Paolo Spriano

In most Western countries, professional standards dictate that physicians should practice medicine with compassion. Patients also expect compassionate care from physicians because it represents a model capable of providing greater patient satisfaction, fostering better doctor-patient relationships, and enabling better psychological states among patients.

The etymology of the term “compassion” derives from the Latin roots “com,” meaning “together with,” and “pati,” meaning “to endure or suffer.” When discussing compassion, it is necessary to distinguish it from empathy, a term generally used to refer to cognitive or emotional processes in which the perspective of the other (in this case, the patient) is taken. Compassion implies or requires empathy and includes the desire to help or alleviate the suffering of others. Compassion in the medical context is likely a specific instance of a more complex adaptive system that has evolved, not only among humans, to motivate recognition and assistance when others suffer.
 

Compassion Fatigue

Physicians’ compassion is expected by patients and the profession. It is fundamental for effective clinical practice. Although compassion is central to medical practice, most research related to the topic has focused on “compassion fatigue,” which is understood as a specific type of professional burnout, as if physicians had a limited reserve of compassion that dwindles or becomes exhausted with use or overuse. This is one aspect of a much more complex problem, in which compassion represents the endpoint of a dynamic process that encompasses the influences of the physician, the patient, the clinic, and the institution.

Compassion Capacity: Conditioning Factors

Chronic exposure of physicians to conflicting work demands may be associated with the depletion of their psychological resources and, consequently, emotional and cognitive fatigue that can contribute to poorer work outcomes, including the ability to express compassion.

Rates of professional burnout in medicine are increasing. The driving factors of this phenomenon are largely rooted in organizations and healthcare systems and include excessive workloads, inefficient work processes, administrative burdens, and lack of input or control by physicians regarding issues concerning their work life. The outcome often is early retirement of physicians, a current, increasingly widespread phenomenon and a critical issue not only for the Italian National Health Service but also for other healthcare systems worldwide.
 

Organizational and Personal Values

There is no clear empirical evidence supporting the hypothesis that working in healthcare environments experienced as discrepant with one’s own values has negative effects on key professional outcomes. However, a study published in the Journal of Internal Medicine highlighted the overall negative effect of misalignment between system values and physicians’ personal values, including impaired ability to provide compassionate care, as well as reduced job satisfaction, burnout, absenteeism, and considering the possibility of early retirement. Results from 1000 surveyed professionals indicate that physicians’ subjective competence in providing compassionate care may remain high, but their ability to express it is compromised. From data analysis, the authors hypothesize that when working in environments with discrepant values, occupational contingencies may repeatedly require physicians to set aside their personal values, which can lead them to refrain from using available skills to keep their performance in line with organizational requirements.

These results and hypotheses are not consistent with the notion of compassion fatigue as a reflection of the cost of care resulting from exposure to repeated suffering. Previous evidence shows that expressing compassion in healthcare facilitates greater understanding, suggesting that providing compassion does not impoverish physicians but rather supports them in the effectiveness of interventions and in their satisfaction.

In summary, this study suggests that what prevents compassion is the inability to provide it when hindered by factors related to the situation in which the physician operates. Improving compassion does not simply depend on motivating individual professionals to be more compassionate or on promoting fundamental skills, but probably on the creation of organizational and clinical conditions in which physician compassion can thrive.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

In most Western countries, professional standards dictate that physicians should practice medicine with compassion. Patients also expect compassionate care from physicians because it represents a model capable of providing greater patient satisfaction, fostering better doctor-patient relationships, and enabling better psychological states among patients.

The etymology of the term “compassion” derives from the Latin roots “com,” meaning “together with,” and “pati,” meaning “to endure or suffer.” When discussing compassion, it is necessary to distinguish it from empathy, a term generally used to refer to cognitive or emotional processes in which the perspective of the other (in this case, the patient) is taken. Compassion implies or requires empathy and includes the desire to help or alleviate the suffering of others. Compassion in the medical context is likely a specific instance of a more complex adaptive system that has evolved, not only among humans, to motivate recognition and assistance when others suffer.
 

Compassion Fatigue

Physicians’ compassion is expected by patients and the profession. It is fundamental for effective clinical practice. Although compassion is central to medical practice, most research related to the topic has focused on “compassion fatigue,” which is understood as a specific type of professional burnout, as if physicians had a limited reserve of compassion that dwindles or becomes exhausted with use or overuse. This is one aspect of a much more complex problem, in which compassion represents the endpoint of a dynamic process that encompasses the influences of the physician, the patient, the clinic, and the institution.

Compassion Capacity: Conditioning Factors

Chronic exposure of physicians to conflicting work demands may be associated with the depletion of their psychological resources and, consequently, emotional and cognitive fatigue that can contribute to poorer work outcomes, including the ability to express compassion.

Rates of professional burnout in medicine are increasing. The driving factors of this phenomenon are largely rooted in organizations and healthcare systems and include excessive workloads, inefficient work processes, administrative burdens, and lack of input or control by physicians regarding issues concerning their work life. The outcome often is early retirement of physicians, a current, increasingly widespread phenomenon and a critical issue not only for the Italian National Health Service but also for other healthcare systems worldwide.
 

Organizational and Personal Values

There is no clear empirical evidence supporting the hypothesis that working in healthcare environments experienced as discrepant with one’s own values has negative effects on key professional outcomes. However, a study published in the Journal of Internal Medicine highlighted the overall negative effect of misalignment between system values and physicians’ personal values, including impaired ability to provide compassionate care, as well as reduced job satisfaction, burnout, absenteeism, and considering the possibility of early retirement. Results from 1000 surveyed professionals indicate that physicians’ subjective competence in providing compassionate care may remain high, but their ability to express it is compromised. From data analysis, the authors hypothesize that when working in environments with discrepant values, occupational contingencies may repeatedly require physicians to set aside their personal values, which can lead them to refrain from using available skills to keep their performance in line with organizational requirements.

These results and hypotheses are not consistent with the notion of compassion fatigue as a reflection of the cost of care resulting from exposure to repeated suffering. Previous evidence shows that expressing compassion in healthcare facilitates greater understanding, suggesting that providing compassion does not impoverish physicians but rather supports them in the effectiveness of interventions and in their satisfaction.

In summary, this study suggests that what prevents compassion is the inability to provide it when hindered by factors related to the situation in which the physician operates. Improving compassion does not simply depend on motivating individual professionals to be more compassionate or on promoting fundamental skills, but probably on the creation of organizational and clinical conditions in which physician compassion can thrive.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

In most Western countries, professional standards dictate that physicians should practice medicine with compassion. Patients also expect compassionate care from physicians because it represents a model capable of providing greater patient satisfaction, fostering better doctor-patient relationships, and enabling better psychological states among patients.

The etymology of the term “compassion” derives from the Latin roots “com,” meaning “together with,” and “pati,” meaning “to endure or suffer.” When discussing compassion, it is necessary to distinguish it from empathy, a term generally used to refer to cognitive or emotional processes in which the perspective of the other (in this case, the patient) is taken. Compassion implies or requires empathy and includes the desire to help or alleviate the suffering of others. Compassion in the medical context is likely a specific instance of a more complex adaptive system that has evolved, not only among humans, to motivate recognition and assistance when others suffer.
 

Compassion Fatigue

Physicians’ compassion is expected by patients and the profession. It is fundamental for effective clinical practice. Although compassion is central to medical practice, most research related to the topic has focused on “compassion fatigue,” which is understood as a specific type of professional burnout, as if physicians had a limited reserve of compassion that dwindles or becomes exhausted with use or overuse. This is one aspect of a much more complex problem, in which compassion represents the endpoint of a dynamic process that encompasses the influences of the physician, the patient, the clinic, and the institution.

Compassion Capacity: Conditioning Factors

Chronic exposure of physicians to conflicting work demands may be associated with the depletion of their psychological resources and, consequently, emotional and cognitive fatigue that can contribute to poorer work outcomes, including the ability to express compassion.

Rates of professional burnout in medicine are increasing. The driving factors of this phenomenon are largely rooted in organizations and healthcare systems and include excessive workloads, inefficient work processes, administrative burdens, and lack of input or control by physicians regarding issues concerning their work life. The outcome often is early retirement of physicians, a current, increasingly widespread phenomenon and a critical issue not only for the Italian National Health Service but also for other healthcare systems worldwide.
 

Organizational and Personal Values

There is no clear empirical evidence supporting the hypothesis that working in healthcare environments experienced as discrepant with one’s own values has negative effects on key professional outcomes. However, a study published in the Journal of Internal Medicine highlighted the overall negative effect of misalignment between system values and physicians’ personal values, including impaired ability to provide compassionate care, as well as reduced job satisfaction, burnout, absenteeism, and considering the possibility of early retirement. Results from 1000 surveyed professionals indicate that physicians’ subjective competence in providing compassionate care may remain high, but their ability to express it is compromised. From data analysis, the authors hypothesize that when working in environments with discrepant values, occupational contingencies may repeatedly require physicians to set aside their personal values, which can lead them to refrain from using available skills to keep their performance in line with organizational requirements.

These results and hypotheses are not consistent with the notion of compassion fatigue as a reflection of the cost of care resulting from exposure to repeated suffering. Previous evidence shows that expressing compassion in healthcare facilitates greater understanding, suggesting that providing compassion does not impoverish physicians but rather supports them in the effectiveness of interventions and in their satisfaction.

In summary, this study suggests that what prevents compassion is the inability to provide it when hindered by factors related to the situation in which the physician operates. Improving compassion does not simply depend on motivating individual professionals to be more compassionate or on promoting fundamental skills, but probably on the creation of organizational and clinical conditions in which physician compassion can thrive.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.

Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.

Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
 

CV Effects

OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.

Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
 

Snoring and Hypertension

A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m²) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:

An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.

The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.

Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.

Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
 

Implications for Practice

This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.

Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.

Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.

Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.

Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
 

CV Effects

OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.

Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
 

Snoring and Hypertension

A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m²) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:

An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.

The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.

Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.

Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
 

Implications for Practice

This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.

Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.

Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.

Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.

Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
 

CV Effects

OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.

Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
 

Snoring and Hypertension

A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m²) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:

An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.

The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.

Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.

Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
 

Implications for Practice

This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.

Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.

Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Communicating bad news to patients is one of the most stressful and challenging clinical tasks for any physician, regardless of his or her specialty. Delivering bad news to a patient or their close relative is demanding because the information provided during the dialogue can substantially alter the person’s perspective on life. This task is more frequent for physicians caring for oncology patients and can also affect the physician’s emotional state.

The manner in which bad news is communicated plays a significant role in the psychological burden on the patient, and various communication techniques and guidelines have been developed to enable physicians to perform this difficult task effectively.

Revealing bad news in person whenever possible, to address the emotional responses of patients or relatives, is part of the prevailing expert recommendations. However, it has been acknowledged that in certain situations, communicating bad news over the phone is more feasible.

Since the beginning of the COVID-19 pandemic, the disclosure of bad news over the phone has become a necessary substitute for in-person visits and an integral part of clinical practice worldwide. It remains to be clarified what the real psychological impact on patients and their closest relatives is when delivering bad news over the phone compared with delivering it in person.

Right and Wrong Ways

The most popular guideline for communicating bad news is SPIKES, a six-phase protocol with a special application for cancer patients. It is used in various countries (eg, the United States, France, and Germany) as a guide for this sensitive practice and for training in communication skills in this context. The SPIKES acronym refers to the following six recommended steps for delivering bad news:

• Setting: Set up the conversation.
• Perception: Assess the patient’s perception.
• Invitation: Ask the patient what he or she would like to know.
• Knowledge: Provide the patient with knowledge and information, breaking it down into small parts.
• Emotions: Acknowledge and empathetically address the patient’s emotions.
• Strategy and Summary: Summarize and define a medical action plan.

The lesson from SPIKES is that when a person experiences strong emotions, it is difficult to continue discussing anything, and they will struggle to hear anything. Allowing for silence is fundamental. In addition, empathy allows the patient to express his or her feelings and concerns, as well as provide support. The aim is not to argue but to allow the expression of emotions without criticism. However, these recommendations are primarily based on expert opinion and less on empirical evidence, due to the difficulty of studies in assessing patient outcomes in various phases of these protocols.

A recent study analyzed the differences in psychological distress between patients who received bad news over the phone vs those who received it in person. The study was a systematic review and meta-analysis.

The investigators examined 5944 studies, including 11 qualitative analysis studies, nine meta-analyses, and four randomized controlled trials.

In a set of studies ranging from moderate to good quality, no difference in psychological distress was found when bad news was disclosed over the phone compared with in person, regarding anxiety, depression, and posttraumatic stress disorder.

There was no average difference in patient satisfaction levels when bad news was delivered over the phone compared with in person. The risk for dissatisfaction was similar between groups.

Clinical Practice Guidelines

The demand for telemedicine, including the disclosure of bad news, is growing despite the limited knowledge of potential adverse effects. The results of existing studies suggest that the mode of disclosure may play a secondary role, and the manner in which bad news is communicated may be more important.

Therefore, it is paramount to prepare patients or their families for the possibility of receiving bad news well in advance and, during the conversation, to ensure first and foremost that they are in an appropriate environment. The structure and content of the conversation may be relevant, and adhering to dedicated communication strategies can be a wise choice for the physician and the interlocutor.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Communicating bad news to patients is one of the most stressful and challenging clinical tasks for any physician, regardless of his or her specialty. Delivering bad news to a patient or their close relative is demanding because the information provided during the dialogue can substantially alter the person’s perspective on life. This task is more frequent for physicians caring for oncology patients and can also affect the physician’s emotional state.

