Tag: smoking

Early onset of menstruation and menopause associated with increased risk of COPD

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In a recent study published in Thorax, a group of researchers evaluated the association between female reproductive factors such as age at menarche, stillbirth, number of children, infertility, miscarriage, and age at natural menopause—and the risk of developing chronic obstructive pulmonary disease (COPD).

Study: Female reproductive histories and the risk of chronic obstructive pulmonary disease. Image Credit: Image Point Fr/Shutterstock.com

Background

COPD is a significant global health issue, with a prevalence of approximately 3.9% in 2017, showing slight gender differences in rates between men and women. Notably, women are more susceptible to developing severe COPD at younger ages than men, and the majority of non-smokers with COPD are women.

This suggests that female sex hormones, such as estrogen and progesterone, play crucial roles in lung development and the pathogenesis of COPD. These hormones influence bronchodilation, inflammation, and cellular proliferation, key factors in COPD development.

The variability in the female hormonal environment throughout different reproductive stages- menarche, pregnancy, menopause, and conditions like infertility or pregnancy loss- highlights the complex relationship between female reproductive health and COPD risk.

However, research specifically exploring this connection remains limited, indicating a need for further research into how reproductive history impacts COPD risk.

About the study

The present study conducted by the International Collaboration for a Life Course Approach to Reproductive Health and Chronic Disease Events (InterLACE) consortium utilized data from over 850,000 women across 12 countries.

It focused on three cohorts with information on reproductive factors and COPD: the Australian Longitudinal Study on Women’s Health, the United Kingdom (UK) Biobank, and the Swedish Women’s Lifestyle and Health Study.

To ensure accuracy, the study excluded women who had developed COPD by age 40 from analyses involving infertility, miscarriage, stillbirths, and parity due to the absence of specific ages for these events.

Only women who had experienced natural menopause were considered for analysis regarding menopause age, and those with COPD before natural menopause were omitted.

The researchers carefully handled missing data, ensuring participants had complete records on critical factors such as race, education, smoking history, body mass index, and asthma.

To address potential biases, including the impacts of coronavirus disease 2019 (COVID-19), follow-up adjustments were made across cohorts, and reproductive histories were detailed, including menarche to menopause.

COPD was identified through diverse data, ensuring accuracy. Statistical analysis, including Cox regression and sensitivity tests, explored reproductive factors’ influence on COPD risk, highlighting their importance in women’s health research.

Study results

In the present comprehensive study encompassing 283,070 women with a median age of 54 years, researchers embarked on an 11-year journey to unravel the intricate relationship between women’s reproductive history and the development of COPD.

Throughout this period, 3.8% of the participants, equivalent to 10,737 women, were diagnosed with COPD at a median age of 63 years.

The identification of COPD cases varied, with 7,983 cases recognized through a singular data source—ranging from survey data to hospital records—and 2,754 through multiple sources.

The initial characteristics of these women highlighted certain risk factors, including advanced age at cohort entry, lower educational attainment, higher body mass indices, significant smoking histories, and pre-existing asthma conditions.

The researchers excluded 53,205 women due to incomplete data, particularly regarding smoking habits and body mass index, ensuring the robustness of their findings.

A nuanced pattern emerged, linking the age of menarche with COPD risk; notably, women who experienced menarche at age 11 or younger, as well as those who began menstruating after 13, saw an increased risk, with a particularly sharp rise observed in those who started menstruating at age 14 or beyond.

Furthermore, the study revealed that motherhood also influenced COPD risk, with women having one or more children facing higher risks compared to childless counterparts. This risk escalated with the number of children borne.

Additionally, experiences of infertility and miscarriages further intensified COPD risks, painting a complex picture of how reproductive history shapes respiratory health.

Women who had undergone natural menopause presented an inverse risk relationship with COPD, dependent on the age at menopause. Those entering menopause before age 40 faced the highest risk, whereas the risk diminished for women experiencing menopause at or beyond age 54.

The study also used rigorous sensitivity analyses, including random effects modeling and competing risk analysis, to validate these findings.

