Category: 8. Health

A potential treatment for glioblastoma crafted by scientists at The Wertheim UF Scripps Institute renders the deadly brain cancer newly sensitive to both radiation and chemotherapy drugs, and blocks the cancer’s ability to invade other tissue, a new study shows.

The experimental medication, called MT-125, has received approval from the FDA to move to clinical trials as a possible first-line treatment for the most aggressive form of the brain cancer.

Each year, 14,000 people in the United States receive the devastating news that they have glioblastoma. It is a cancer with an average survival of just 14 to 16 months. Standard treatments include surgery, radiation and chemotherapy. But half of glioblastoma patients have a subtype that doesn’t respond to any approved cancer drugs, said Courtney Miller, Ph.D., a professor and academic affairs director at The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology.

New options are urgently needed for those patients, said Miller, a member of the University of Florida Health Cancer Center.

We know glioblastoma patients are awaiting a breakthrough, and we are moving as fast as humanly possible.”

Courtney Miller, Ph.D., professor and academic affairs director at The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology

Miller and her colleagues have long focused on molecular “motors” in the cell, nanoscale proteins called myosin. They look and act like machines, converting the cell’s energy into activity. Myosin motors enable cells to move, connect to other cells or contract and expand, Miller said. They are found throughout the body, including in heart, muscle and brain tissue.

As a result, they have potential as therapeutic targets for a wide range of conditions, from cancer to substance use disorders, she said. However, there are no current medications that target them, or even selective drug-like tools that scientists can use to study them.

Miller teamed up with her Wertheim UF Scripps colleagues to design a spectrum of potential drug candidates to block myosin motors in different contexts. Their work was published Tuesday, July 1, in the scientific journal Cell.

Medicinal chemist Theodore Kamenecka, Ph.D., engineered the array of compounds, in consultation with structural biologist Patrick Griffin, Ph.D., The Wertheim UF Scripps Institute’s scientific director.

To test the oncology potential of the myosin motor drugs, the team joined forces with Steven Rosenfeld, M.D., Ph.D., a scientist and neuro-oncologist at the Mayo Clinic in Jacksonville. Their out-of-the-box strategy appears to have opened a new route to attacking the hardest-to-treat glioblastoma. It works in four ways, the scientists reported in a companion paper published in Cell on June 10.

“In animal studies, MT-125 makes malignant cells that were previously resistant to radiation responsive to it,” Miller said. “You also end up with multinucleated cells that cannot separate, and so they get marked for cell death.”

MT-125 also blocks the cells’ ability to squeeze and change shape, which means they cannot proliferate and invade other parts of the brain, she said. And if MT-125 is combined with existing chemotherapy drugs, including sunitinib, the drug appears to deliver a very powerful response, Rosenfeld said. Sunitinib belongs to a class of chemotherapy drugs called kinase inhibitors.

“We found in mice that combining MT-125 with a number of kinase inhibitors created long periods of a disease-free state that we haven’t seen in these mouse models before,” Rosenfeld said. 

The scientists cautioned that many potential drugs that perform well in mice fail in human studies, due to differences in biology, so it will take time and study to learn if MT-125 is the hoped-for breakthrough, Rosenfeld said.

Toxicity is another worry. But because the cancer cells are much more sensitive to MT-125 than healthy cells, and because the drug doesn’t stay in the body long, pulsed administration of the medication over a brief period seems to address the issue, Rosenfeld said.

“I have been in the field for 35 years, and I always thought the solution to this problem would have to come from out-of-the-box thinking,” Rosenfeld said. “The tried-and-true methods don’t seem to work for this disease.”

The compound, MT-125, has been licensed to a Jupiter, Florida-based biotechnology company started by the scientists, Myosin Therapeutics. They are working hard to begin first-in-human clinical trials within the year in glioblastoma patients, Miller said. The U.S. Food and Drug Administration has given them the green light to proceed. They are awaiting release of a federal grant that has internal approval, she said. The National Institutes of Health has provided study funding, as well as the William Potter Glioblastoma Research Fund at The Wertheim UF Scripps Institute, which was established by William Potter’s wife, Ronnie Potter, in his memory.