The manner in which bad news is communicated plays a significant role in the psychological burden on the patient, and various communication techniques and guidelines have been developed to enable physicians to perform this difficult task effectively.

Revealing bad news in person whenever possible, to address the emotional responses of patients or relatives, is part of the prevailing expert recommendations. However, it has been acknowledged that in certain situations, communicating bad news over the phone is more feasible.

Since the beginning of the COVID-19 pandemic, the disclosure of bad news over the phone has become a necessary substitute for in-person visits and an integral part of clinical practice worldwide. It remains to be clarified what the real psychological impact on patients and their closest relatives is when delivering bad news over the phone compared with delivering it in person.

Right and Wrong Ways

The most popular guideline for communicating bad news is SPIKES, a six-phase protocol with a special application for cancer patients. It is used in various countries (eg, the United States, France, and Germany) as a guide for this sensitive practice and for training in communication skills in this context. The SPIKES acronym refers to the following six recommended steps for delivering bad news:

• Setting: Set up the conversation.
• Perception: Assess the patient’s perception.
• Invitation: Ask the patient what he or she would like to know.
• Knowledge: Provide the patient with knowledge and information, breaking it down into small parts.
• Emotions: Acknowledge and empathetically address the patient’s emotions.
• Strategy and Summary: Summarize and define a medical action plan.

The lesson from SPIKES is that when a person experiences strong emotions, it is difficult to continue discussing anything, and they will struggle to hear anything. Allowing for silence is fundamental. In addition, empathy allows the patient to express his or her feelings and concerns, as well as provide support. The aim is not to argue but to allow the expression of emotions without criticism. However, these recommendations are primarily based on expert opinion and less on empirical evidence, due to the difficulty of studies in assessing patient outcomes in various phases of these protocols.

A recent study analyzed the differences in psychological distress between patients who received bad news over the phone vs those who received it in person. The study was a systematic review and meta-analysis.

The investigators examined 5944 studies, including 11 qualitative analysis studies, nine meta-analyses, and four randomized controlled trials.

In a set of studies ranging from moderate to good quality, no difference in psychological distress was found when bad news was disclosed over the phone compared with in person, regarding anxiety, depression, and posttraumatic stress disorder.

There was no average difference in patient satisfaction levels when bad news was delivered over the phone compared with in person. The risk for dissatisfaction was similar between groups.

Clinical Practice Guidelines

The demand for telemedicine, including the disclosure of bad news, is growing despite the limited knowledge of potential adverse effects. The results of existing studies suggest that the mode of disclosure may play a secondary role, and the manner in which bad news is communicated may be more important.

Therefore, it is paramount to prepare patients or their families for the possibility of receiving bad news well in advance and, during the conversation, to ensure first and foremost that they are in an appropriate environment. The structure and content of the conversation may be relevant, and adhering to dedicated communication strategies can be a wise choice for the physician and the interlocutor.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Communicating bad news to patients is one of the most stressful and challenging clinical tasks for any physician, regardless of his or her specialty. Delivering bad news to a patient or their close relative is demanding because the information provided during the dialogue can substantially alter the person’s perspective on life. This task is more frequent for physicians caring for oncology patients and can also affect the physician’s emotional state.

The manner in which bad news is communicated plays a significant role in the psychological burden on the patient, and various communication techniques and guidelines have been developed to enable physicians to perform this difficult task effectively.

Revealing bad news in person whenever possible, to address the emotional responses of patients or relatives, is part of the prevailing expert recommendations. However, it has been acknowledged that in certain situations, communicating bad news over the phone is more feasible.

Since the beginning of the COVID-19 pandemic, the disclosure of bad news over the phone has become a necessary substitute for in-person visits and an integral part of clinical practice worldwide. It remains to be clarified what the real psychological impact on patients and their closest relatives is when delivering bad news over the phone compared with delivering it in person.

Right and Wrong Ways

The most popular guideline for communicating bad news is SPIKES, a six-phase protocol with a special application for cancer patients. It is used in various countries (eg, the United States, France, and Germany) as a guide for this sensitive practice and for training in communication skills in this context. The SPIKES acronym refers to the following six recommended steps for delivering bad news:

• Setting: Set up the conversation.
• Perception: Assess the patient’s perception.
• Invitation: Ask the patient what he or she would like to know.
• Knowledge: Provide the patient with knowledge and information, breaking it down into small parts.
• Emotions: Acknowledge and empathetically address the patient’s emotions.
• Strategy and Summary: Summarize and define a medical action plan.

The lesson from SPIKES is that when a person experiences strong emotions, it is difficult to continue discussing anything, and they will struggle to hear anything. Allowing for silence is fundamental. In addition, empathy allows the patient to express his or her feelings and concerns, as well as provide support. The aim is not to argue but to allow the expression of emotions without criticism. However, these recommendations are primarily based on expert opinion and less on empirical evidence, due to the difficulty of studies in assessing patient outcomes in various phases of these protocols.

A recent study analyzed the differences in psychological distress between patients who received bad news over the phone vs those who received it in person. The study was a systematic review and meta-analysis.

The investigators examined 5944 studies, including 11 qualitative analysis studies, nine meta-analyses, and four randomized controlled trials.

In a set of studies ranging from moderate to good quality, no difference in psychological distress was found when bad news was disclosed over the phone compared with in person, regarding anxiety, depression, and posttraumatic stress disorder.

There was no average difference in patient satisfaction levels when bad news was delivered over the phone compared with in person. The risk for dissatisfaction was similar between groups.

Clinical Practice Guidelines

The demand for telemedicine, including the disclosure of bad news, is growing despite the limited knowledge of potential adverse effects. The results of existing studies suggest that the mode of disclosure may play a secondary role, and the manner in which bad news is communicated may be more important.

Therefore, it is paramount to prepare patients or their families for the possibility of receiving bad news well in advance and, during the conversation, to ensure first and foremost that they are in an appropriate environment. The structure and content of the conversation may be relevant, and adhering to dedicated communication strategies can be a wise choice for the physician and the interlocutor.

This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Violence against women by partners is a serious human rights violation and a significant global public health issue. Overall, an estimated 27% of women aged 15-49 years who have been in a relationship have experienced physical or sexual violence (SV) at the hands of a partner. According to 2019 data from the US Department of Justice, SV in the United States occurs every 73 seconds, with child victims every 9 minutes. Lifetime rates of SV are around 17%-18% for women and 3% for men.

The emergency department remains the most common place where patients who have experienced SV seek comprehensive care, including emergency contraception, prophylaxis against sexually transmitted infections, forensic evidence collection for rape cases, and treatment for injuries.

Physical injuries from SV are not always detectable. Studies report variable percentages, ranging from 30%-80% of patients with traumatic SV injuries. Evidence regarding their severity is conflicting. Genital injuries are more common in assaults by acquaintances and in victims not using hormonal contraceptives.

The presence or absence of anogenital injuries following SV is a factor that can influence both victims’ willingness to report a crime and the judicial decision-making process regarding accusations and convictions. 

Rape Myths

The mythology of rape has been under discussion for more than 50 years, encompassing concerns that rape myths reinforce ideas about what does and does not constitute SV and who is a credible victim.

Rape myths, classically defined in the 1980s, are “prejudiced, stereotyped, and false beliefs about rape, rape victims, and rapists,” designed to “deny or minimize perceived harm or blame victims for their victimization.” The concept remains relevant to contemporary societal beliefs and concerns.

A systematic review analyzed elements of rape myths related to victim characteristics and their impact on credibility and blame attribution in the investigative process. Victims who knew the (male) perpetrator and were deemed provocative based on attire were assigned greater blame. In addition, detail and consistency in victims› statements and the presence of physical evidence and injuries increased credibility. However, in certain situations, rape myths may lead to blaming victims who do not fit the “real victim” stereotype, thus resulting in secondary victimization or revictimization.

Anogenital Injuries 

Anogenital injuries can occur in relation to consensual sexual activity (CSA), and SV may not be associated with injuries. Therefore, the presence of anogenital injuries does not “prove” SV nor does their absence exclude rape.

This statement is supported by a systematic review and meta-analysis investigating the prevalence of anogenital injuries in women following SV and CSA, using consistent examination techniques for better forensic evidence evaluation in criminal proceedings.

The following two groups were defined for comparison: SV, indicating any nonconsensual sexual contact with the survivor’s anogenital area, and CSA, representing the same type of sexual contact with participants’ consent.

The outcome measure was the presence of anogenital injury (defined as any genital, anal, or perineal injury detected using described techniques in each study). With no universal definition of genital trauma, the result assessment was dichotomous: The presence or absence of injury.

The systematic search yielded 1401 results, and 10 cohort studies published from 1997 to 2022 met the inclusion criteria. The study participants were 3165 women, with 59% (1874/3165) surviving SV.

Anogenital injuries were found in 48% of women who experienced SV (901/1874) and in 31% of those with CSA (394/1291). Anogenital injuries were significantly more likely in women who had experienced SV, compared with those with CSA (risk ratio, 1.59; P < .001). However, both groups had cases where anogenital injuries were either detected or not.

Some SV survivors had no identified anogenital injuries, and women examined after CSA had detectable anogenital injuries. Subgroup analysis for high-quality studies showed no significant differences between groups. These data support the hypothesis that the presence of anogenital injuries does not prove SV, and the absence of injuries does not disprove it.

Point for Practice

Numerous myths reinforce cultural attitudes toward reporting SV. One myth suggests that physical violence, and thus injuries, are inevitable accompaniments to rape. If the victim does not react physically, it might be argued that it was not really rape, or without physical trauma, one might be less inclined to believe that a rape occurred.

Physicians and healthcare professionals involved in the care and support of SV survivors must explicitly reassure them that the lack of anogenital injury evidence does not diminish the credibility of their account.
 

This article was translated from Univadis Italy, which is part of the Medscape Professional Network. A version of this article appeared on Medscape.com.

Violence against women by partners is a serious human rights violation and a significant global public health issue. Overall, an estimated 27% of women aged 15-49 years who have been in a relationship have experienced physical or sexual violence (SV) at the hands of a partner. According to 2019 data from the US Department of Justice, SV in the United States occurs every 73 seconds, with child victims every 9 minutes. Lifetime rates of SV are around 17%-18% for women and 3% for men.

The emergency department remains the most common place where patients who have experienced SV seek comprehensive care, including emergency contraception, prophylaxis against sexually transmitted infections, forensic evidence collection for rape cases, and treatment for injuries.

Physical injuries from SV are not always detectable. Studies report variable percentages, ranging from 30%-80% of patients with traumatic SV injuries. Evidence regarding their severity is conflicting. Genital injuries are more common in assaults by acquaintances and in victims not using hormonal contraceptives.

The presence or absence of anogenital injuries following SV is a factor that can influence both victims’ willingness to report a crime and the judicial decision-making process regarding accusations and convictions. 

Rape Myths

The mythology of rape has been under discussion for more than 50 years, encompassing concerns that rape myths reinforce ideas about what does and does not constitute SV and who is a credible victim.

Rape myths, classically defined in the 1980s, are “prejudiced, stereotyped, and false beliefs about rape, rape victims, and rapists,” designed to “deny or minimize perceived harm or blame victims for their victimization.” The concept remains relevant to contemporary societal beliefs and concerns.

A systematic review analyzed elements of rape myths related to victim characteristics and their impact on credibility and blame attribution in the investigative process. Victims who knew the (male) perpetrator and were deemed provocative based on attire were assigned greater blame. In addition, detail and consistency in victims› statements and the presence of physical evidence and injuries increased credibility. However, in certain situations, rape myths may lead to blaming victims who do not fit the “real victim” stereotype, thus resulting in secondary victimization or revictimization.

Anogenital Injuries 

Anogenital injuries can occur in relation to consensual sexual activity (CSA), and SV may not be associated with injuries. Therefore, the presence of anogenital injuries does not “prove” SV nor does their absence exclude rape.

This statement is supported by a systematic review and meta-analysis investigating the prevalence of anogenital injuries in women following SV and CSA, using consistent examination techniques for better forensic evidence evaluation in criminal proceedings.

The following two groups were defined for comparison: SV, indicating any nonconsensual sexual contact with the survivor’s anogenital area, and CSA, representing the same type of sexual contact with participants’ consent.

The outcome measure was the presence of anogenital injury (defined as any genital, anal, or perineal injury detected using described techniques in each study). With no universal definition of genital trauma, the result assessment was dichotomous: The presence or absence of injury.

The systematic search yielded 1401 results, and 10 cohort studies published from 1997 to 2022 met the inclusion criteria. The study participants were 3165 women, with 59% (1874/3165) surviving SV.

Anogenital injuries were found in 48% of women who experienced SV (901/1874) and in 31% of those with CSA (394/1291). Anogenital injuries were significantly more likely in women who had experienced SV, compared with those with CSA (risk ratio, 1.59; P < .001). However, both groups had cases where anogenital injuries were either detected or not.

Some SV survivors had no identified anogenital injuries, and women examined after CSA had detectable anogenital injuries. Subgroup analysis for high-quality studies showed no significant differences between groups. These data support the hypothesis that the presence of anogenital injuries does not prove SV, and the absence of injuries does not disprove it.