Notably, the association between infertility and COPD risk diminished in some analyses, yet the overarching trends remained consistent across various subgroups, including smokers and non-smokers, as well as women with and without a history of asthma.

The analysis extended to explore the impact of bilateral oophorectomy age on COPD risk, finding a heightened risk among women who underwent the procedure at younger ages.

Further, the study delved into the specific effects of reproductive history facets such as age at menarche, miscarriages, stillbirths, and menopause timing on COPD risk, with findings echoing across individual cohort studies and meta-analyses.

Despite some variability, especially concerning the age at menarche, most evidence pointed towards a consistent relationship between reproductive factors and the development of COPD.

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February 14, 2024
New study shows dramatic health benefits of quitting smoking

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People who quit smoking see major gains in life expectancy after just a few years, according to a new study by University of Toronto researchers at Unity Health Toronto.

The study, published in NEJM Evidence, shows that smokers who quit smoking before age 40 can expect to live almost as long as those who never smoked. Those who quit at any age return close to never-smoker survival 10 years after quitting, and about half that benefit occurs within just three years.

“Quitting smoking is ridiculously effective in reducing the risk of death, and people can reap those rewards remarkably quickly,” said Prabhat Jha, a professor at U of T’s Dalla Lana School of Public Health and Temerty Faculty of Medicine, who is executive director of the Centre for Global Health Research at Unity Health Toronto.

The observational study included 1.5 million adults in four countries (the U.S., UK, Canada and Norway), followed over 15 years. Smokers between the ages of 40 and 79 had an almost three-fold risk of dying compared to those who never smoked, meaning on average they lost 12 to 13 years of life.

Former smokers lowered their risk of death to 1.3-fold (or 30 per cent higher) compared to never smokers. Stopping smoking at any age was associated with longer survival, and even those who quit for less than three years gained up to six years in life expectancy.

Many people think it’s too late to quit smoking, especially in middle age. But these results counter that line of thought. It’s never too late, the impact is fast and you can reduce risk across major diseases, meaning a longer and better quality of life.”

Prabhat Jha, Professor at U of T’s Dalla Lana School of Public Health and Temerty Faculty of Medicine

The researchers found that quitting smoking reduced the risk of dying from vascular disease and cancer, in particular. Former smokers also reduced their risk of death from respiratory disease, but slightly less so, likely due to residual lung damage.

There are currently about 60 million smokers in the four countries involved in the study, and over a billion worldwide. The global rate of smoking has fallen by more than 25 per cent since 1990, but tobacco is still a leading cause of preventable death.

Jha said the findings should add urgency to efforts by governments to support people who want to stop smoking. “Helping smokers quit is one of most effective ways to substantially improve health. And we know how to do that, by raising taxes on cigarettes and improving cessation supports.”

Canada is long overdue for an increase in the federal excise tax on cigarettes, and many other countries could lower smoking rates by raising taxes, Jha said. Cessation supports can include clinical guidelines and patient resources such as helplines, but also a whole-health-system approach.

“When smokers interact with the health care system in any way, physicians and health professionals can encourage them to quit, pointing out how well quitting works,” Jha said. “This can be done with concern, and without judgement or stigma, recognizing that cigarettes are engineered to be highly addictive.”

Source:

Journal reference:

Cho, E. R., et al. (2024) Smoking Cessation and Short- and Longer-Term Mortality. NEJM Evidence. doi.org/10.1056/EVIDoa2300272.

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February 10, 2024
Chewing tobacco linked to higher stroke and cancer risk, study finds
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In a recent study in the journal Nature Communications, researchers systematically reviewed and synthesized the literature on the health risks associated with chewing tobacco. Their results indicate that people who chew tobacco are significantly more likely to suffer from strokes and several cancers.

While chewing tobacco is not as prevalent as smoking cigarettes, estimates suggest that more than 270 million people use smokeless tobacco products, of whom the majority live in India and Bangladesh. Smoking has declined since the 1990s, while the popularity of chewing tobacco appears to have increased, including among women.

The health risks of chewing tobacco are less understood compared to the almost universal consensus on the harms caused by cigarettes and other forms of smoking. However, smokeless tobacco is thought to be a carcinogen.