Looking ahead, Miller says there is evidence that MT-125 could prove beneficial not only against the aggressive variant of glioblastoma, but for malignant gliomas and other cancers.

In parallel, Miller and her collaborators are working to prepare a clinical trial for a related compound, MT-110, which appears to block drug cravings for people with methamphetamine use disorder. This compound is described in more detail in the July 1 Cell study.

Our study adds to the growing body of literature by investigating the relationship between pulmonary function and stroke in a large NHANES cohort. We observed a consistent inverse association between pulmonary function, as measured by spirometry-derived metrics such as FEV1, FVC, and PEF, and the risk of stroke, suggesting that preserved lung function may confer protective effects against stroke risk.

These findings are consistent with previous studies that have reported associations between lung function and cardiovascular events, including stroke [14, 15, 16]. Logitudinal studies found that a higher pulmonary function was associated with lower risk of new-onset stroke using data from the UK Biobank [11]. However, a two-sample Mendelian randomisation study confirmed that there was weak evidence that reduced lung function increased risk of ischaemic stroke [12]. Greater longitudinal declines in these spirometric measures are further associated with cardiovascular morbidity and mortality. Previous conclusions were mostly based on the patients with chronic obstructive pulmonary disease. Our study extended the association in general adults, affirming the significance of respiratory health in cardiovascular outcomes [17, 18]. Interestingly, we observed that the association between reduced pulmonary function and stroke was significantly stronger among participants aged 60 years and older. This age-dependent interaction may reflect cumulative vascular injury, reduced physiologic reserve, and heightened susceptibility to systemic inflammation and hypoxia in older adults. These findings suggest that pulmonary health maintenance may be particularly critical in mitigating stroke risk among the aging population. The inverse association between physical activity and stroke risk observed in our study is consistent with prior research. Physical activity improves vascular health through mechanisms such as lowering blood pressure, enhancing insulin sensitivity, and reducing inflammation. It also helps control key risk factors like obesity and dyslipidemia. Epidemiological studies, including the ARIC and Nurses’ Health Study, have similarly reported reduced stroke incidence with higher activity levels.

The mechanisms linking pulmonary function to stroke risk are complex and likely involve multiple pathways. Reduced pulmonary function cause reduced oxygen exchange and contribute to systemic inflammation [19], endothelial dysfunction [20], and impaired vascular homeostasis [21], all of which are implicated in the pathogenesis of atherosclerosis and cerebrovascular disease. Additionally, impaired lung function may lead to hypoxemia and neurovascular dysfunction [22, 23], thereby predisposing individuals to ischemic stroke. Finally, reduced pulmonary function may alter coagulation and platelet aggregation, increasing the risk of thromboembolic events, including stroke.

Our study builds on previous research by using a nationally representative cohort, which includes a broad range of demographic, clinical, and pulmonary function variables. However, several limitations should be considered when interpreting our findings. First, the cross-sectional design of NHANES precludes determination of temporal or causal relationships between pulmonary function and stroke risk. Stroke survivors may experience reduced physical activity, neuromuscular dysfunction, and an increased risk of aspiration pneumonia, all of which can impair respiratory mechanics and lung capacity. Second, stroke history was based on self-report, which may be affected by recall bias or misclassification. However, previous studies suggest that self-reported stroke in NHANES has reasonable validity. Third, despite extensive adjustment for confounders, residual confounding cannot be entirely excluded, such as a history of cerebrovascular disease and prior use of medications like hypoglycemic agents and statins. Forth, spirometry-derived metrics may not fully capture the complexity of respiratory physiology, and other measures of lung function, such as diffusion capacity and airway resistance, were not assessed in our study. Finally, we acknowledge that group size imbalance may still introduce residual confounding. We did not apply propensity score matching in the current analysis. Therefore, future studies with larger event numbers consider incorporating PSM as a complementary strategy will strengthen causal inference and improve the robustness of results.

