Medical Bulletin 15/February/2024

Here are the top medical news for the day:

Early periods and early menopause raise COPD risk

A research, published online in the journal Thorax, finds that various reproductive factors, such as the age at which menstruation begins and early menopause, are associated with an increased risk of COPD—a collective term for progressive lung diseases that leads to breathing difficulties.

Miscarriage, stillbirth, infertility, and having 3 or more children are also associated with a heightened risk of COPD, which includes emphysema and chronic bronchitis.

For the study, the researchers analysed data from three groups of women—totalling 283,070, with an average age of 54—across the Australian Longitudinal Study on Women’s Health 1946–51 (ALSWH-mid), the UK Biobank, and the Swedish Women’s Lifestyle and Health Study (WLH), focusing on reproductive factors and COPD. Tracking in the ALSWH-mid and UK Biobank groups continued until the end of December 2019, while the WLH group was monitored until the end of 2010.

Data on reproductive factors was collected along with potentially influential factors such as birth year, ethnicity, educational level, duration of smoking, asthma, and weight (BMI).Several reproductive factors were associated with the risk of COPD, including age when periods first started; number of children; a history of infertility, miscarriage or stillbirth, and age at menopause.

The findings revealed a U-shaped association between the onset age of menstruation and COPD risk, with increased risks for those starting before age 11 (17% higher) and after age 16 (24% higher), compared to starting at age 13. Women with children faced greater COPD risks than childless ones, particularly those with more than three children (34% higher risk) or one child (18% higher). Infertility and a history of miscarriage or stillbirth also elevated COPD risk by 13%, 15-36%, and 42% respectively, with risks escalating with the number of miscarriages or stillbirths. Early menopause (before age 40) significantly raised COPD risk by 69%, whereas menopause at or after age 54 reduced it by 21%.

“The overall effect of oestrogen might differ depending on the timing,” researchers suggest. “In the early or middle reproductive stage, long or higher accumulated exposure to oestrogen would be detrimental to the lung, leading to a higher risk of COPD among women with early menarche or multiple live births. In the later stage, oestrogen may be protective, since earlier age at menopause or [ovary removal] (indicates shorter exposure to oestrogen) were associated with a higher risk of COPD.”

Reference:DOI: 10.1136/thorax-2023-220388

Anabolic steroids raise heart disease risk

A new study has found that anabolic steroid users may be elevating their risk of developing atrial fibrillation, a heart condition.

The research is published in the Journal of Physiology and conducted by an interdisciplinary consortium of clinicians and researchers led by University of Birmingham and collaborators in Germany.

The team discovered that male sex hormones, such as testosterone, also called androgenic anabolic steroids (AAS), which are misused for muscle building particularly among in young men can increase the risk of atrial fibrillation in individuals genetically predisposed to heart diseases.

Dr LauraSommerfeld, Postdoctoral Researcher at the UKE Hamburg said: “Our study can significantly contribute to understanding the impact on the heart health of young men who misuse anabolic steroids to increase muscle mass. Recent reports have shown that young men in particular are being targeted on social media such as TikTok being sold testosterone products, but we have shown how the misuse of steroids carries a specific risk that many people will not be aware of.”

The researchers investigated the impact on arrhythmogenic right ventricular cardiomyopathy (ARVC), a genetic condition mainly caused by disruptions in cell connections essential for heart muscle stability. Analysing clinical data from UHB and other sources, they verified that ARVC is more common and severe in men than women. Laboratory experiments revealed that six weeks of anabolic-androgenic steroids (AAS) intake, coupled with compromised cell connections, could diminish sodium channel function in heart tissue and slow down signal conduction in the atria.

“Heart muscle diseases like ARVC affect young, athletic individuals and can lead to life-threatening heart rhythm disturbances. Atrial fibrillation is a common condition in the general population. Elevated testosterone levels can result in an earlier onset of these diseases.” researchers concluded.

Reference: DOI: 10.1113/JP284597

Study shows nicotine's varied effects on brain's reward and aversion centers

A new study, led by researchers at the Marshall University Joan C. Edwards School of Medicinehighlight the intricate interplay of brain regions involved in nicotine's effects on the human brain.

The study, published in the open-access journal eNeuro by the Society for Neuroscience, examines nicotine's complex effects on brain regions tied to reward and aversion. It highlights the nuanced interaction that is influenced by factors like dosage, the presence of additives such as menthol, and the sex of the individual. The focus is on the medial habenula (MHb), critical for nicotine aversion, where researchers observed variable activity levels based on these factors. This variability contrasts with the behaviour in reward-related areas such as the ventral tegmental area, offering new insights into nicotine's differential impact on the brain.

"This study demonstrates that the activity of crucial brain regions associated with nicotine dependence is altered in different ways based on nicotine dosage and sex,” said lead researcher Nathan Olszewski, a biomedical research doctoral student at Marshall University in the laboratory of Brandon J. Henderson, Ph.D. “Nicotine usage affects individuals uniquely, making it advisable for users to exercise caution."

The study employed a method where mice inhaled nicotine vapor by poking their noses into a device, mimicking how humans might self-administer nicotine. The researchers used advanced techniques to study how nicotine affects nerve cell activity in two brain areas, the medial habenula and the ventral tegmental area, looking at differences based on the amount of nicotine and whether the mice were male or female. They also measured how nicotine changed the release of dopamine, a chemical related to pleasure, in another part of the brain called the nucleus accumbens.

The researchers plan to broaden their study to include additional brain areas, especially looking at the connection between the medial habenula (MHb) and the interpeduncular nucleus (IPN). This pathway is key for controlling nicotine consumption and managing withdrawal symptoms. Further research will use techniques like electrophysiology, confocal microscopy, and RNA-fluorescent in situ hybridization (FISH) to explore how nicotine impacts the behaviour and levels of nicotinic acetylcholine receptors within this critical circuit.

"In our field, attention has predominantly focused on specific regions like the ventral tegmental area,” said Henderson, an associate professor of biomedical sciences at Marshall University. “This study underscores the necessity of exploring other brain areas controlling the negative aspects of nicotine exposure."

Reference: “Neuronal excitability in the medial habenula and ventral tegmental area is differentially modulated by nicotine dosage and menthol in a sex-specific manner”DOI: 10.1523/ENEURO.0380-23.2024