Study: Health effects associated with chewing tobacco: a Burden of Proof study. Image Credit: bildfokus.se / Shutterstock

About the study

In this study, researchers conducted a systematic review and meta-analysis across three scientific databases (Global Index Medicus, Web of Science, and PubMed) to analyze relationships between chewing tobacco and stroke, ischemic heart disease, and five types of cancer of the neck and head.

The search included publications regardless of their language and papers published from 1970 onwards. They used meta-regressions and Bayesian methods to estimate a measure of pooled relative risk and then obtained an effect size for each health outcome. Of the literature obtained from the search, 4,480 were excluded, and 111 were included in the analysis.

Findings

Three studies conducted in Bangladesh and India included data on chewing tobacco and stroke; the meta-analysis suggested that conservatively, using smoking tobacco products increased the risk of stroke by 16%. This association is classified as a ‘weak’ relationship. However, these findings were robust to various validations; no publication or covariate bias was detected.

Eight studies examined associations between smokeless tobacco and ischemic heart disease, most of which were conducted in Bangladesh, India, and the United States. The meta-analysis found no evidence that chewing tobacco significantly changed ischemic heart disease risk; again, researchers found no evidence of publication bias or covariate bias.

For esophageal cancer, 22 studies were identified; analysis suggested that using chewing tobacco significantly increased the risk of cancer by 2% conservatively. However, a meta-analytic approach yielded a higher estimate of a 2.14-fold increase in esophageal cancer risk. Smoking status, sex, and age were adjusted for in the final analysis, and no publication bias was detected.

A total of 70 studies examined associations between smokeless tobacco products and cancers of the lip and oral cavity. The analysis incorporated numerous sources of uncertainty and found a relative risk factor of 3.64, and the association was characterized as weak; the risk of developing these forms of cancer increased when the sample was restricted to studies conducted in Asian countries.

The effect size for laryngeal cancer was estimated from 24 studies. Researchers found that evidence regarding this outcome was weak after accounting for sources of uncertainty, while the relative risk factor was 2.66. However, for a single study, the relationship between smokeless tobacco and laryngeal cancer was significantly higher.

17 studies were included for nasopharyngeal cancer, and weak evidence of a relationship with a relative risk measure of 2.50 was seen. Age and sex were included in the model after covariate selection, and no evidence of publication bias was found.

The outcome included in the meta-analysis was other cancers of the pharynx; data for this model was obtained from 31 studies. The relative risk factor was 2.33, and the association was characterized as weak. However, using a subset of the data, a higher risk measure of 4.38 was found, showing a stronger association.

Conclusions

The study had various strengths, including reducing the impact of geographical variation. Of the seven health outcomes included, six showed at least weak evidence of increased risk faced by smokeless tobacco users; the only outcome for which no evidence was found was ischemic heart disease. The highest risks were of stroke and esophageal cancer, with a conservative estimate suggesting an increase in incidence of 2-16%.

An important conclusion was that while chewing tobacco is considered a carcinogen, the literature predominantly examined its relationship with lip, oral cavity, and esophageal cancer, highlighting the need for more high-quality studies on associations with other cancers of the head and neck. Specifically, nasopharyngeal and laryngeal cancer should also merit careful observation in the future, as should stroke.

Limitations of the study included the variety of smokeless tobacco products, exposure definitions, and geographical settings. The approach followed in this study was also not able to estimate dose-response relationships. However, these findings can be used by public health workers to better counsel clients on harms associated with smoking tobacco products and advocate for more effective public health policies, while they may also be of interest to community awareness campaigns.
Journal reference:

Health effects associated with chewing tobacco: A Burden of Proof study. Gil, G.F., Anderson, J.A., Aravkin, A., Bhangdia, K., Carr, S., Dai, X., Flor, L.S., Hay, S.I., Matthew, M.J., McLaughlin, S.A., Mullany, E.C., Murray, C.J.L., O’Connell, E.M., Okereke, C., Sorensen, R.J.D., Whisnant, J., Zheng, P., Gakidou, E. Nature Communications (2024). 10.1038/s41467-024-45074-9, https://www.nature.com/articles/s41467-024-45074-9
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February 8, 2024
Study shows how low dose of cadmium produces deleterious stress in lung epithelial cells

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Cigarette smoke exposure is associated with the development and severity of chronic obstructive pulmonary disease, or COPD, which is the third leading cause of death worldwide.