These findings suggest that pulmonary function testing could serve as a useful adjunct in stroke risk assessment, especially among older adults. Although our findings suggest that lower pulmonary function is associated with higher stroke prevalence, our study does not evaluate whether pulmonary function measures add incremental predictive value beyond traditional risk scores such as the Framingham Stroke Risk Profile. Therefore, the clinical utility of incorporating pulmonary function testing into routine stroke risk assessment remains uncertain. Future studies should investigate whether pulmonary function improves risk prediction models and whether interventions aimed at preserving or improving lung function can reduce the burden of stroke.

Putting the brakes on an enzyme might rescue neurons that are dying due to a type of Parkinson’s disease that’s caused by a single genetic mutation, according to a new Stanford Medicine-led study conducted in mice.

The genetic mutation causes an enzyme called leucine-rich repeat kinase 2, or LRRK2, to be overactive. Too much LRRK2 enzyme activity changes the structure of brain cells in a way that disrupts crucial communication between neurons that make the neurotransmitter dopamine and cells in the striatum, a region deep in the brain that is part of the dopamine system and is involved in movement, motivation and decision making.

Findings from this study suggest that inhibiting the LRRK2 enzyme could stabilize the progression of symptoms if patients can be identified early enough.”

Suzanne Pfeffer, PhD, the Emma Pfeiffer Merner Professor in Medical Sciences and professor of biochemistry

Researchers can mitigate overactive LRRK2 using MLi-2 LRRK2 kinase inhibitor, a molecule that attaches to the enzyme and decreases its activity.

Pfeffer added that because the genetic mutation is not the only way to end up with overactive LRRK2 enzyme, the inhibitor treatment might help with other types of Parkinson’s disease or even other neurodegenerative diseases.

Pfeffer is the senior author of the study to be published in Science Signaling on July 1. Ebsy Jaimon, PhD, a postdoctoral scholar in biochemistry, is the lead author. The work is part of a longstanding collaboration with Dario Alessi, PhD, at the University of Dundee in Scotland.

Cellular antennae

About 25% of Parkinson’s disease cases are caused by genetic mutations, and the single genetic mutation that makes the LRRK2 enzyme too active is one of the most common. An overactive LRRK2 enzyme causes cells to lose their primary cilia, a cellular appendage that acts like an antenna, sending and receiving chemical messages. A cell that has lost its primary cilia is like your mobile phone when the network is down – no messages come through or are sent.

In a healthy brain, many messages are sent back and forth between dopamine neurons in a region of the brain called the substantia nigra and the striatum. These cellular “conversations” are possible because dopamine neuron axons, which are tubular extensions coming off the cell body, reach all the way to the striatum to communicate with neurons and glia, cells that support neuronal function.

An important communication that is disrupted by too much LRRK2 enzyme activity occurs when dopamine neurons are stressed and release a signal in the striatum called sonic hedgehog (named after the cartoon character). In a healthy brain, it causes certain neurons and astrocytes, a type of glial support cell, in the striatum to produce proteins called neuroprotective factors. As their name suggests, these proteins help shield other cells from dying. When there is too much LRRK2 enzyme activity, many of the striatal cells lose their primary cilia – and their ability to receive the signal from dopamine neurons. This disruption in sonic hedgehog signaling means that needed neuroprotective factors are not produced.

“Many kinds of processes necessary for cells to survive are regulated through cilia sending and receiving signals. The cells in the striatum that secrete neuroprotective factors in response to hedgehog signals also need hedgehog to survive. We think that when cells have lost their cilia, they are also on the pathway to death because they need cilia to receive signals that keep them alive,” Pfeffer explained.

