, but a recent study from the University of Georgia suggests that it’s not just the physical movement itself that affects mental well-being. Instead, it’s the why, where, and how you exercise that makes all the difference.

Historically, research on physical activity has focused on the length and intensity of exercise sessions, with little attention paid to the context in which they take place. However, this approach may be oversimplifying the complex relationship between exercise and mental health. As co-author Patrick O’Connor explains, “The ‘dose’ of exercise has been the dominant way researchers have tried to understand how physical activity might influence mental health, while often ignoring whether those minutes were spent exercising with a friend or as part of a game.”

Leisure-time physical activity, such as going for a run, taking a yoga class, or biking for fun, has been shown to correlate with better mental health outcomes. However, these benefits may vary significantly depending on the environment and circumstances surrounding the activity. For example, exercising alone in a gym may have different effects than working out with friends in a park.

Multiple studies have found that people who engage in regular leisure-time physical activity tend to report lower levels of depression and anxiety. However, it’s less clear whether other forms of physical activity, such as cleaning the house or working for a lawn care company, have similar benefits.

The context of exercise can also play a significant role in its impact on mental health. As O’Connor notes, “If you do the exact same exercise but miss the goal and people are blaming you, you likely feel very differently.” This highlights the importance of considering not only the physical activity itself but also the social and emotional aspects surrounding it.

Randomized controlled trials have shown that adopting regular exercise routines can boost mental health, especially for individuals with existing mental health disorders. However, these studies were typically based on small, short-term, and homogenous samples, so their results may not be generalizable to larger, more diverse groups.

The average effects of exercise on mental health are small across all the randomized controlled studies, partly because most of them focused on people who were not depressed or anxious. This suggests that larger- and longer-term controlled studies are needed to make a compelling case for whether exercise does, or does not, truly impact mental health.

Ultimately, understanding contextual factors is crucial in determining the impact of exercise on mental health. As O’Connor concludes, “If we’re trying to help people’s mental health with exercise, then not only do we need to think about the dose and the mode, we also need to ask: What is the context?” By considering these factors, researchers can develop more effective strategies for promoting mental well-being through physical activity.

The way we perceive and respond to physical pain is more than just a physical sensation – it also carries an emotional weight. This emotional discomfort can motivate us to take action and helps us learn to associate negative feelings with situations so we can avoid them in the future. However, when our ability to tolerate pain becomes too sensitive or lasts too long, it can result in chronic and affective pain disorders such as fibromyalgia, migraines, and post-traumatic stress disorder (PTSD).

Researchers at the Salk Institute have now identified a brain circuit that gives physical pain its emotional tone. Published in the Proceedings of the National Academy of Sciences, the study reveals a group of neurons in the central brain area called the thalamus that appears to mediate the emotional or affective side of pain in mice.

The prevailing view for decades was that the brain processes sensory and emotional aspects of pain through separate pathways. However, this new pathway challenges the textbook understanding of how pain is processed in the brain and body. The physical sensation of pain allows you to immediately detect it, assess its intensity, and identify its source, while the affective part of pain makes it unpleasant.

This distinction is crucial because most people start to perceive pain at the same stimulus intensities. However, our ability to tolerate pain varies greatly, with some individuals being more sensitive than others. The affective processing determines how much we suffer or feel threatened by pain. If this becomes too sensitive or lasts too long, it can result in a pain disorder.

The researchers used advanced techniques to manipulate the activity of specific brain cells and discovered a new spinothalamic pathway in mice. In this circuit, pain signals are sent from the spinal cord into a different part of the thalamus, which has connections to the amygdala, the brain’s emotional processing center. This particular group of neurons can be identified by their expression of CGRP (calcitonin gene-related peptide).

When these CGRP neurons were “turned off,” the mice still reacted to mild pain stimuli but didn’t seem to associate lasting negative feelings with these situations. However, when these same neurons were “turned on,” the mice showed clear signs of distress and learned to avoid that area, even when no pain stimuli had been used.

“Pain processing is not just about nerves detecting pain; it’s about the brain deciding how much that pain matters,” says first author Sukjae Kang. Understanding the biology behind these two distinct processes will help us find treatments for the kinds of pain that don’t respond to traditional drugs.

Many chronic pain conditions, such as fibromyalgia and migraine, involve long, intense, unpleasant experiences of pain often without a clear physical source or injury. Some patients also report extreme sensitivity to ordinary stimuli like light, sound, or touch which others would not perceive as painful.

Han says overactivation of the CGRP spinothalamic pathway may contribute to these conditions by making the brain misinterpret or overreact to sensory inputs. In fact, transcriptomic analysis of the CGRP neurons showed that they express many of the genes associated with migraine and other pain disorders.

Several CGRP blockers are already being used to treat migraines. This study may help explain why these medications work and could inspire new nonaddictive treatments for affective pain disorders. Han also sees potential relevance for psychiatric conditions that involve heightened threat perception, such as PTSD. Quieting this pathway with CGRP blockers could offer a new approach to easing fear, avoidance, and hypervigilance in trauma-related disorders.

Importantly, the relationship between the CGRP pathway and the psychological pain associated with social experiences like grief, loneliness, and heartbreak remains unclear and requires further study.

“Our discovery of the CGRP affective pain pathway gives us a molecular and circuit-level explanation for the difference between detecting physical pain and suffering from it,” says Han. “We’re excited to continue exploring this pathway and enabling future therapies that can reduce this suffering.”