Cigarette smoke contains 2 to 3 micrograms of cadmium, a highly toxic metal and environmental pollutant, per cigarette. Burning tobacco releases cadmium oxide that can be adsorbed onto microparticles in smoke that travel deep into the lungs. Furthermore, the body is not able to remove cadmium, which accumulates in longtime smokers.

In a Scientific Reports study, University of Alabama at Birmingham researchers show how a low dose of cadmium produces a deleterious stress in lung epithelial cells, and their findings highlight potential therapeutic targets to be explored in cadmium-exposure and subsequent lung injury.

The research, led by Veena Antony, M.D., a professor in the UAB Department of Medicine, focuses on microRNA-381, and the expression of a chloride channel gene called ANO1 in lung tissue samples and airway epithelial cells. ANO1 helps produce mucus in the airway; but overproduction of mucus in chronic lung disease can lead to airway thickening and mucus blockage, adding to severity of the disease. Thus, overexpression of ANO1 can exacerbate COPD.

The UAB researchers compared lung tissue samples from nine “never” smokers, who had zero history of cigarette smoking, and lung tissue samples from 13 “ever” smokers with COPD who had a history of smoking that ranged from 15 to 25 pack years per person. One pack year is generally defined as smoking one pack of cigarettes a day for one year. The researchers found that “ever” smokers, in contrast to “never” smokers, had upregulated ANO1 expression in airway epithelial cells.

Similarly, airway epithelial cells in a bronchoalveolar lavage fluid from one non-COPD subject and one smoker with COPD showed greater ANO1 expression in the COPD-subject cells.

The researchers next tested the direct effect of very low doses of cadmium on normal human airway epithelial cells. These cells were grown on an air-liquid interface that allows the airway cells to differentiate normally. Two weeks of exposure to 0.5 or 1.0 micromolar cadmium chloride in the liquid layer increased expression of ANO1 12 to 14 times.

MicroRNAs have the ability to downregulate expression of a gene by direct interaction with that gene’s mRNA sequence. The UAB team used computer software analysis to identify microRNA-381 as the microRNA with most interaction with ANO1 mRNAs, suggesting that microRNA-381 is a negative regulator of ANO1. Some heavy metals are known to negatively regulate microRNAs.

Antony and colleagues used a synthetic inhibitor for microRNA-381 to inhibit the expression of microRNA-381 in primary human airway epithelial cells from subjects with COPD, and found that ANO1 expression was upregulated significantly. In contrast, adding a microRNA-381-mimic -; a synthetic RNA that acts like microRNA-381 to increase the amount of negative regulation -; to those cells decreased ANO1 expression. These results strengthened the premise of the UAB researchers that cadmium negatively regulates microRNA-381 expression to upregulate ANO1 expression in airway epithelial cells.

Lastly, researchers found that, even when primary human airway epithelial cells from subjects with COPD were also exposed to 1 micromolar cadmium chloride, the microRNA-381 inhibitor still upregulated ANO1 and the mimic still downregulated ANO1.

Our observations from experiments involving low-dose cadmium-exposure of epithelial cells suggest that ANO1 is a direct target for miR-381, which is downregulated upon low-dose cadmium exposure. Thus, cigarette-induced cadmium-toxicity may alter cellular homeostasis mechanisms at very low concentrations, and cadmium-exposure in a person with an existing pulmonary condition can have an additive or adverse effect with increased susceptibility toward infections and environmental allergens.

This interaction of cadmium, microRNA-381 and ANO1 suggests that microRNAs may act as potential therapeutic targets to be explored further in cadmium-exposure and subsequent lung injury.”

Veena Antony, M.D., Professor, UAB Department of Medicine

At UAB, Antony holds the Endowed Professorship in Environmental Medicine, directs the Superfund Research Center, and is a member of the Division of Pulmonary, Allergy and Critical Care Medicine.