Restored cilia were unexpected

The goal of the study was to test if the MLi-2 LRRK2 kinase inhibitor reversed the effects of too much LRRK2 enzyme activity. Because the neurons and glia that were examined in this study were fully mature and no longer reproducing through cell division, the researchers were initially unsure whether cilia could regrow. Working with mice with the genetic mutation that causes overactive LRRK2 and symptoms consistent with early Parkinson’s disease, the scientists first tried feeding the mice the inhibitor for two weeks. There were no changes detected in brain structure, signaling or the viability of the dopamine neurons.

Recent findings on neurons involved in regulating circadian rhythms, or sleep-wake cycles, inspired the researchers to try again. The primary cilia on those cells – which were also no longer dividing – grew and shrank every 12 hours.

“The findings that other non-dividing cells grow cilia made us realize that it was theoretically possible for the inhibitor to work,” Pfeffer said.

The team decided to see what happened after mice with overactive LRRK2 enzyme consumed the inhibitor for a longer period of time; Pfeffer described the results as “astounding.”

After three months of eating the inhibitor, the percentage of striatal neurons and glia typically affected by the overactive LRRK2 enzyme that had primary cilia in mice with the genetic mutation was indistinguishable from that in mice without the genetic mutation. In the same way moving from an area with spotty cell service to one with good service restores our ability to send and receive text messages, the increase in primary cilia restored communication between dopamine neurons and the striatum.

The striatal neurons and glia were again secreting neuroprotective factors in response to hedgehog signaling from dopamine neurons in the same amounts as the brains of mice without the genetic mutation. The hedgehog signaling from dopamine neurons decreased, suggesting they were under less stress. And, indicators of the density of dopamine nerve endings within the striatum doubled, suggesting an initial recovery for neurons that had been in the process of dying.

“These findings suggest that it might be possible to improve, not just stabilize, the condition of patients with Parkinson’s disease,” Pfeffer said.

The earliest symptoms of Parkinson’s disease begin about 15 years before someone notices a tremor. Typically, these symptoms are a loss of smell, constipation and a sleep disorder in which people act out their dreams while still sleeping, according to Pfeffer. She said the hope is that people who have the LRRK2 genetic mutation can start a treatment that inhibits the enzyme as early as possible.

The next step for the research team is to test whether other forms of Parkinson’s disease that are not associated with the LRRK2 genetic mutation could benefit from this type of treatment.

“We are so excited about these findings. They suggest this approach has great promise to help patients in terms of restoring neuronal activity in this brain circuit,” Pfeffer said. “There are multiple LRRK2 inhibitor clinical trials underway, and our hope is that these findings in mice will hold true for patients in the future.”

The study was funded by The Michael J. Fox Foundation for Parkinson’s Research, the Aligning Science Across Parkinson’s initiative and the United Kingdom Medical Research Council.

BBC

Suncream ‘makes a difference’

Researchers estimate that approximately 200 million people worldwide are affected by age-related macular degeneration (AMD), a condition that impairs central vision and can cause blurriness or other visual disturbances.

There are two forms of AMD. The more common type is dry AMD, which involves gradual damage to the macula—a region at the back of the retina—as part of the natural aging process. Wet AMD, on the other hand, occurs when abnormal blood vessels grow behind the eye and damage the macula, reported Medical News Today.

A recent study featured in the journal Food Science & Nutrition suggests that a mix of genetic factors and consuming instant coffee could raise the risk of developing dry age-related macular degeneration (AMD).

In this study, researchers gathered coffee consumption data from over 500,000 individuals using the UK Biobank genome-wide association studies (GWAS) summary statistics. Participants were categorised based on their coffee preferences: decaffeinated, ground, or instant coffee.

Additionally, data on both dry and wet age-related macular degeneration (AMD) in adults aged 50 and older was sourced from the Finngen GWAS dataset.