Point for Practice

Numerous myths reinforce cultural attitudes toward reporting SV. One myth suggests that physical violence, and thus injuries, are inevitable accompaniments to rape. If the victim does not react physically, it might be argued that it was not really rape, or without physical trauma, one might be less inclined to believe that a rape occurred.

Physicians and healthcare professionals involved in the care and support of SV survivors must explicitly reassure them that the lack of anogenital injury evidence does not diminish the credibility of their account.
 

This article was translated from Univadis Italy, which is part of the Medscape Professional Network. A version of this article appeared on Medscape.com.

Violence against women by partners is a serious human rights violation and a significant global public health issue. Overall, an estimated 27% of women aged 15-49 years who have been in a relationship have experienced physical or sexual violence (SV) at the hands of a partner. According to 2019 data from the US Department of Justice, SV in the United States occurs every 73 seconds, with child victims every 9 minutes. Lifetime rates of SV are around 17%-18% for women and 3% for men.

The emergency department remains the most common place where patients who have experienced SV seek comprehensive care, including emergency contraception, prophylaxis against sexually transmitted infections, forensic evidence collection for rape cases, and treatment for injuries.

Physical injuries from SV are not always detectable. Studies report variable percentages, ranging from 30%-80% of patients with traumatic SV injuries. Evidence regarding their severity is conflicting. Genital injuries are more common in assaults by acquaintances and in victims not using hormonal contraceptives.

The presence or absence of anogenital injuries following SV is a factor that can influence both victims’ willingness to report a crime and the judicial decision-making process regarding accusations and convictions. 

Rape Myths

The mythology of rape has been under discussion for more than 50 years, encompassing concerns that rape myths reinforce ideas about what does and does not constitute SV and who is a credible victim.

Rape myths, classically defined in the 1980s, are “prejudiced, stereotyped, and false beliefs about rape, rape victims, and rapists,” designed to “deny or minimize perceived harm or blame victims for their victimization.” The concept remains relevant to contemporary societal beliefs and concerns.

A systematic review analyzed elements of rape myths related to victim characteristics and their impact on credibility and blame attribution in the investigative process. Victims who knew the (male) perpetrator and were deemed provocative based on attire were assigned greater blame. In addition, detail and consistency in victims› statements and the presence of physical evidence and injuries increased credibility. However, in certain situations, rape myths may lead to blaming victims who do not fit the “real victim” stereotype, thus resulting in secondary victimization or revictimization.

Anogenital Injuries 

Anogenital injuries can occur in relation to consensual sexual activity (CSA), and SV may not be associated with injuries. Therefore, the presence of anogenital injuries does not “prove” SV nor does their absence exclude rape.

This statement is supported by a systematic review and meta-analysis investigating the prevalence of anogenital injuries in women following SV and CSA, using consistent examination techniques for better forensic evidence evaluation in criminal proceedings.

The following two groups were defined for comparison: SV, indicating any nonconsensual sexual contact with the survivor’s anogenital area, and CSA, representing the same type of sexual contact with participants’ consent.

The outcome measure was the presence of anogenital injury (defined as any genital, anal, or perineal injury detected using described techniques in each study). With no universal definition of genital trauma, the result assessment was dichotomous: The presence or absence of injury.

The systematic search yielded 1401 results, and 10 cohort studies published from 1997 to 2022 met the inclusion criteria. The study participants were 3165 women, with 59% (1874/3165) surviving SV.

Anogenital injuries were found in 48% of women who experienced SV (901/1874) and in 31% of those with CSA (394/1291). Anogenital injuries were significantly more likely in women who had experienced SV, compared with those with CSA (risk ratio, 1.59; P < .001). However, both groups had cases where anogenital injuries were either detected or not.

Some SV survivors had no identified anogenital injuries, and women examined after CSA had detectable anogenital injuries. Subgroup analysis for high-quality studies showed no significant differences between groups. These data support the hypothesis that the presence of anogenital injuries does not prove SV, and the absence of injuries does not disprove it.

Point for Practice

Numerous myths reinforce cultural attitudes toward reporting SV. One myth suggests that physical violence, and thus injuries, are inevitable accompaniments to rape. If the victim does not react physically, it might be argued that it was not really rape, or without physical trauma, one might be less inclined to believe that a rape occurred.

Physicians and healthcare professionals involved in the care and support of SV survivors must explicitly reassure them that the lack of anogenital injury evidence does not diminish the credibility of their account.
 

This article was translated from Univadis Italy, which is part of the Medscape Professional Network. A version of this article appeared on Medscape.com.

Poor adherence to medication is a real challenge in health care. Despite evidence indicating therapeutic benefit from adhering to a prescribed regimen, it is estimated that around 50% of patients around the world don’t take their medication as it is prescribed – and some simply don’t take them at all.

Nonadherence to medication can be primary or secondary. Primary medication nonadherence occurs when a new medication is prescribed for a patient, but the patient does not obtain the medication or an appropriate alternative within an acceptable period after it was prescribed. Secondary nonadherence measures prescription refills among patients who previously filled their first prescriptions. With most medication adherence research to date focused on secondary nonadherence, PMN has been identified as a major research gap.

Growth in electronic prescribing has partially resolved this issue, and new measures have emerged linking electronic prescribing databases with pharmacy dispensing databases. A study conducted in a network of primary care services in Canada has sought to identify the predictive factors of primary nonadherence and which drugs could be at greatest risk of primary nonadherence when prescribed by a primary care physician
 

Adherence measures

Measuring medication adherence is challenging but can be done using various approaches. It comprises the following approaches:

• Subjective measurements obtained by asking patients, family members, caregivers, and physicians about the patient’s medication use
• Objective measurements obtained by counting pills, examining pharmacy refill records, or using electronic medication event monitoring systems
• Biochemical measurements obtained by adding a nontoxic marker to the medication and detecting its presence in blood or urine or measurement of serum drug levels.

Determining factors

A myriad of factors contributes to poor medication adherence. Some are related to patients (e.g., suboptimal health literacy and lack of involvement in the treatment decision-making process), others are related to physicians (e.g., prescription of complex drug regimens, communication barriers, ineffective communication of information about adverse effects, and provision of care by multiple physicians), and still others are related to health care systems (e.g., office visit time limitations, limited access to care, and lack of health information technology).

Primary nonadherence

The literature has reported substantial variation in primary nonadherence, with estimates ranging from as little as 1.9% of incident prescriptions never filled to as much as 75%.

Investigators for the Canadian study estimated the rate of primary nonadherence, defined as failure to dispense a new medication or its equivalent within 6 months of the prescription date, using data from 150,565 new prescriptions issued to 34,243 patients.
 

Rate of nonadherence

The following patterns of primary nonadherence were observed:

• Primary nonadherence was lowest for prescriptions issued by prescribers aged 35 years or younger (17.1%) and male prescribers (15.1%).
• It was similar among patients of both sexes.
• It was lowest in the oldest subjects, decreasing with age (odds ratio, 0.91 for each additional 10 years).
• It was highest for drugs prescribed mostly on an as-needed basis, including topical corticosteroids (35.1%) and antihistamines (23.4%).

Predictors of nonadherence

The odds of primary nonadherence exhibited the following patterns:

• Lower for prescriptions issued by male clinicians (OR, 0.66)
• Significantly greater, compared with anti-infectives, for dermatological agents (OR, 1.36) and lowest for cardiovascular agents (OR, 0.46).
• Lower across therapeutic drug categories (except for respiratory agents) for those aged 65 years and older than for those younger than age 65.

In conclusion, in a general medicine setting, the odds of primary nonadherence were higher for younger patients, those who received primary care services from female prescribers, and older patients who were prescribed more medications. Across therapeutic categories, the odds of primary nonadherence were lowest for cardiovascular system agents and highest for dermatological agents.

To date, the lack of a standardized terminology, operational definition, and measurement methods of primary nonadherence has limited our understanding of the extent to which patients do not avail themselves of prescriber-ordered pharmaceutical treatment. These results reaffirm the need to compare the prevalence of such nonadherence in different health care settings.

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Poor adherence to medication is a real challenge in health care. Despite evidence indicating therapeutic benefit from adhering to a prescribed regimen, it is estimated that around 50% of patients around the world don’t take their medication as it is prescribed – and some simply don’t take them at all.

Nonadherence to medication can be primary or secondary. Primary medication nonadherence occurs when a new medication is prescribed for a patient, but the patient does not obtain the medication or an appropriate alternative within an acceptable period after it was prescribed. Secondary nonadherence measures prescription refills among patients who previously filled their first prescriptions. With most medication adherence research to date focused on secondary nonadherence, PMN has been identified as a major research gap.

Growth in electronic prescribing has partially resolved this issue, and new measures have emerged linking electronic prescribing databases with pharmacy dispensing databases. A study conducted in a network of primary care services in Canada has sought to identify the predictive factors of primary nonadherence and which drugs could be at greatest risk of primary nonadherence when prescribed by a primary care physician
 

Adherence measures

Measuring medication adherence is challenging but can be done using various approaches. It comprises the following approaches:

• Subjective measurements obtained by asking patients, family members, caregivers, and physicians about the patient’s medication use
• Objective measurements obtained by counting pills, examining pharmacy refill records, or using electronic medication event monitoring systems
• Biochemical measurements obtained by adding a nontoxic marker to the medication and detecting its presence in blood or urine or measurement of serum drug levels.

Determining factors

A myriad of factors contributes to poor medication adherence. Some are related to patients (e.g., suboptimal health literacy and lack of involvement in the treatment decision-making process), others are related to physicians (e.g., prescription of complex drug regimens, communication barriers, ineffective communication of information about adverse effects, and provision of care by multiple physicians), and still others are related to health care systems (e.g., office visit time limitations, limited access to care, and lack of health information technology).

Primary nonadherence

The literature has reported substantial variation in primary nonadherence, with estimates ranging from as little as 1.9% of incident prescriptions never filled to as much as 75%.

Investigators for the Canadian study estimated the rate of primary nonadherence, defined as failure to dispense a new medication or its equivalent within 6 months of the prescription date, using data from 150,565 new prescriptions issued to 34,243 patients.
 

Rate of nonadherence

The following patterns of primary nonadherence were observed:

• Primary nonadherence was lowest for prescriptions issued by prescribers aged 35 years or younger (17.1%) and male prescribers (15.1%).
• It was similar among patients of both sexes.
• It was lowest in the oldest subjects, decreasing with age (odds ratio, 0.91 for each additional 10 years).
• It was highest for drugs prescribed mostly on an as-needed basis, including topical corticosteroids (35.1%) and antihistamines (23.4%).

Predictors of nonadherence

The odds of primary nonadherence exhibited the following patterns:

• Lower for prescriptions issued by male clinicians (OR, 0.66)
• Significantly greater, compared with anti-infectives, for dermatological agents (OR, 1.36) and lowest for cardiovascular agents (OR, 0.46).
• Lower across therapeutic drug categories (except for respiratory agents) for those aged 65 years and older than for those younger than age 65.

In conclusion, in a general medicine setting, the odds of primary nonadherence were higher for younger patients, those who received primary care services from female prescribers, and older patients who were prescribed more medications. Across therapeutic categories, the odds of primary nonadherence were lowest for cardiovascular system agents and highest for dermatological agents.

To date, the lack of a standardized terminology, operational definition, and measurement methods of primary nonadherence has limited our understanding of the extent to which patients do not avail themselves of prescriber-ordered pharmaceutical treatment. These results reaffirm the need to compare the prevalence of such nonadherence in different health care settings.

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Poor adherence to medication is a real challenge in health care. Despite evidence indicating therapeutic benefit from adhering to a prescribed regimen, it is estimated that around 50% of patients around the world don’t take their medication as it is prescribed – and some simply don’t take them at all.

Nonadherence to medication can be primary or secondary. Primary medication nonadherence occurs when a new medication is prescribed for a patient, but the patient does not obtain the medication or an appropriate alternative within an acceptable period after it was prescribed. Secondary nonadherence measures prescription refills among patients who previously filled their first prescriptions. With most medication adherence research to date focused on secondary nonadherence, PMN has been identified as a major research gap.

Growth in electronic prescribing has partially resolved this issue, and new measures have emerged linking electronic prescribing databases with pharmacy dispensing databases. A study conducted in a network of primary care services in Canada has sought to identify the predictive factors of primary nonadherence and which drugs could be at greatest risk of primary nonadherence when prescribed by a primary care physician
 

Adherence measures

Measuring medication adherence is challenging but can be done using various approaches. It comprises the following approaches:

• Subjective measurements obtained by asking patients, family members, caregivers, and physicians about the patient’s medication use
• Objective measurements obtained by counting pills, examining pharmacy refill records, or using electronic medication event monitoring systems
• Biochemical measurements obtained by adding a nontoxic marker to the medication and detecting its presence in blood or urine or measurement of serum drug levels.

Determining factors

A myriad of factors contributes to poor medication adherence. Some are related to patients (e.g., suboptimal health literacy and lack of involvement in the treatment decision-making process), others are related to physicians (e.g., prescription of complex drug regimens, communication barriers, ineffective communication of information about adverse effects, and provision of care by multiple physicians), and still others are related to health care systems (e.g., office visit time limitations, limited access to care, and lack of health information technology).

Primary nonadherence

The literature has reported substantial variation in primary nonadherence, with estimates ranging from as little as 1.9% of incident prescriptions never filled to as much as 75%.

Investigators for the Canadian study estimated the rate of primary nonadherence, defined as failure to dispense a new medication or its equivalent within 6 months of the prescription date, using data from 150,565 new prescriptions issued to 34,243 patients.
 