Co-authors with Antony in the study, “Low dose cadmium exposure regulates miR‑381–ANO1 interaction in airway epithelial cells,” are Pooja Singh, Fu Jun Li, Kevin Dsouza, Crystal T. Stephens, Huaxiu Zheng and Mark T. Dransfield, UAB Department of Medicine Division of Pulmonary, Allergy and Critical Care Medicine; and Abhishek Kumar, UAB Superfund Center Advisory Board, Gainesville, Florida.

Support came from National Institute of Environmental Health Sciences grant ES027723.

Source:

University of Alabama at Birmingham

Journal reference:

Singh, P., et al. (2024). Low dose cadmium exposure regulates miR-381–ANO1 interaction in airway epithelial cells. Scientific Reports. doi.org/10.1038/s41598-023-50471-z.

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February 3, 2024
Study explores the mediatory role of gut microbiota in metabolic syndrome and sleep disorders

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In a systematic review published in Nutrients, researchers described gut microbiota and metabolic alterations common to metabolic syndrome (MetS) and sleep disorders.

Study: The Microbiota–Gut–Brain Axis in Metabolic Syndrome and Sleep Disorders: A Systematic Review. Image Credit: Kmpzzz/Shutterstock.com

Background

One of the key mediators of the association between sleep disorders and MetS is diet. Yet, scientific evidence on its impact on human metabolism and sleep is scarce.

Moreover, studies have not unveiled the biological mechanisms governing the intricate crosstalk between neuroendocrine, immune, and metabolic pathways that connect sleep disorders to MetS.

Furthermore, several factors, such as smoking, alcohol consumption, and poor dietary habits, may lead to gut dysbiosis, which, in turn, adversely affects the gut–brain axis. However, how precisely the gut microbiota affects sleep homeostasis and MetS remains unclear.

Study methodology

Researchers conducted two separate thorough literature searches in the Medline-Pubmed databases to review observational studies and randomized clinical trials (RCTs) published in the last ten years investigating the microbial composition in adults with MetS and sleep disorders.

The database search returned 117 articles, of which they selected 59 articles for extensive full-text search. The final sample set comprised 36 articles, 11 for sleep disorders and 25 for MetS.

The gut-brain axis

The communication between the gut and the brain is facilitated through multiple pathways. One such pathway involves the afferent vagus nerve, which innervates the gut and relays signals to the central nervous system (CNS).

This nerve is responsive to various substances, such as microbial neurotransmitters, hormones, fatty acids, and cytokines.

Among the diverse neuromodulators, acetylcholine (ACh), norepinephrine (NE), and γ-aminobutyric acid (GABA) are particularly notable.

These are produced and metabolized by gut microbes, playing a crucial role in directly and indirectly stimulating the connection between the gut’s afferent neurons and the CNS.

Specifically, studies have identified that Lactobacillus and Bifidobacterium spp. strains can synthesize GABA. This synthesis impacts neurological functions, including the modulation of sleep disorders and memory.

Additionally, the gut microbe Clostridium sporogenes converts tryptophan (Trp) into 5-hydroxy-tryptophan, a precursor of serotonin.

This conversion enhances the inhibitory neuroregulatory effect of L-tryptophan (Trp) by interacting with trace amine-associated receptors.

Moreover, the gut microbiome is involved in the neuroprotective effects of melatonin against cognitive impairment caused by sleep deprivation (SD), as demonstrated in mouse studies.

The gut microbiome also influences immune cell activity, both directly and indirectly, which in turn contributes to regulating the circadian clock.

For example, Lactobacillus rhamnosum can stimulate regulatory T-cells both indirectly, through the modulation of immune signaling via microbial cell wall components like lipopolysaccharides (LPS), and directly, through pattern-recognition receptors (PRRs).

Lastly, gut microbes are known to modulate the expression of genes that regulate circadian rhythms, such as Rev-ERBA.

Host-microbial mechanisms influencing sleep disorders and MetS

The studies included in this review demonstrated how the internal biological clock (or circadian rhythm) altered metabolic homeostasis, and any changes in nutritional and metabolic statuses affected the circadian rhythm; thus, this link was reciprocal.