Using the collected data, researchers applied several analytical methods—such as Mendelian randomisation and linkage disequilibrium score regression (LDSC)—to explore potential genetic links.

By the end of the study, they discovered a genetic overlap between a predisposition for drinking instant coffee and an increased risk of developing dry AMD.

Moreover, within this genetic connection, they found that consuming instant coffee—as opposed to other types—was associated with a roughly sevenfold higher risk of dry AMD.

In this study, we analyzed the temporal trends in the burden of kidney cancer (KC) in China from 1990 to 2021. In 2021, the number of incident KC cases in China reached 65,799 (4.62 cases per 100,000 total population). Additionally, KC resulted in 24,867 deaths (1.75 deaths per 100,000 total population). Over the past 30 years, both the prevalence and mortality of KC have increased significantly. We observed a notable rise in the incidence, mortality, and disability-adjusted life years (DALYs) of kidney cancer in China over the three-decade period, with more pronounced increases in males than in females. The China age-standardized incidence rate (ASIR) of kidney cancer increased from 1.79 per 100,000 in 1990 to 3.31 per 100,000 in 2021. Furthermore, the age-standardized mortality rate (ASMR) of kidney cancer also rose, from 1.14 per 100,000 in 1990 to 2.25 per 100,000 in 2021.

The increasing burden of kidney cancer can be attributed to several key factors. First, population aging is a major driver, as the incidence of kidney cancer increases with age [26, 27]. China’s population is rapidly aging, with the proportion of individuals aged 65 and older projected to rise from 15.6% in 2024 to 26% in 2050 [28]. This demographic shift toward an older population contributes to a higher risk of developing kidney cancer [7]. Risk factors such as smoking, alcohol consumption, overweight, and hypertension have important implications for both kidney cancer incidence and mortality [14, 29, 30]. Our study showed that the burden of KC in males was consistently higher than in females across different age groups. Males are generally exposed to these risk factors for longer durations, making them more susceptible to KC. For example, the global smoking rate was estimated to be 32.6% in males and 6.5% in females in 2020 [31]. Previous studies have also indicated that males tend to have higher BMIs than females [32]. Moreover, industries with higher male participation may expose individuals to occupational hazards associated with urinary tract cancers [33] Reports suggest that males are approximately twice as likely as females to be occupationally exposed to trichloroethylene, and males also exhibit higher prevalence in jobs involving trichloroethylene exposure [34]. Between 1990 and 2021, smoking and high BMI were the primary drivers of KC in individuals aged 65 and older. Smoking significantly increases the risk of KC incidence and mortality [35].

Previous epidemiological evidence has indicated that age is an independent and critical risk factor for KC, with varying numbers of deaths across different age groups [11]. According to age-period-cohort analysis, KC prevalence and mortality increase with advancing age. After the 60–64 age group, the risk trend of the age effect increases roughly exponentially. Middle-aged and elderly individuals are more likely to have long-term smoking and obesity, which elevate their risk of KC [36]. The period effect refers to changes in medical technology, diagnostic methods, and economic and cultural factors that influence the disease burden of KC during specific time periods. According to the current study, the period effect on KC prevalence showed a slight decrease, possibly due to the recent popularization of medical knowledge in China, which has reduced some KC cases. The cohort effect highlights socioeconomic, behavioral, and environmental exposures in early life and the risks of different birth cohorts. In our study, the cohort effect on KC prevalence showed a downward trend: earlier birth cohorts had a higher risk of KC, while more recent cohorts had a lower risk. In addition to age, this decreasing effect can be attributed to better education and higher health awareness among younger generations.