Rate of nonadherence

The following patterns of primary nonadherence were observed:

• Primary nonadherence was lowest for prescriptions issued by prescribers aged 35 years or younger (17.1%) and male prescribers (15.1%).
• It was similar among patients of both sexes.
• It was lowest in the oldest subjects, decreasing with age (odds ratio, 0.91 for each additional 10 years).
• It was highest for drugs prescribed mostly on an as-needed basis, including topical corticosteroids (35.1%) and antihistamines (23.4%).

Predictors of nonadherence

The odds of primary nonadherence exhibited the following patterns:

• Lower for prescriptions issued by male clinicians (OR, 0.66)
• Significantly greater, compared with anti-infectives, for dermatological agents (OR, 1.36) and lowest for cardiovascular agents (OR, 0.46).
• Lower across therapeutic drug categories (except for respiratory agents) for those aged 65 years and older than for those younger than age 65.

In conclusion, in a general medicine setting, the odds of primary nonadherence were higher for younger patients, those who received primary care services from female prescribers, and older patients who were prescribed more medications. Across therapeutic categories, the odds of primary nonadherence were lowest for cardiovascular system agents and highest for dermatological agents.

To date, the lack of a standardized terminology, operational definition, and measurement methods of primary nonadherence has limited our understanding of the extent to which patients do not avail themselves of prescriber-ordered pharmaceutical treatment. These results reaffirm the need to compare the prevalence of such nonadherence in different health care settings.

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Treatment options for patients with cancer that is detected at a late stage are severely limited, which usually leads to an unfavorable prognosis for such patients. Indeed, the options available for patients with metastatic solid cancers are scarcely curative. Therefore, early diagnosis of neoplasia remains a fundamental mainstay for improving outcomes for cancer patients.

Histopathology is the current gold standard for cancer diagnosis. Biopsy is an invasive procedure that provides physicians with further samples to test but that furnishes limited information concerning tumor heterogeneity. Biopsy specimens are usually obtained only when there is clinical evidence of neoplasia, which significantly limits their usefulness in early diagnosis.

Around 20 years ago, it was discovered that the presence of circulating tumor cells (CTC) in patients with metastatic breast cancer who were about to begin a new line of treatment was predictive of overall and progression-free survival. The prognostic value of CTC was independent of the line of treatment (first or second) and was greater than that of the site of metastasis, the type of therapy, and the time to metastasis after complete primary resection. These results support the idea that the presence of CTC could be used to modify the system for staging advanced disease.

Since then, research into liquid biopsy assays has expanded rapidly, and many biomarkers have been studied in various body fluids for their usefulness in assessing solid tumors.
 

Liquid vs. tissue

Liquid biopsy is a minimally invasive tool that is easy to use. It is employed to detect cancer, to assess treatment response, or to monitor disease progression. Liquid biopsy produces test material from primary and metastatic (or micrometastatic) sites and provides a more heterogeneous picture of the entire tumor cell population, compared with specimens obtained with tissue biopsy.

Metastasis

The notion that metastatic lesions are formed from cancer cells that have disseminated from advanced primary tumors has been substantially revised following the identification of disseminated tumor cells (DTC) in the bone marrow of patients with early-stage disease. These results have led researchers to no longer view cancer metastasis as a linear cascade of events but rather as a series of concurrent, partially overlapping processes, as metastasizing cells assume new phenotypes while abandoning older behaviors.

The initiation of metastasis is not simply a cell-autonomous event but is heavily influenced by complex tissue microenvironments. Although colonization of distant tissues by DTC is an extremely inefficient process, at times, relatively numerous CTC can be detected in the blood of cancer patients (> 1,000 CTC/mL of blood plasma), whereas the number of clinically detectable metastases is disproportionately low, confirming that tumor cell diffusion can happen at an early stage but usually occurs later on.
 

Early dissemination

Little is currently known about the preference of cancer subtypes for distinct tissues or about the receptiveness of a tissue as a metastatic site. What endures as one of the most confounding clinical phenomena is that patients may undergo tumor resection and remain apparently disease free for months, years, and even decades, only to experience relapse and be diagnosed with late-stage metastatic disease. This course may be a result of cell seeding from minimal residual disease after resection of the primary tumor or of preexisting clinically undetectable micrometastases. It may also arise from early disseminated cells that remain dormant and resistant to therapy until they suddenly reawaken to initiate proliferation into clinically detectable macrometastases.

Dormant DTC could be the main reason for delayed detection of metastases. It is thought that around 40% of patients with prostate cancer who undergo radical prostatectomy present with biochemical recurrence, suggesting that it is likely that hidden DTC or micrometastases are present at the time of the procedure. The finding is consistent with the detection of DTC many years after tumor resection, suggesting they were released before surgical treatment. Nevertheless, research into tumor cell dormancy is limited, owing to the invasive and technically challenging nature of obtaining DTC samples, which are predominantly taken from the bone marrow.
 

CTC metastases

Cancer cells can undergo epithelial-to-mesenchymal transition to facilitate their detachment from the primary tumor and intravasation into the blood circulation (step 1). Dissemination of cancer cells from the primary tumor into circulation can involve either single cells or cell clusters containing multiple CTC as well as immune cells and platelets, known as microemboli. CTC that can survive in circulation (step 2) can exit the bloodstream (step 3) and establish metastatic tumors (step 4), or they can enter dormancy and reside in distant organs, such as the bone marrow.

Use in practice

CTC were discovered over a century ago, but only in recent years has technology been sufficiently advanced to study CTC and to assess their usefulness as biomarkers. Recent evidence suggests that not only do the number of CTC increase during sleep and rest phases but also that these CTC are better able to metastasize, compared to those generated during periods of wakefulness or activity.

CTC clusters (microemboli) are defined as groups of two or more CTC. They can consist of CTC alone (homotypic) or can include various stromal cells, such as cancer-associated fibroblasts or platelets and immune cells (heterotypic). CTC clusters (with or without leukocytes) seem to have greater metastatic capacity, compared with individual CTC.

A multitude of characteristics can be measured in CTC, including genetics and epigenetics, as well as protein levels, which might help in understanding many processes involved in the formation of metastases.

Quantitative assessment of CTC could indicate tumor burden in patients with aggressive cancers, as has been seen in patients with primary lung cancer.
 

Early cancer diagnosis

Early research into CTC didn’t explore their usefulness in diagnosing early-stage tumors because it was thought that CTC were characteristic of advanced-stage disease. This hypothesis was later rejected following evidence of local intravascular invasion of very early cancer cells, even over a period of several hours. This feature may allow CTC to be detected before the clinical diagnosis of cancer.

CTC have been detected in various neoplastic conditions: in breast cancer, seen in 20% of patients with stage I disease, in 26.8% with stage II disease, and 26.7% with stage III disease; in nonmetastatic colorectal cancer, including stage I and II disease; and in prostate cancer, seen in over 50% of patients with localized disease.

The presence of CTC has been proven to be an unfavorable prognostic predictor of overall survival among patients with early-stage non–small cell lung cancer. It distinguishes patients with pancreatic ductal adenocarcinoma from those with noncancerous pancreatic diseases with a sensitivity of 75% and a specificity of 96.3%.

CTC positivity scoring (appropriately defined), combined with serum prostate-specific antigen level, was predictive of a biopsy diagnosis of clinically significant prostate cancer.

All these data support the utility of CTC in early cancer diagnosis. Their link with metastases, and thus with aggressive tumors, gives them an advantage over other (noninvasive or minimally invasive) biomarkers in the early identification of invasive tumors for therapeutic intervention with better cure rates.
 

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Treatment options for patients with cancer that is detected at a late stage are severely limited, which usually leads to an unfavorable prognosis for such patients. Indeed, the options available for patients with metastatic solid cancers are scarcely curative. Therefore, early diagnosis of neoplasia remains a fundamental mainstay for improving outcomes for cancer patients.

Histopathology is the current gold standard for cancer diagnosis. Biopsy is an invasive procedure that provides physicians with further samples to test but that furnishes limited information concerning tumor heterogeneity. Biopsy specimens are usually obtained only when there is clinical evidence of neoplasia, which significantly limits their usefulness in early diagnosis.

Around 20 years ago, it was discovered that the presence of circulating tumor cells (CTC) in patients with metastatic breast cancer who were about to begin a new line of treatment was predictive of overall and progression-free survival. The prognostic value of CTC was independent of the line of treatment (first or second) and was greater than that of the site of metastasis, the type of therapy, and the time to metastasis after complete primary resection. These results support the idea that the presence of CTC could be used to modify the system for staging advanced disease.

Since then, research into liquid biopsy assays has expanded rapidly, and many biomarkers have been studied in various body fluids for their usefulness in assessing solid tumors.
 

Liquid vs. tissue

Liquid biopsy is a minimally invasive tool that is easy to use. It is employed to detect cancer, to assess treatment response, or to monitor disease progression. Liquid biopsy produces test material from primary and metastatic (or micrometastatic) sites and provides a more heterogeneous picture of the entire tumor cell population, compared with specimens obtained with tissue biopsy.

Metastasis

The notion that metastatic lesions are formed from cancer cells that have disseminated from advanced primary tumors has been substantially revised following the identification of disseminated tumor cells (DTC) in the bone marrow of patients with early-stage disease. These results have led researchers to no longer view cancer metastasis as a linear cascade of events but rather as a series of concurrent, partially overlapping processes, as metastasizing cells assume new phenotypes while abandoning older behaviors.

The initiation of metastasis is not simply a cell-autonomous event but is heavily influenced by complex tissue microenvironments. Although colonization of distant tissues by DTC is an extremely inefficient process, at times, relatively numerous CTC can be detected in the blood of cancer patients (> 1,000 CTC/mL of blood plasma), whereas the number of clinically detectable metastases is disproportionately low, confirming that tumor cell diffusion can happen at an early stage but usually occurs later on.
 

Early dissemination

Little is currently known about the preference of cancer subtypes for distinct tissues or about the receptiveness of a tissue as a metastatic site. What endures as one of the most confounding clinical phenomena is that patients may undergo tumor resection and remain apparently disease free for months, years, and even decades, only to experience relapse and be diagnosed with late-stage metastatic disease. This course may be a result of cell seeding from minimal residual disease after resection of the primary tumor or of preexisting clinically undetectable micrometastases. It may also arise from early disseminated cells that remain dormant and resistant to therapy until they suddenly reawaken to initiate proliferation into clinically detectable macrometastases.

Dormant DTC could be the main reason for delayed detection of metastases. It is thought that around 40% of patients with prostate cancer who undergo radical prostatectomy present with biochemical recurrence, suggesting that it is likely that hidden DTC or micrometastases are present at the time of the procedure. The finding is consistent with the detection of DTC many years after tumor resection, suggesting they were released before surgical treatment. Nevertheless, research into tumor cell dormancy is limited, owing to the invasive and technically challenging nature of obtaining DTC samples, which are predominantly taken from the bone marrow.
 

CTC metastases

Cancer cells can undergo epithelial-to-mesenchymal transition to facilitate their detachment from the primary tumor and intravasation into the blood circulation (step 1). Dissemination of cancer cells from the primary tumor into circulation can involve either single cells or cell clusters containing multiple CTC as well as immune cells and platelets, known as microemboli. CTC that can survive in circulation (step 2) can exit the bloodstream (step 3) and establish metastatic tumors (step 4), or they can enter dormancy and reside in distant organs, such as the bone marrow.

Use in practice

CTC were discovered over a century ago, but only in recent years has technology been sufficiently advanced to study CTC and to assess their usefulness as biomarkers. Recent evidence suggests that not only do the number of CTC increase during sleep and rest phases but also that these CTC are better able to metastasize, compared to those generated during periods of wakefulness or activity.

CTC clusters (microemboli) are defined as groups of two or more CTC. They can consist of CTC alone (homotypic) or can include various stromal cells, such as cancer-associated fibroblasts or platelets and immune cells (heterotypic). CTC clusters (with or without leukocytes) seem to have greater metastatic capacity, compared with individual CTC.

A multitude of characteristics can be measured in CTC, including genetics and epigenetics, as well as protein levels, which might help in understanding many processes involved in the formation of metastases.

Quantitative assessment of CTC could indicate tumor burden in patients with aggressive cancers, as has been seen in patients with primary lung cancer.
 

Early cancer diagnosis

Early research into CTC didn’t explore their usefulness in diagnosing early-stage tumors because it was thought that CTC were characteristic of advanced-stage disease. This hypothesis was later rejected following evidence of local intravascular invasion of very early cancer cells, even over a period of several hours. This feature may allow CTC to be detected before the clinical diagnosis of cancer.

CTC have been detected in various neoplastic conditions: in breast cancer, seen in 20% of patients with stage I disease, in 26.8% with stage II disease, and 26.7% with stage III disease; in nonmetastatic colorectal cancer, including stage I and II disease; and in prostate cancer, seen in over 50% of patients with localized disease.

The presence of CTC has been proven to be an unfavorable prognostic predictor of overall survival among patients with early-stage non–small cell lung cancer. It distinguishes patients with pancreatic ductal adenocarcinoma from those with noncancerous pancreatic diseases with a sensitivity of 75% and a specificity of 96.3%.

CTC positivity scoring (appropriately defined), combined with serum prostate-specific antigen level, was predictive of a biopsy diagnosis of clinically significant prostate cancer.