Moreover, any perturbation to the delicate circadian pattern leads to internal desynchrony and organ failure, as commonly observed in sleep disorders, such as sleep apnea, narcolepsy, insomnia, and circadian rhythm sleep disorders, categorized based on their clinical manifestations.

Several controlled trials addressed the need to establish a cause-and-effect association between sleep duration and gastrointestinal (GI) disorders.

They found that gut microbial neurometabolites and amino acids, such as Trp and alpha-lactalbumin (A-LAC), affected the sleepgut–brain axis.

Thus, many studies have shown that intake of Trp-rich foods, such as milk, is linked to improved sleep quality.

In an RCT, Schaafsma et al. showed that three weeks of supplementation of a dairy-based product in subjects with sleep disorders effectively ameliorated their Pittsburgh Sleep Quality Index (PSQI) score and reduced their cholesterol levels.

Intriguingly, fecal samples collected at the end of the study showed an abundance of Bifidobacteraceae. This gut microbe produces an active form of GABA; thus, it is a crucial player in the stress/anxiety/sleep axis.

MetS is an ensemble of dyslipidemia, hypertension, central obesity, disrupted insulin sensitivity, and low-grade systemic inflammation and is a well-recognized marker of microbial dysbiosis in MetS.

In addition, MetS patients exhibit a deficiency in short-chain fatty acid (SCFA) producing gut microbes.

Some studies included in this review showed that metabolic impairments observed in MetS were due to a decline in bacterial deconjugation activity of primary bile acids.

Other studies showed that microbial-derived metabolites called branched-chain aromatic amino acids (BCAAs), e.g., leucine, were involved in obesity-associated insulin resistance via an mTOR-dependent mechanism.

More and more studies have also pointed out the importance of feeding time and rhythmicity in shaping gut microbiota communities that can achieve this.

Thus, only long-term dietary interventions may permanently alter the gut microbial composition to ameliorate MetS.

Moreover, multiple animal studies and studies with human subjects demonstrated that higher ingested dietary fiber intake leads to a higher prevalence of bacterial SCFA producers in the gut, which are beneficial for glucose homeostasis and ameliorating metabolic parameters in MetS.

Interestingly, this effect correlates with the enrichment of Bifidobacterium observed in the case of sleep improvements.

Conclusions

Overall, this review highlights the importance of diets rich in fiber to modulate the beneficial bacteria in the gut microbiota composition of subjects with MetS and sleep disorders.

In sleep disorders, a potential common microbial signature is the lower abundances of butyrate (a SCFA) producers, especially Faecalibacterium prausnitzii, coupled with a reduction in some members of the Lachnospiraceae family, like Roseburia, and an enrichment in the Bacteroidetes phylum.

This pattern is similar to the observed decrease in SCFA producers in MetS. Since MetS cohorts examined in this review were larger, more controlled, and better taxonomically defined, their microbial pattern is more consistent for further investigation.

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January 31, 2024
How bad is vaping for your health? We’re finally getting answers

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AS THE old joke goes, when I read about the dangers of smoking, I gave up reading. If you are a vaper, you might feel like you want to stop reading now. Don’t: you need to know this.

I am a vaper. Like many others, I used to smoke and switched to vaping for health reasons. I plan to quit completely, but I haven’t managed it yet. I am sure vaping is better for me than smoking, but I am also sure it is worse than not vaping. I cough in the morning and feel massively addicted to the nicotine. I don’t even really know what I am inhaling. I worry that it will be hard to quit, that I am causing long-term damage to my body and that by vaping, I am susceptible to slipping back down the slope to cigarettes. I also have the same worries for the teenagers I see coming out of school and immediately enveloping themselves in sweet-smelling clouds.

As vaping has increased throughout the Western world, these fears have been repeated often. Part of last month’s King’s Speech in the UK focused on new legislation aiming to create a smoke-free generation in part by cracking down on youth vaping. Worldwide, there have been calls for tougher regulation and more investigation into vaping’s health effects as increasing numbers of children admit to taking up the habit.

But there hasn’t been a huge amount to say on whether fears over health effects are well-founded – until recently. Now, vaping…

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December 6, 2023