Monitoring disease prevalence and predicting trends are essential components of disease prevention and control. As a predictive model, the Bayesian age-period-cohort (BAPC) model has been proven reliable [4]. Therefore, we conducted BAPC analysis to project trends in the age-standardized incidence and mortality rates of kidney cancer. According to the BAPC model, the prevalence and mortality of KC are expected to rise to 4.58 per 100,000 and 1.31 per 100,000 by 2036. The large gap between high KC prevalence and low awareness/treatment may partially explain the consistent increase in mortality in recent years. Thus, a comprehensive strategy is needed, including risk factor prevention at the primary care level, KC screening for the elderly and high-risk populations, and access to high-quality medical services, to reduce the burden of KC and achieve better health outcomes for KC patients.

Given the exponential rise in kidney cancer (KC) risk after 60–64 years of age and China’s rapidly aging population—with individuals aged ≥ 65 projected to account for 26% of the population by 2050—integrating age-stratified screening into primary care for older adults is critical. Priorities include expanding low-cost, non-invasive screening tools (e.g., urine cytology, renal ultrasound) for high-risk groups, particularly those with smoking or obesity histories. Multisectoral policies must address modifiable risks: strengthening tobacco taxation and smoke-free legislation, promoting population-wide body mass index (BMI) management through dietary and physical activity initiatives, and enhancing workplace safety regulations to reduce occupational carcinogen exposure—especially among male workers.

The lower KC risk observed in younger generations, likely linked to improved education and health awareness, highlights the need to scale public education programs emphasizing early detection, risk avoidance, and regular screening. Additionally, to address the projected rise in KC burden through 2036, healthcare infrastructure upgrades—particularly in resource-constrained regions—are essential to ensure equitable access to diagnostics and advanced therapies, such as targeted treatments for advanced KC.

Collectively, translating these findings into action requires a synergistic strategy integrating primary prevention (risk factor control), age- and sex-tailored screening, and tertiary care optimization, supported by robust surveillance models like the Bayesian age-period-cohort framework, to curtail rising KC burden and improve outcomes for at-risk populations in China.

Limitations

This analysis provides valuable data reference for KC prevention and control efforts. However, the study has several limitations. First, the data provided in GBD 2021 are based on estimates and mathematical modeling, which may affect the accuracy and reliability of burden estimates. Second, several types of KC, such as clear cell renal cell carcinoma, chromophobe renal cell carcinoma, and papillary renal cell carcinoma, are not included in the GBD database, precluding subtype-specific analysis of the KC burden. Third, our analysis of the KC burden was conducted at the national level without further exploration of the complex interactions between genetic and environmental factors contributing to KC development.

BBC

BBC

This study developed and validated a comprehensive questionnaire (Supplementary Table 3) aimed at identifying factors influencing hookah smoking behavior across personal, interpersonal, and organizational levels. The initial version of the questionnaire was informed by a qualitative study, which provided valuable insights into relevant factors. Through an iterative process, certain items were removed to enhance clarity and relevance, resulting in a refined instrument that was subsequently tested for content validity. The results confirmed the reliability and validity of the questionnaire. The final questionnaire included 81 items aligned with 16 factors. Having tested the face validity, content validity, and construct validity were substantiated. The results offer evidence that this questionnaire is a valid and reliable tool for assessing factors related to hookah smoking among women. To our knowledge, this is the first study to focus specifically on vulnerable populations, such as women who smoke hookah in the Eastern Mediterranean region. Further validation across different sites and cultural contexts would enhance its applicability and provide deeper insights into its broader relevance.