All these data support the utility of CTC in early cancer diagnosis. Their link with metastases, and thus with aggressive tumors, gives them an advantage over other (noninvasive or minimally invasive) biomarkers in the early identification of invasive tumors for therapeutic intervention with better cure rates.
 

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Treatment options for patients with cancer that is detected at a late stage are severely limited, which usually leads to an unfavorable prognosis for such patients. Indeed, the options available for patients with metastatic solid cancers are scarcely curative. Therefore, early diagnosis of neoplasia remains a fundamental mainstay for improving outcomes for cancer patients.

Histopathology is the current gold standard for cancer diagnosis. Biopsy is an invasive procedure that provides physicians with further samples to test but that furnishes limited information concerning tumor heterogeneity. Biopsy specimens are usually obtained only when there is clinical evidence of neoplasia, which significantly limits their usefulness in early diagnosis.

Around 20 years ago, it was discovered that the presence of circulating tumor cells (CTC) in patients with metastatic breast cancer who were about to begin a new line of treatment was predictive of overall and progression-free survival. The prognostic value of CTC was independent of the line of treatment (first or second) and was greater than that of the site of metastasis, the type of therapy, and the time to metastasis after complete primary resection. These results support the idea that the presence of CTC could be used to modify the system for staging advanced disease.

Since then, research into liquid biopsy assays has expanded rapidly, and many biomarkers have been studied in various body fluids for their usefulness in assessing solid tumors.
 

Liquid vs. tissue

Liquid biopsy is a minimally invasive tool that is easy to use. It is employed to detect cancer, to assess treatment response, or to monitor disease progression. Liquid biopsy produces test material from primary and metastatic (or micrometastatic) sites and provides a more heterogeneous picture of the entire tumor cell population, compared with specimens obtained with tissue biopsy.

Metastasis

The notion that metastatic lesions are formed from cancer cells that have disseminated from advanced primary tumors has been substantially revised following the identification of disseminated tumor cells (DTC) in the bone marrow of patients with early-stage disease. These results have led researchers to no longer view cancer metastasis as a linear cascade of events but rather as a series of concurrent, partially overlapping processes, as metastasizing cells assume new phenotypes while abandoning older behaviors.

The initiation of metastasis is not simply a cell-autonomous event but is heavily influenced by complex tissue microenvironments. Although colonization of distant tissues by DTC is an extremely inefficient process, at times, relatively numerous CTC can be detected in the blood of cancer patients (> 1,000 CTC/mL of blood plasma), whereas the number of clinically detectable metastases is disproportionately low, confirming that tumor cell diffusion can happen at an early stage but usually occurs later on.
 

Early dissemination

Little is currently known about the preference of cancer subtypes for distinct tissues or about the receptiveness of a tissue as a metastatic site. What endures as one of the most confounding clinical phenomena is that patients may undergo tumor resection and remain apparently disease free for months, years, and even decades, only to experience relapse and be diagnosed with late-stage metastatic disease. This course may be a result of cell seeding from minimal residual disease after resection of the primary tumor or of preexisting clinically undetectable micrometastases. It may also arise from early disseminated cells that remain dormant and resistant to therapy until they suddenly reawaken to initiate proliferation into clinically detectable macrometastases.

Dormant DTC could be the main reason for delayed detection of metastases. It is thought that around 40% of patients with prostate cancer who undergo radical prostatectomy present with biochemical recurrence, suggesting that it is likely that hidden DTC or micrometastases are present at the time of the procedure. The finding is consistent with the detection of DTC many years after tumor resection, suggesting they were released before surgical treatment. Nevertheless, research into tumor cell dormancy is limited, owing to the invasive and technically challenging nature of obtaining DTC samples, which are predominantly taken from the bone marrow.
 

CTC metastases

Cancer cells can undergo epithelial-to-mesenchymal transition to facilitate their detachment from the primary tumor and intravasation into the blood circulation (step 1). Dissemination of cancer cells from the primary tumor into circulation can involve either single cells or cell clusters containing multiple CTC as well as immune cells and platelets, known as microemboli. CTC that can survive in circulation (step 2) can exit the bloodstream (step 3) and establish metastatic tumors (step 4), or they can enter dormancy and reside in distant organs, such as the bone marrow.

Use in practice

CTC were discovered over a century ago, but only in recent years has technology been sufficiently advanced to study CTC and to assess their usefulness as biomarkers. Recent evidence suggests that not only do the number of CTC increase during sleep and rest phases but also that these CTC are better able to metastasize, compared to those generated during periods of wakefulness or activity.

CTC clusters (microemboli) are defined as groups of two or more CTC. They can consist of CTC alone (homotypic) or can include various stromal cells, such as cancer-associated fibroblasts or platelets and immune cells (heterotypic). CTC clusters (with or without leukocytes) seem to have greater metastatic capacity, compared with individual CTC.

A multitude of characteristics can be measured in CTC, including genetics and epigenetics, as well as protein levels, which might help in understanding many processes involved in the formation of metastases.

Quantitative assessment of CTC could indicate tumor burden in patients with aggressive cancers, as has been seen in patients with primary lung cancer.
 

Early cancer diagnosis

Early research into CTC didn’t explore their usefulness in diagnosing early-stage tumors because it was thought that CTC were characteristic of advanced-stage disease. This hypothesis was later rejected following evidence of local intravascular invasion of very early cancer cells, even over a period of several hours. This feature may allow CTC to be detected before the clinical diagnosis of cancer.

CTC have been detected in various neoplastic conditions: in breast cancer, seen in 20% of patients with stage I disease, in 26.8% with stage II disease, and 26.7% with stage III disease; in nonmetastatic colorectal cancer, including stage I and II disease; and in prostate cancer, seen in over 50% of patients with localized disease.

The presence of CTC has been proven to be an unfavorable prognostic predictor of overall survival among patients with early-stage non–small cell lung cancer. It distinguishes patients with pancreatic ductal adenocarcinoma from those with noncancerous pancreatic diseases with a sensitivity of 75% and a specificity of 96.3%.

CTC positivity scoring (appropriately defined), combined with serum prostate-specific antigen level, was predictive of a biopsy diagnosis of clinically significant prostate cancer.

All these data support the utility of CTC in early cancer diagnosis. Their link with metastases, and thus with aggressive tumors, gives them an advantage over other (noninvasive or minimally invasive) biomarkers in the early identification of invasive tumors for therapeutic intervention with better cure rates.
 

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Feelings of inadequacy, in terms of skills and expectations in an ever-changing system, are common emotions that many doctors have experienced since the start of the pandemic.

COVID-19 imposed challenges on health care professionals and systems by forcing changes in how doctors organize themselves professionally as well as in their relationships with patients and in their expectations (realistic or not) of their roles. The situation was bound to generate high rates of frustration and discomfort among younger and older physicians. It was compounded by a generational transition of the profession, which was accelerated by the virus. It was not managed by the decision-makers and was painful for doctors and patients.

Impostor syndrome (IS) is a psychological construct characterized by the persistent belief that one’s success is undeserved, rather than stemming from personal effort, skill, and ability. The phenomenon is common among medics for various reasons, including professional burnout. Recent studies have helped to better define the extent and characteristic features of the syndrome, as well as efforts to combat it.
 

Doctors and burnout

Although occupational burnout among physicians is a systemic issue primarily attributable to problems in the practice environment, professional norms and aspects of medical culture often contribute to the distress that individual physicians experience.

These dimensions have been well characterized and include suggestions that physicians should be impervious to normal human limitations (that is, superhuman), that work should always come first, and that seeking help is a sign of weakness. In aggregate, these attitudes lead many physicians to engage in unhealthy levels of self-sacrifice, manifested by excessive work hours, anxiety about missing something that would benefit their patients, and prioritizing work over personal health. These factors are familiar to many hospital-based and family physicians.
 

The impostor phenomenon

The impostor phenomenon (IP) is a psychological experience of intellectual and professional fraud. Individuals who suffer from it believe that others have inflated perceptions of the individual’s abilities and fear being judged. This fear persists despite continual proof of the individual’s successes. These people ignore praise, are highly self-critical, and attribute their successes to external factors, such as luck, hard work, or receiving help from others, rather than to qualities such as skill, intelligence, or ability.

IP is common among men and women. Some studies suggest it may be more prevalent among women. Studies across industries suggest that the phenomenon is associated with personal consequences (for example, low emotional well-being, problems with work-life integration, anxiety, depression, suicide) and professional consequences (for example, impaired job performance, occupational burnout). Studies involving U.S. medical students have revealed that more than one in four medical students experience IP and that those who experience it are at higher risk for burnout.
 

Surveying IS

IS, which is not a formal psychiatric diagnosis, is defined as having feelings of uncertainty, inadequacy, and being undeserving of one’s achievements despite evidence to the contrary. There are five subtypes of IS:

• Perfectionist: insecurity related to self-imposed, unachievable goals
• Expert: feeling inadequate from lacking sufficient knowledge
• Superperson: assuming excessive workloads just to feel okay among peers
• Natural genius: experiencing shame when it takes effort to develop a skill
• Soloist: believing that requesting help is a sign of weakness

Risk factors

Studies suggest that IS is a problem early in the physician training process. There is limited information on IS among physicians in practice.

Because transitions represent a risk factor for IP, the frequent rotation between clerkships and being a “perpetual novice” during medical school training may contribute to the high prevalence. Qualitative studies suggest that, once in practice, other professional experiences (for example, unfavorable patient outcomes, patient complaints, rejection of grants or manuscripts, and poor teaching evaluations or patient satisfaction scores) may contribute to IP.
 

Impact on doctors

Several methods have been used to classify how much the phenomenon interferes with a person’s life. The Clance Impostor Phenomenon Scale is a 20-item scale that asks respondents to indicate how well each item characterizes their experience on a 5-point scale. Options range from “not at all” to “very true.” The sum of responses to the individual items is used to create an aggregate score (IP score). The higher the score, the more frequently and seriously IP interferes with a person’s life.

A simplified version of the IP score was used in a study of 3,237 U.S. doctors that investigated the association between IS and burnout among doctors and to compare their rates of IS with those of other professionals.

Mean IP scores were higher for female physicians than for male physicians (mean, 10.91 vs. 9.12; P < .001). Scores decreased with age and were lower among those who were married or widowed.

With respect to professional characteristics, IP scores were greater among those in academic practice or who worked in the Veterans Affairs medical system and decreased with years in practice.

The highest IP scores were among pediatric subspecialists, general pediatricians, and emergency medicine physicians. Scores were lowest among ophthalmologists, radiologists, and orthopedic surgeons. IP has been independently associated with the risk of burnout and low professional fulfillment.
 

Lessening the impact

An article commenting on the study highlighted the following expert practice strategies that doctors can use to reduce the impact of IS in their professional life.

• Review and celebrate feats that have led to your professional role.
• Share concerns with trusted colleagues who can validate your accomplishments and normalize your feelings by reporting their own struggles with IS.
• Combat perfectionism by accepting that it is okay to be good enough when meeting the challenges of a demanding profession.
• Exercise self-compassion as an alternative to relying on an external locus of self-worth.
• Understand that IS may be common, especially during transitions, such as when entering medical school, graduate medical training, or starting a new career.

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Feelings of inadequacy, in terms of skills and expectations in an ever-changing system, are common emotions that many doctors have experienced since the start of the pandemic.

COVID-19 imposed challenges on health care professionals and systems by forcing changes in how doctors organize themselves professionally as well as in their relationships with patients and in their expectations (realistic or not) of their roles. The situation was bound to generate high rates of frustration and discomfort among younger and older physicians. It was compounded by a generational transition of the profession, which was accelerated by the virus. It was not managed by the decision-makers and was painful for doctors and patients.

Impostor syndrome (IS) is a psychological construct characterized by the persistent belief that one’s success is undeserved, rather than stemming from personal effort, skill, and ability. The phenomenon is common among medics for various reasons, including professional burnout. Recent studies have helped to better define the extent and characteristic features of the syndrome, as well as efforts to combat it.
 

Doctors and burnout

Although occupational burnout among physicians is a systemic issue primarily attributable to problems in the practice environment, professional norms and aspects of medical culture often contribute to the distress that individual physicians experience.

These dimensions have been well characterized and include suggestions that physicians should be impervious to normal human limitations (that is, superhuman), that work should always come first, and that seeking help is a sign of weakness. In aggregate, these attitudes lead many physicians to engage in unhealthy levels of self-sacrifice, manifested by excessive work hours, anxiety about missing something that would benefit their patients, and prioritizing work over personal health. These factors are familiar to many hospital-based and family physicians.
 

The impostor phenomenon

The impostor phenomenon (IP) is a psychological experience of intellectual and professional fraud. Individuals who suffer from it believe that others have inflated perceptions of the individual’s abilities and fear being judged. This fear persists despite continual proof of the individual’s successes. These people ignore praise, are highly self-critical, and attribute their successes to external factors, such as luck, hard work, or receiving help from others, rather than to qualities such as skill, intelligence, or ability.

IP is common among men and women. Some studies suggest it may be more prevalent among women. Studies across industries suggest that the phenomenon is associated with personal consequences (for example, low emotional well-being, problems with work-life integration, anxiety, depression, suicide) and professional consequences (for example, impaired job performance, occupational burnout). Studies involving U.S. medical students have revealed that more than one in four medical students experience IP and that those who experience it are at higher risk for burnout.
 

Surveying IS

IS, which is not a formal psychiatric diagnosis, is defined as having feelings of uncertainty, inadequacy, and being undeserving of one’s achievements despite evidence to the contrary. There are five subtypes of IS:

• Perfectionist: insecurity related to self-imposed, unachievable goals
• Expert: feeling inadequate from lacking sufficient knowledge
• Superperson: assuming excessive workloads just to feel okay among peers
• Natural genius: experiencing shame when it takes effort to develop a skill
• Soloist: believing that requesting help is a sign of weakness

Risk factors

Studies suggest that IS is a problem early in the physician training process. There is limited information on IS among physicians in practice.

Because transitions represent a risk factor for IP, the frequent rotation between clerkships and being a “perpetual novice” during medical school training may contribute to the high prevalence. Qualitative studies suggest that, once in practice, other professional experiences (for example, unfavorable patient outcomes, patient complaints, rejection of grants or manuscripts, and poor teaching evaluations or patient satisfaction scores) may contribute to IP.
 

Impact on doctors

Several methods have been used to classify how much the phenomenon interferes with a person’s life. The Clance Impostor Phenomenon Scale is a 20-item scale that asks respondents to indicate how well each item characterizes their experience on a 5-point scale. Options range from “not at all” to “very true.” The sum of responses to the individual items is used to create an aggregate score (IP score). The higher the score, the more frequently and seriously IP interferes with a person’s life.

A simplified version of the IP score was used in a study of 3,237 U.S. doctors that investigated the association between IS and burnout among doctors and to compare their rates of IS with those of other professionals.

Mean IP scores were higher for female physicians than for male physicians (mean, 10.91 vs. 9.12; P < .001). Scores decreased with age and were lower among those who were married or widowed.

With respect to professional characteristics, IP scores were greater among those in academic practice or who worked in the Veterans Affairs medical system and decreased with years in practice.

The highest IP scores were among pediatric subspecialists, general pediatricians, and emergency medicine physicians. Scores were lowest among ophthalmologists, radiologists, and orthopedic surgeons. IP has been independently associated with the risk of burnout and low professional fulfillment.
 

Lessening the impact

An article commenting on the study highlighted the following expert practice strategies that doctors can use to reduce the impact of IS in their professional life.

• Review and celebrate feats that have led to your professional role.
• Share concerns with trusted colleagues who can validate your accomplishments and normalize your feelings by reporting their own struggles with IS.
• Combat perfectionism by accepting that it is okay to be good enough when meeting the challenges of a demanding profession.
• Exercise self-compassion as an alternative to relying on an external locus of self-worth.
• Understand that IS may be common, especially during transitions, such as when entering medical school, graduate medical training, or starting a new career.

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Feelings of inadequacy, in terms of skills and expectations in an ever-changing system, are common emotions that many doctors have experienced since the start of the pandemic.

COVID-19 imposed challenges on health care professionals and systems by forcing changes in how doctors organize themselves professionally as well as in their relationships with patients and in their expectations (realistic or not) of their roles. The situation was bound to generate high rates of frustration and discomfort among younger and older physicians. It was compounded by a generational transition of the profession, which was accelerated by the virus. It was not managed by the decision-makers and was painful for doctors and patients.

Impostor syndrome (IS) is a psychological construct characterized by the persistent belief that one’s success is undeserved, rather than stemming from personal effort, skill, and ability. The phenomenon is common among medics for various reasons, including professional burnout. Recent studies have helped to better define the extent and characteristic features of the syndrome, as well as efforts to combat it.
 

Doctors and burnout

Although occupational burnout among physicians is a systemic issue primarily attributable to problems in the practice environment, professional norms and aspects of medical culture often contribute to the distress that individual physicians experience.

These dimensions have been well characterized and include suggestions that physicians should be impervious to normal human limitations (that is, superhuman), that work should always come first, and that seeking help is a sign of weakness. In aggregate, these attitudes lead many physicians to engage in unhealthy levels of self-sacrifice, manifested by excessive work hours, anxiety about missing something that would benefit their patients, and prioritizing work over personal health. These factors are familiar to many hospital-based and family physicians.
 

The impostor phenomenon

The impostor phenomenon (IP) is a psychological experience of intellectual and professional fraud. Individuals who suffer from it believe that others have inflated perceptions of the individual’s abilities and fear being judged. This fear persists despite continual proof of the individual’s successes. These people ignore praise, are highly self-critical, and attribute their successes to external factors, such as luck, hard work, or receiving help from others, rather than to qualities such as skill, intelligence, or ability.

IP is common among men and women. Some studies suggest it may be more prevalent among women. Studies across industries suggest that the phenomenon is associated with personal consequences (for example, low emotional well-being, problems with work-life integration, anxiety, depression, suicide) and professional consequences (for example, impaired job performance, occupational burnout). Studies involving U.S. medical students have revealed that more than one in four medical students experience IP and that those who experience it are at higher risk for burnout.
 

Surveying IS

IS, which is not a formal psychiatric diagnosis, is defined as having feelings of uncertainty, inadequacy, and being undeserving of one’s achievements despite evidence to the contrary. There are five subtypes of IS:

• Perfectionist: insecurity related to self-imposed, unachievable goals
• Expert: feeling inadequate from lacking sufficient knowledge
• Superperson: assuming excessive workloads just to feel okay among peers
• Natural genius: experiencing shame when it takes effort to develop a skill
• Soloist: believing that requesting help is a sign of weakness

Risk factors

Studies suggest that IS is a problem early in the physician training process. There is limited information on IS among physicians in practice.

Because transitions represent a risk factor for IP, the frequent rotation between clerkships and being a “perpetual novice” during medical school training may contribute to the high prevalence. Qualitative studies suggest that, once in practice, other professional experiences (for example, unfavorable patient outcomes, patient complaints, rejection of grants or manuscripts, and poor teaching evaluations or patient satisfaction scores) may contribute to IP.
 

Impact on doctors

Several methods have been used to classify how much the phenomenon interferes with a person’s life. The Clance Impostor Phenomenon Scale is a 20-item scale that asks respondents to indicate how well each item characterizes their experience on a 5-point scale. Options range from “not at all” to “very true.” The sum of responses to the individual items is used to create an aggregate score (IP score). The higher the score, the more frequently and seriously IP interferes with a person’s life.

A simplified version of the IP score was used in a study of 3,237 U.S. doctors that investigated the association between IS and burnout among doctors and to compare their rates of IS with those of other professionals.

Mean IP scores were higher for female physicians than for male physicians (mean, 10.91 vs. 9.12; P < .001). Scores decreased with age and were lower among those who were married or widowed.

With respect to professional characteristics, IP scores were greater among those in academic practice or who worked in the Veterans Affairs medical system and decreased with years in practice.

The highest IP scores were among pediatric subspecialists, general pediatricians, and emergency medicine physicians. Scores were lowest among ophthalmologists, radiologists, and orthopedic surgeons. IP has been independently associated with the risk of burnout and low professional fulfillment.
 

Lessening the impact

An article commenting on the study highlighted the following expert practice strategies that doctors can use to reduce the impact of IS in their professional life.

• Review and celebrate feats that have led to your professional role.
• Share concerns with trusted colleagues who can validate your accomplishments and normalize your feelings by reporting their own struggles with IS.
• Combat perfectionism by accepting that it is okay to be good enough when meeting the challenges of a demanding profession.
• Exercise self-compassion as an alternative to relying on an external locus of self-worth.
• Understand that IS may be common, especially during transitions, such as when entering medical school, graduate medical training, or starting a new career.

This article was translated from Univadis Italy. A version appeared on Medscape.com.

Cardiovascular disease (CVD) is the main cause of premature death and disability in the general population, and according to the World Health Organization, the incidence of CVD is increasing throughout the world. Conventional risk factors that contribute to the occurrence and worsening of CVD have been identified and widely studied. They include high cholesterol levels, high blood pressure, diabetes, obesity, smoking, and lack of physical activity. Despite the introduction of measures to prevent and treat these risk factors with lipid-lowering drugs, antihypertensives, antiplatelet drugs, and anticoagulants, the mortality rate related to CVD remains high.
 

Despite the effectiveness of many currently available treatment options, there are still significant gaps in risk assessment and treatment of CVD.

In the past few years, new coronary risk factors have emerged. They are detailed in an editorial published in The American Journal of Medicine that describes their role and their impact on our cardiovascular health.
 

Systemic inflammation

The new coronary risk factors include the following diseases characterized by systemic inflammation:

• Gout – Among patients who have experienced a recent flare of gout, the probability of experiencing an acute cardiovascular event such as a myocardial infarction or stroke is increased.
• Rheumatoid arthritis and systemic lupus erythematous – Patients with one or both of these conditions are at higher odds of experiencing concomitant premature and extremely premature coronary artery disease.
• Inflammatory bowel disease (Crohn’s disease or ulcerative colitis) – Patients with this disease have increased odds of developing coronary artery disease.
• Psoriasis – Patients with psoriasis are up to 50% more likely to develop CVD.

Maternal and childhood factors

The following maternal and childhood factors are associated with an increased risk of developing coronary artery disease: gestational diabetes; preeclampsia; delivering a child of low birth weight; preterm delivery; and premature or surgical menopause. The factor or factors that increase the risk of coronary artery disease associated with each of these conditions are not known but may be the result of increased cytokine and oxidative stress.

An unusual and yet unexplained association has been observed between migraine headaches with aura in women and incident CVD.

Also of interest is the association of early life trauma and the risk of adverse cardiovascular outcomes in young and middle-aged individuals who have a history of myocardial infarction.

Transgender patients who present for gender-affirming care are also at increased cardiovascular risk. Among these patients, the increase in coronary artery disease risk may be related to high rates of anxiety and depression.
 

Environmental factors

Low socioeconomic status has emerged as a risk factor. Increased psychosocial stressors, limited educational and economic opportunities, and lack of peer influence favoring healthier lifestyle choices may be causative elements leading to enhanced coronary artery disease among individuals with low socioeconomic living conditions.

Air pollution was estimated to have caused 9 million deaths worldwide in 2019, with 62% due to CVD and 31.7% to coronary artery disease. Severely polluted environmental aerosols contain several toxic metals, such as lead, mercury, arsenic, and cadmium. Transient exposure to various air pollutants may trigger the onset of an acute coronary syndrome.
 

Lifestyle factors

Long working hours by patients who have experienced a first myocardial infarction increase the risk for a recurrent event, possibly because of prolonged exposure to work stressors.

Skipping breakfast has been linked to increased cardiovascular and all-cause mortality.

Long-term consumption of drinks containing sugar and artificial sweeteners has also been associated with increased cardiovascular mortality.

Recognizing the presence of one or more of these new risk factors could help prompt and improve behaviors for reducing more conventional CV risk factors to a minimum.

This article was translated from Univadis Italy, which is part of the Medscape Professional Network.

A version of this article first appeared on Medscape.com.

Cardiovascular disease (CVD) is the main cause of premature death and disability in the general population, and according to the World Health Organization, the incidence of CVD is increasing throughout the world. Conventional risk factors that contribute to the occurrence and worsening of CVD have been identified and widely studied. They include high cholesterol levels, high blood pressure, diabetes, obesity, smoking, and lack of physical activity. Despite the introduction of measures to prevent and treat these risk factors with lipid-lowering drugs, antihypertensives, antiplatelet drugs, and anticoagulants, the mortality rate related to CVD remains high.
 

Despite the effectiveness of many currently available treatment options, there are still significant gaps in risk assessment and treatment of CVD.

In the past few years, new coronary risk factors have emerged. They are detailed in an editorial published in The American Journal of Medicine that describes their role and their impact on our cardiovascular health.
 

Systemic inflammation

The new coronary risk factors include the following diseases characterized by systemic inflammation:

• Gout – Among patients who have experienced a recent flare of gout, the probability of experiencing an acute cardiovascular event such as a myocardial infarction or stroke is increased.
• Rheumatoid arthritis and systemic lupus erythematous – Patients with one or both of these conditions are at higher odds of experiencing concomitant premature and extremely premature coronary artery disease.
• Inflammatory bowel disease (Crohn’s disease or ulcerative colitis) – Patients with this disease have increased odds of developing coronary artery disease.
• Psoriasis – Patients with psoriasis are up to 50% more likely to develop CVD.

Maternal and childhood factors

The following maternal and childhood factors are associated with an increased risk of developing coronary artery disease: gestational diabetes; preeclampsia; delivering a child of low birth weight; preterm delivery; and premature or surgical menopause. The factor or factors that increase the risk of coronary artery disease associated with each of these conditions are not known but may be the result of increased cytokine and oxidative stress.

An unusual and yet unexplained association has been observed between migraine headaches with aura in women and incident CVD.

Also of interest is the association of early life trauma and the risk of adverse cardiovascular outcomes in young and middle-aged individuals who have a history of myocardial infarction.

Transgender patients who present for gender-affirming care are also at increased cardiovascular risk. Among these patients, the increase in coronary artery disease risk may be related to high rates of anxiety and depression.
 

Environmental factors

Low socioeconomic status has emerged as a risk factor. Increased psychosocial stressors, limited educational and economic opportunities, and lack of peer influence favoring healthier lifestyle choices may be causative elements leading to enhanced coronary artery disease among individuals with low socioeconomic living conditions.