The need for a questionnaire on women’s hookah smoking in Iran is urgent due to the significant increase in hookah smoking among Iranian women and the adverse effects of consuming this tobacco product on health [24, 25]. Gender differences exist in why men and women start hookah smoking. For example, Iranian men with Turkmen ethnicity often begin smoking due to cultural identity and sense of adulthood [26], while women are more influenced by social approval and emotional needs [14, 27]. These differences suggest that public health strategies should be tailored by gender, and because of this, we need a gender-specific questionnaire. The lack of a questionnaire specifically designed for women shows the need to design one to measure the effective factors in the initiation and continuation of hookah smoking among women. This questionnaire can help develop systematic health promotion initiatives and interventions that specifically address women’s needs and behaviors. There are several questionnaires to evaluate hookah smoking, such as the Hookah Smoking Initiation for Women Questionnaire (HIWQ). This questionnaire was designed using an exploratory sequential mixed methods approach to include six dimensions: drawing the attention of other people, the need to have fun and be relaxed, hookah smoking in the family, availability of hookah, curiosity and having a positive attitude toward hookah. HIWQ aims to assess the initiation of hookah smoking by women. In the questionnaire used in the present study, besides these factors, other issues have also been addressed such as socio-economic deficiencies and role of advertisement and education [13]. Hookah Smoking Obscenity Measurement Scale for Adolescents evaluates the level of obscenity related to hookah smoking among adolescents. This instrument is not specifically designed for women, and considers a specific age group (i.e., adolescents) [12]. The Questionnaire on Smoking Urges for Assessment of Hookah Smoking evaluates the tendency to smoke hookah and, like the previous questionnaire, it is not specifically designed for women [11]. These questionnaires provide a basis for the development of a comprehensive and culturally relevant instrument. It evaluated the beginning and continuation of hookah, which, besides the factors included in these questionnaires, also deals with other factors at the personal, interpersonal and organizational levels.

These factors include socioeconomic deficiencies, role of advertisement and education, availability, fun and entertainment, hookah smoking in family and relatives, search for peace, attracting others’ attention and approval, physical and mental dependence, color, flavor and sound of hookah, happy environment of coffee shops, pleasant experience of the first puff of hookah smoking, The prevalence of acceptability of hookah smoking in society, false beliefs, Low self-efficacy, Peer pressure, and Family tendencies. These factors showed adequate internal consistency and construct validity and supported their use in evaluating the key factors underlying hookah smoking behavior.

Our developed and validated questionnaire addresses many dimensions, including low self-efficacy, physical/mental dependence, attracting others’ attention and approval, search for peace, positive attitude towards hookah, false beliefs about personal factors underlying hookah smoking, the color, taste, and sound of hookah, and the pleasant experience of the first puff of hookah. Low self-efficacy, or belief in one’s ability to resist hookah smoking, is a main factor that contributes to hookah smoking. Women with low self-efficacy are more likely to initiate and continue hookah smoking [15]. Self-efficacy assessment helps understand people’s vulnerability to hookah smoking. Moreover, hookah smoking can become addictive and make it hard for women to quit. Assessing the degree of dependence provides insights into the intensity of hookah smoking and the challenges of cessation [15]. Having a positive attitude towards hookah is a major reason for smoking among women. Women who hold more favorable beliefs about hookah are less likely to quit [14, 28]. Assessing attitudes helps identify women at risk of hookah smoking and guides researchers to design interventions to change these attitudes. Meanwhile, the spread of false beliefs about the harmlessness of hookah smoking affects people’s attitudes toward this tobacco product [29]. Some women believe that hookah is less harmful than cigarettes or even has health benefits. The belief that hookah smoking is pleasant and acceptable may add to its popularity among women. It is important to assess these misconceptions to correct them through education. Therefore, individual factors can be effective in women’s hookah smoking, and including relevant questions in questionnaires provides a comprehensive assessment of the risk of hookah smoking in women. This information can guide systematic interventions to prevent hookah initiation, reduce smoking, and promote hookah cessation.