Air pollution was estimated to have caused 9 million deaths worldwide in 2019, with 62% due to CVD and 31.7% to coronary artery disease. Severely polluted environmental aerosols contain several toxic metals, such as lead, mercury, arsenic, and cadmium. Transient exposure to various air pollutants may trigger the onset of an acute coronary syndrome.
 

Lifestyle factors

Long working hours by patients who have experienced a first myocardial infarction increase the risk for a recurrent event, possibly because of prolonged exposure to work stressors.

Skipping breakfast has been linked to increased cardiovascular and all-cause mortality.

Long-term consumption of drinks containing sugar and artificial sweeteners has also been associated with increased cardiovascular mortality.

Recognizing the presence of one or more of these new risk factors could help prompt and improve behaviors for reducing more conventional CV risk factors to a minimum.

This article was translated from Univadis Italy, which is part of the Medscape Professional Network.

A version of this article first appeared on Medscape.com.

Cardiovascular disease (CVD) is the main cause of premature death and disability in the general population, and according to the World Health Organization, the incidence of CVD is increasing throughout the world. Conventional risk factors that contribute to the occurrence and worsening of CVD have been identified and widely studied. They include high cholesterol levels, high blood pressure, diabetes, obesity, smoking, and lack of physical activity. Despite the introduction of measures to prevent and treat these risk factors with lipid-lowering drugs, antihypertensives, antiplatelet drugs, and anticoagulants, the mortality rate related to CVD remains high.
 

Despite the effectiveness of many currently available treatment options, there are still significant gaps in risk assessment and treatment of CVD.

In the past few years, new coronary risk factors have emerged. They are detailed in an editorial published in The American Journal of Medicine that describes their role and their impact on our cardiovascular health.
 

Systemic inflammation

The new coronary risk factors include the following diseases characterized by systemic inflammation:

• Gout – Among patients who have experienced a recent flare of gout, the probability of experiencing an acute cardiovascular event such as a myocardial infarction or stroke is increased.
• Rheumatoid arthritis and systemic lupus erythematous – Patients with one or both of these conditions are at higher odds of experiencing concomitant premature and extremely premature coronary artery disease.
• Inflammatory bowel disease (Crohn’s disease or ulcerative colitis) – Patients with this disease have increased odds of developing coronary artery disease.
• Psoriasis – Patients with psoriasis are up to 50% more likely to develop CVD.

Maternal and childhood factors

The following maternal and childhood factors are associated with an increased risk of developing coronary artery disease: gestational diabetes; preeclampsia; delivering a child of low birth weight; preterm delivery; and premature or surgical menopause. The factor or factors that increase the risk of coronary artery disease associated with each of these conditions are not known but may be the result of increased cytokine and oxidative stress.

An unusual and yet unexplained association has been observed between migraine headaches with aura in women and incident CVD.

Also of interest is the association of early life trauma and the risk of adverse cardiovascular outcomes in young and middle-aged individuals who have a history of myocardial infarction.

Transgender patients who present for gender-affirming care are also at increased cardiovascular risk. Among these patients, the increase in coronary artery disease risk may be related to high rates of anxiety and depression.
 

Environmental factors

Low socioeconomic status has emerged as a risk factor. Increased psychosocial stressors, limited educational and economic opportunities, and lack of peer influence favoring healthier lifestyle choices may be causative elements leading to enhanced coronary artery disease among individuals with low socioeconomic living conditions.

Air pollution was estimated to have caused 9 million deaths worldwide in 2019, with 62% due to CVD and 31.7% to coronary artery disease. Severely polluted environmental aerosols contain several toxic metals, such as lead, mercury, arsenic, and cadmium. Transient exposure to various air pollutants may trigger the onset of an acute coronary syndrome.
 

Lifestyle factors

Long working hours by patients who have experienced a first myocardial infarction increase the risk for a recurrent event, possibly because of prolonged exposure to work stressors.

Skipping breakfast has been linked to increased cardiovascular and all-cause mortality.

Long-term consumption of drinks containing sugar and artificial sweeteners has also been associated with increased cardiovascular mortality.

Recognizing the presence of one or more of these new risk factors could help prompt and improve behaviors for reducing more conventional CV risk factors to a minimum.

This article was translated from Univadis Italy, which is part of the Medscape Professional Network.

A version of this article first appeared on Medscape.com.

Intake of salt is a biological necessity, inextricably woven into physiologic systems. However, excessive salt intake is associated with high blood pressure. Hypertension is linked to increased cardiovascular morbidity and mortality, and it is estimated that excessive salt intake causes approximately 5 million deaths per year worldwide. Reducing salt intake lowers blood pressure, but processed foods contain “hidden” salt, which makes dietary control of salt difficult. This problem is compounded by growing inequalities in food systems, which present another hurdle to sustaining individual dietary control of salt intake.

Salt_spoon_web.jpg

Of the 87 risk factors included in the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, high systolic blood pressure was identified as the leading risk factor for disease burden at the global level and for its effect on human health. A range of strategies, including primary care management and reduction in sodium intake, are known to reduce the burden of this critical risk factor. Two questions remain unanswered: “What is the relationship between mortality and adding salt to foods?” and “How much does a reduction in salt intake influence people’s health?”
 

Cardiovascular disease and death

Because dietary sodium intake has been identified as a risk factor for cardiovascular disease and premature death, high sodium intake can be expected to curtail life span. A study tested this hypothesis by analyzing the relationship between sodium intake and life expectancy and survival in 181 countries. Sodium intake correlated positively with life expectancy and inversely with all-cause mortality worldwide and in high-income countries, which argues against dietary sodium intake curtailing life span or a being risk factor for premature death. These results help fuel a scientific debate about sodium intake, life expectancy, and mortality. The debate requires interpreting composite data of positive linear, J-shaped, or inverse linear correlations, which underscores the uncertainty regarding this issue.

In a prospective study of 501,379 participants from the UK Biobank, researchers found that higher frequency of adding salt to foods was significantly associated with a higher risk of premature mortality and lower life expectancy independently of diet, lifestyle, socioeconomic level, and preexisting diseases. They found that the positive association appeared to be attenuated with increasing intake of high-potassium foods (vegetables and fruits).

In addition, the researchers made the following observations:

• For cause-specific premature mortality, they found that higher frequency of adding salt to foods was significantly associated with a higher risk of cardiovascular disease mortality and cancer mortality (P-trend < .001 and P-trend < .001, respectively).
• Always adding salt to foods was associated with the lower life expectancy at the age of 50 years by 1.50 (95% confidence interval, 0.72-2.30) and 2.28 (95% CI, 1.66-2.90) years for women and men, respectively, compared with participants who never or rarely added salt to foods.

The researchers noted that adding salt to foods (usually at the table) is common and is directly related to an individual’s long-term preference for salty foods and habitual salt intake. Indeed, in the Western diet, adding salt at the table accounts for 6%-20% of total salt intake. In addition, commonly used table salt contains 97%-99% sodium chloride, minimizing the potential confounding effects of other dietary factors, including potassium. Therefore, adding salt to foods provides a way to evaluate the association between habitual sodium intake and mortality – something that is relevant, given that it has been estimated that in 2010, a total of 1.65 million deaths from cardiovascular causes were attributable to consumption of more than 2.0 g of sodium per day.
 

Salt sensitivity

Current evidence supports a recommendation for moderate sodium intake in the general population (3-5 g/day). Persons with hypertension should consume salt at the lower end of that range. Some dietary guidelines recommend consuming less than 2,300 mg dietary sodium per day for persons aged 14 years or older and less for persons aged 2-13 years. Although low sodium intake (< 2.0 g/day) has been achieved in short-term clinical trials, sustained low sodium intake has not been achieved in any of the longer-term clinical trials (duration > 6 months).

The controversy continues as to the relationship between low sodium intake and blood pressure or cardiovascular diseases. Most studies show that both in individuals with hypertension and those without, blood pressure is reduced by consuming less sodium. However, it is not necessarily lowered by reducing sodium intake (< 3-5 g/day). With a sodium-rich diet, most normotensive individuals experienced a minimal change in mean arterial pressure; for many individuals with hypertension, the values increased by about 4 mm Hg. In addition, among individuals with hypertension who are “salt sensitive,” arterial pressure can increase by > 10 mm Hg in response to high sodium intake.
 

The effect of potassium

Replacing some of the sodium chloride in regular salt with potassium chloride may mitigate some of salt’s harmful cardiovascular effects. Indeed, salt substitutes that have reduced sodium levels and increased potassium levels have been shown to lower blood pressure.

In one trial, researchers enrolled over 20,000 persons from 600 villages in rural China and compared the use of regular salt (100% sodium chloride) with the use of a salt substitute (75% sodium chloride and 25% potassium chloride by mass).

The participants were at high risk for stroke, cardiovascular events, and death. The mean duration of follow-up was 4.74 years. The results were surprising. The rate of stroke was lower with the salt substitute than with regular salt (29.14 events vs. 33.65 events per 1,000 person-years; rate ratio, 0.86; 95% CI, 0.77-0.96; P = .006), as were the rates of major cardiovascular events and death from any cause. The rate of serious adverse events attributed to hyperkalemia was not significantly higher with the salt substitute than with regular salt.

Although there is an ongoing debate about the extent of salt’s effects on the cardiovascular system, there is no doubt that in most places in the world, people are consuming more salt than the body needs.

A lot depends upon the kind of diet consumed by a particular population. Processed food is rarely used in rural areas, such as those involved in the above-mentioned trial, with dietary sodium chloride being added while preparing food at home. This is a determining factor with regard to cardiovascular outcomes, but it cannot be generalized to other social-environmental settings.

In much of the world, commercial food preservation introduces a lot of sodium chloride into the diet, and most salt intake could not be fully attributed to the use of salt substitutes. Indeed, by comparing the sodium content of cereal-based products currently sold on the Italian market with the respective benchmarks proposed by the World Health Organization, researchers found that for most items, the sodium content is much higher than the benchmarks, especially with flatbreads, leavened breads, and crackers/savory biscuits. This shows that there is work to be done to achieve the World Health Organization/United Nations objective of a 30% global reduction in sodium intake by 2025.

This article was translated from Univadis Italy. A version of this article first appeared on Medscape.com.

Intake of salt is a biological necessity, inextricably woven into physiologic systems. However, excessive salt intake is associated with high blood pressure. Hypertension is linked to increased cardiovascular morbidity and mortality, and it is estimated that excessive salt intake causes approximately 5 million deaths per year worldwide. Reducing salt intake lowers blood pressure, but processed foods contain “hidden” salt, which makes dietary control of salt difficult. This problem is compounded by growing inequalities in food systems, which present another hurdle to sustaining individual dietary control of salt intake.

Salt_spoon_web.jpg

Of the 87 risk factors included in the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, high systolic blood pressure was identified as the leading risk factor for disease burden at the global level and for its effect on human health. A range of strategies, including primary care management and reduction in sodium intake, are known to reduce the burden of this critical risk factor. Two questions remain unanswered: “What is the relationship between mortality and adding salt to foods?” and “How much does a reduction in salt intake influence people’s health?”
 

Cardiovascular disease and death

Because dietary sodium intake has been identified as a risk factor for cardiovascular disease and premature death, high sodium intake can be expected to curtail life span. A study tested this hypothesis by analyzing the relationship between sodium intake and life expectancy and survival in 181 countries. Sodium intake correlated positively with life expectancy and inversely with all-cause mortality worldwide and in high-income countries, which argues against dietary sodium intake curtailing life span or a being risk factor for premature death. These results help fuel a scientific debate about sodium intake, life expectancy, and mortality. The debate requires interpreting composite data of positive linear, J-shaped, or inverse linear correlations, which underscores the uncertainty regarding this issue.

In a prospective study of 501,379 participants from the UK Biobank, researchers found that higher frequency of adding salt to foods was significantly associated with a higher risk of premature mortality and lower life expectancy independently of diet, lifestyle, socioeconomic level, and preexisting diseases. They found that the positive association appeared to be attenuated with increasing intake of high-potassium foods (vegetables and fruits).

In addition, the researchers made the following observations:

• For cause-specific premature mortality, they found that higher frequency of adding salt to foods was significantly associated with a higher risk of cardiovascular disease mortality and cancer mortality (P-trend < .001 and P-trend < .001, respectively).
• Always adding salt to foods was associated with the lower life expectancy at the age of 50 years by 1.50 (95% confidence interval, 0.72-2.30) and 2.28 (95% CI, 1.66-2.90) years for women and men, respectively, compared with participants who never or rarely added salt to foods.

The researchers noted that adding salt to foods (usually at the table) is common and is directly related to an individual’s long-term preference for salty foods and habitual salt intake. Indeed, in the Western diet, adding salt at the table accounts for 6%-20% of total salt intake. In addition, commonly used table salt contains 97%-99% sodium chloride, minimizing the potential confounding effects of other dietary factors, including potassium. Therefore, adding salt to foods provides a way to evaluate the association between habitual sodium intake and mortality – something that is relevant, given that it has been estimated that in 2010, a total of 1.65 million deaths from cardiovascular causes were attributable to consumption of more than 2.0 g of sodium per day.
 

Salt sensitivity

Current evidence supports a recommendation for moderate sodium intake in the general population (3-5 g/day). Persons with hypertension should consume salt at the lower end of that range. Some dietary guidelines recommend consuming less than 2,300 mg dietary sodium per day for persons aged 14 years or older and less for persons aged 2-13 years. Although low sodium intake (< 2.0 g/day) has been achieved in short-term clinical trials, sustained low sodium intake has not been achieved in any of the longer-term clinical trials (duration > 6 months).