Interpersonal factors also play a significant role in hookah smoking among women. These factors in the current study include the influence of peers and friends, family preferences, and the role of the family in hookah smoking. These factors are of utmost importance and need to be included in the questionnaire. The role of peers and friends is admittedly an important interpersonal factor involved in hookah smoking among women. Hookah smoking has deep roots in the culture and history of many societies. Climate and cultural norms can affect the prevalence of hookah smoking among women. For example, in some societies like Iran, hookah smoking is considered a social norm and a way to communicate with others as opposed to cigarette which carries stigma for women who smoke [14, 28, 29]. Social norms and peer pressure can initiate, encourage or prohibit the use of hookah. If people closely related to women are hookah smokers, it is more likely that they begin to smoke hookahs too [29]. Friends’ and acquaintances’ smoking can tempt women to smoke hookahs. Including questions about peer pressure in the questionnaire helps recognize the effect of social networks on hookah smoking and informs professionals about interventions that address these relationships. In some cultures, family members may encourage or prohibit hookah smoking, and women may be strongly influenced in their hookah smoking behavior. In this regard, researchers reported that familial habits like having hookah-smoking family members, especially parents or siblings can influence women’s decision to go for hookahs [29, 30]. It can be argued that people can copy hookah smoking by friends and family members and be tempted to smoke due to the availability of hookahs, or the environments that facilitate its use. Including questions about family tendencies in the questionnaire can highlight the role of family in hookah smoking and contribute to interventions that address family dynamics.

Organizational factors are among the other factors included in this questionnaire as advertisement and education. Advertising can promote hookah smoking by introducing hookah as a social and cultural norm. This could lead to a higher prevalence of hookah smoking among women, as they are more influenced by social norms and cultural expectations [28, 31]. Education can play a significant role in reducing the rate of hookah smoking among women. Educating women on the health risks of hookah smoking can help them make informed decisions about their health.

In the current study, social factors were also included in the questionnaire. Social factors play a significant role in women’s hookah smoking. These factors included availability, fun and entertainment, socio-economic deficiencies, and happy environment of coffee shops. Easy access to hookah and its low cost are the main factors underlying its prevalence. When hookah is readily available and affordable, women tend more to try it [16]. Moreover, recreational centers where hookah is sold, such as coffee shops and restaurants, can further encourage hookah smoking by providing a pleasant social environment and easy access to hookahs [14, 29]. In addition to the prevalence of hookah smoking in families, the prevalence in public places like coffee shops also familiarizes the young with hookah and gives them easy access to it. The lower cost of hookah compared to other recreational drugs has also attracted many people. The lack of appropriate and large enough social contexts for women, especially recreational facilities, can affect their hookah smoking patterns. This points to the necessity of considering the social and political factors that shape the opportunities and limitations facing women [15]. The political and regulatory system significantly affects the availability of hookahs [27]. Therefore, including questions about social factors in the questionnaire is essential to consider the role of these factors in hookah smoking among women. These factors can provide valuable insights into the social effects of hookah smoking.

The comprehensive nature of this questionnaire, which includes a wide range of factors, increases its effectiveness in capturing the multidimensional aspects of hookah smoking. Nevertheless, this study has some limitations. First, it was conducted in a single city in Iran, limiting the generalizability of the findings to the wider population of women in Iran or beyond. Further testing in different regions is necessary to enhance the study’s broader applicability. The questionnaire can indeed be applicable to women in other MENA countries as well as in other similar contexts. Second, all data were self-reported, which may introduce recall or reporting biases. Lastly, variations in the use of flavored and non-flavored hookah tobacco, which may influence users’ perceptions and behaviors, were not assessed in this study. Although women in Iran typically smoke mildly flavored hookah tobacco, future studies should account for this important factor.

Implications of the study

The present study has major implications for understanding and measuring the complex nature of hookah smoking behavior. Recognition and measurement of these factors give researchers and public health professionals a deeper understanding of the causes and effects of hookah smoking. This knowledge can help with the development of systematic interventions and policies aimed at reducing hookah smoking and its health risks. Future research can use this valid questionnaire to further investigate the factors affecting hookah smoking in different populations and environments. By expanding the scope of research and interventions based on the present findings, stakeholders can attempt to develop goal-oriented strategies to address the complex interplay of personal, interpersonal, and social factors underlying hookah smoking.

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