The controversy continues as to the relationship between low sodium intake and blood pressure or cardiovascular diseases. Most studies show that both in individuals with hypertension and those without, blood pressure is reduced by consuming less sodium. However, it is not necessarily lowered by reducing sodium intake (< 3-5 g/day). With a sodium-rich diet, most normotensive individuals experienced a minimal change in mean arterial pressure; for many individuals with hypertension, the values increased by about 4 mm Hg. In addition, among individuals with hypertension who are “salt sensitive,” arterial pressure can increase by > 10 mm Hg in response to high sodium intake.
 

The effect of potassium

Replacing some of the sodium chloride in regular salt with potassium chloride may mitigate some of salt’s harmful cardiovascular effects. Indeed, salt substitutes that have reduced sodium levels and increased potassium levels have been shown to lower blood pressure.

In one trial, researchers enrolled over 20,000 persons from 600 villages in rural China and compared the use of regular salt (100% sodium chloride) with the use of a salt substitute (75% sodium chloride and 25% potassium chloride by mass).

The participants were at high risk for stroke, cardiovascular events, and death. The mean duration of follow-up was 4.74 years. The results were surprising. The rate of stroke was lower with the salt substitute than with regular salt (29.14 events vs. 33.65 events per 1,000 person-years; rate ratio, 0.86; 95% CI, 0.77-0.96; P = .006), as were the rates of major cardiovascular events and death from any cause. The rate of serious adverse events attributed to hyperkalemia was not significantly higher with the salt substitute than with regular salt.

Although there is an ongoing debate about the extent of salt’s effects on the cardiovascular system, there is no doubt that in most places in the world, people are consuming more salt than the body needs.

A lot depends upon the kind of diet consumed by a particular population. Processed food is rarely used in rural areas, such as those involved in the above-mentioned trial, with dietary sodium chloride being added while preparing food at home. This is a determining factor with regard to cardiovascular outcomes, but it cannot be generalized to other social-environmental settings.

In much of the world, commercial food preservation introduces a lot of sodium chloride into the diet, and most salt intake could not be fully attributed to the use of salt substitutes. Indeed, by comparing the sodium content of cereal-based products currently sold on the Italian market with the respective benchmarks proposed by the World Health Organization, researchers found that for most items, the sodium content is much higher than the benchmarks, especially with flatbreads, leavened breads, and crackers/savory biscuits. This shows that there is work to be done to achieve the World Health Organization/United Nations objective of a 30% global reduction in sodium intake by 2025.

This article was translated from Univadis Italy. A version of this article first appeared on Medscape.com.

Intake of salt is a biological necessity, inextricably woven into physiologic systems. However, excessive salt intake is associated with high blood pressure. Hypertension is linked to increased cardiovascular morbidity and mortality, and it is estimated that excessive salt intake causes approximately 5 million deaths per year worldwide. Reducing salt intake lowers blood pressure, but processed foods contain “hidden” salt, which makes dietary control of salt difficult. This problem is compounded by growing inequalities in food systems, which present another hurdle to sustaining individual dietary control of salt intake.

Salt_spoon_web.jpg

Of the 87 risk factors included in the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, high systolic blood pressure was identified as the leading risk factor for disease burden at the global level and for its effect on human health. A range of strategies, including primary care management and reduction in sodium intake, are known to reduce the burden of this critical risk factor. Two questions remain unanswered: “What is the relationship between mortality and adding salt to foods?” and “How much does a reduction in salt intake influence people’s health?”
 

Cardiovascular disease and death

Because dietary sodium intake has been identified as a risk factor for cardiovascular disease and premature death, high sodium intake can be expected to curtail life span. A study tested this hypothesis by analyzing the relationship between sodium intake and life expectancy and survival in 181 countries. Sodium intake correlated positively with life expectancy and inversely with all-cause mortality worldwide and in high-income countries, which argues against dietary sodium intake curtailing life span or a being risk factor for premature death. These results help fuel a scientific debate about sodium intake, life expectancy, and mortality. The debate requires interpreting composite data of positive linear, J-shaped, or inverse linear correlations, which underscores the uncertainty regarding this issue.

In a prospective study of 501,379 participants from the UK Biobank, researchers found that higher frequency of adding salt to foods was significantly associated with a higher risk of premature mortality and lower life expectancy independently of diet, lifestyle, socioeconomic level, and preexisting diseases. They found that the positive association appeared to be attenuated with increasing intake of high-potassium foods (vegetables and fruits).

In addition, the researchers made the following observations:

• For cause-specific premature mortality, they found that higher frequency of adding salt to foods was significantly associated with a higher risk of cardiovascular disease mortality and cancer mortality (P-trend < .001 and P-trend < .001, respectively).
• Always adding salt to foods was associated with the lower life expectancy at the age of 50 years by 1.50 (95% confidence interval, 0.72-2.30) and 2.28 (95% CI, 1.66-2.90) years for women and men, respectively, compared with participants who never or rarely added salt to foods.

The researchers noted that adding salt to foods (usually at the table) is common and is directly related to an individual’s long-term preference for salty foods and habitual salt intake. Indeed, in the Western diet, adding salt at the table accounts for 6%-20% of total salt intake. In addition, commonly used table salt contains 97%-99% sodium chloride, minimizing the potential confounding effects of other dietary factors, including potassium. Therefore, adding salt to foods provides a way to evaluate the association between habitual sodium intake and mortality – something that is relevant, given that it has been estimated that in 2010, a total of 1.65 million deaths from cardiovascular causes were attributable to consumption of more than 2.0 g of sodium per day.
 

Salt sensitivity

Current evidence supports a recommendation for moderate sodium intake in the general population (3-5 g/day). Persons with hypertension should consume salt at the lower end of that range. Some dietary guidelines recommend consuming less than 2,300 mg dietary sodium per day for persons aged 14 years or older and less for persons aged 2-13 years. Although low sodium intake (< 2.0 g/day) has been achieved in short-term clinical trials, sustained low sodium intake has not been achieved in any of the longer-term clinical trials (duration > 6 months).

The controversy continues as to the relationship between low sodium intake and blood pressure or cardiovascular diseases. Most studies show that both in individuals with hypertension and those without, blood pressure is reduced by consuming less sodium. However, it is not necessarily lowered by reducing sodium intake (< 3-5 g/day). With a sodium-rich diet, most normotensive individuals experienced a minimal change in mean arterial pressure; for many individuals with hypertension, the values increased by about 4 mm Hg. In addition, among individuals with hypertension who are “salt sensitive,” arterial pressure can increase by > 10 mm Hg in response to high sodium intake.
 

The effect of potassium

Replacing some of the sodium chloride in regular salt with potassium chloride may mitigate some of salt’s harmful cardiovascular effects. Indeed, salt substitutes that have reduced sodium levels and increased potassium levels have been shown to lower blood pressure.

In one trial, researchers enrolled over 20,000 persons from 600 villages in rural China and compared the use of regular salt (100% sodium chloride) with the use of a salt substitute (75% sodium chloride and 25% potassium chloride by mass).

The participants were at high risk for stroke, cardiovascular events, and death. The mean duration of follow-up was 4.74 years. The results were surprising. The rate of stroke was lower with the salt substitute than with regular salt (29.14 events vs. 33.65 events per 1,000 person-years; rate ratio, 0.86; 95% CI, 0.77-0.96; P = .006), as were the rates of major cardiovascular events and death from any cause. The rate of serious adverse events attributed to hyperkalemia was not significantly higher with the salt substitute than with regular salt.

Although there is an ongoing debate about the extent of salt’s effects on the cardiovascular system, there is no doubt that in most places in the world, people are consuming more salt than the body needs.

A lot depends upon the kind of diet consumed by a particular population. Processed food is rarely used in rural areas, such as those involved in the above-mentioned trial, with dietary sodium chloride being added while preparing food at home. This is a determining factor with regard to cardiovascular outcomes, but it cannot be generalized to other social-environmental settings.

In much of the world, commercial food preservation introduces a lot of sodium chloride into the diet, and most salt intake could not be fully attributed to the use of salt substitutes. Indeed, by comparing the sodium content of cereal-based products currently sold on the Italian market with the respective benchmarks proposed by the World Health Organization, researchers found that for most items, the sodium content is much higher than the benchmarks, especially with flatbreads, leavened breads, and crackers/savory biscuits. This shows that there is work to be done to achieve the World Health Organization/United Nations objective of a 30% global reduction in sodium intake by 2025.

This article was translated from Univadis Italy. A version of this article first appeared on Medscape.com.

It is projected that by 2050, 1.6 billion women in the world will have reached menopause or the postmenopausal period, a significant increase, compared with a billion women in 2020. Of all menopausal women, around 75% are affected by troublesome menopause symptoms, such as hot flashes and night sweats.

Around 84% of postmenopausal women experience genitourinary symptoms, such as vulvovaginal atrophy and incontinence.

Menopausal hormone therapy (MHT) is the most effective treatment for managing these symptoms; however, its effects on numerous aspects of female health remain uncertain, in particular with regard to breast cancer. The influence of MHT on breast cancer remains unsettled, with discordant findings from observational studies and randomized clinical trials, a factor that affects the decisions made by doctors concerning hormone therapy in menopausal women.
 

Background

Conjugated equine estrogens (CEEs) were introduced into clinical practice in the 1940s. For decades, MHT was the main treatment in conventional medicine for the symptoms of menopause. MHT was used in Western countries for about 600 million women starting from 1970, and it progressively increased during the 1990s. Professional organizations recommended MHT for the prevention of osteoporosis and chronic heart disease (CHD), and a third of prescriptions were for women older than 60 years.

Against this background, the National Institutes of Health launched randomized trials of MHT through the Women’s Health Initiative (WHI) to test whether the association with reduced risk for CHD found in observational studies was real and to obtain reliable information on the overall risks and benefits regarding the prevention of chronic disease for postmenopausal women aged 50-79 years.

The WHI trials tested standard-dose oral CEEs with and without standard-dose continuous medroxyprogesterone acetate (EPT). In 2002, the results of the WHI studies raised a series of concerns about the long-term safety of MHT, in particular the finding of an increased risk of breast cancer for women undergoing therapy. That risk exceeded the benefits from reductions in hip fractures and colorectal cancer.

The WHI findings received wide attention. Prescriptions for MHT dropped precipitously after 2002 and continued to decline in subsequent years. Declines were most marked for standard-dose EPT and in older women. The results of the CEE study were less negative, compared with those for EPT, as they showed no effect on CHD, a nonsignificant reduction in the risk of breast cancer, and a more favorable risk-benefit ratio for younger women, compared with older women. A decade later, it had become widely accepted that MHT should not be used for the prevention of chronic disease in older women; however, short-term use for treatment of vasomotor symptoms remains an accepted indication.
 

Risks and outcomes

Emerging from a series of WHI reports are complex models on the effect of hormonal therapy on the risk and outcome of breast cancer. In one study, women with an intact uterus received CEEs plus medroxyprogesterone acetate (MPA). An increase in the risk of breast cancer was observed over a median of 5.6 years of treatment, followed by a moderate reduction, with the risk increasing after 13 years of cumulative follow-up. For women treated with CEE alone, the reduction in risk observed over an average of 7.2 years of treatment was maintained for 13 years of follow-up.

Results from observational studies contrast with those from randomized controlled trials, particularly those concerning the use of estrogens only. A meta-analysis by the Collaborative Group on Hormonal Factors in Breast Cancer showed that both EPT and CEE were associated with a higher risk of breast neoplasia. Results of the Million Women Study showed a higher death rate.
 

Treatment methods and duration

Information from prospective studies on the effects of commencing MHT at various ages between 40 and 59 years show that for women who commenced treatment at any time within this age range, the relative risk was similar and was highly significant for all ages. Few women had started MHT treatment well after menopause at ages 60-69 years, and their excess risks during years 5-14 of current use were significant for estrogen-progestogen but not for estrogen-only MHT.

If these associations are largely causal, then for women of average weight in developed countries, 5 years of MHT, starting at age 50 years, would increase breast cancer incidence at ages 50-69 years by about 1 in every 50 users of estrogen plus daily progestogen preparations; 1 in every 70 users of estrogen plus intermittent progestogen preparations; and 1 in every 200 users of estrogen-only preparations. The corresponding excesses from 10 years of MHT would be about twice as great.

During 5-14 years of MHT use, the RRs were similarly increased if MHT use had started at ages 40-44 years, 45-49 years, 50-54 years, and 55-59 years; RRs appeared to be attenuated if MHT use had started after age 60 years. They were also attenuated by adiposity, particularly for estrogen-only MHT (which had little effect in obese women). After MHT use ceased, some excess risk of breast cancer persisted for more than a decade; this is directly correlated with the duration of treatment.

Therefore, it can be expected that the effects of MHT may vary between participants on the basis of age or time since menopause, as well as treatments (MHT type, dose, formulation, duration of use, and route of administration). Regarding formulation effects on the risk of breast cancer, new evidence shows an increased risk of 28%. Progestogens appeared to be differentially associated with breast cancer (micronized progesterone: odds ratio, 0.99; 95% confidence interval 0.55-1.79; synthetic progestin: OR, 1.28; 95% CI, 1.22-1.35). When prescribing MHT, micronized progesterone may be the safer progestogen to use.

In conclusion, MHT has a complex balance of benefits and risk on various health outcomes. Some effects differ qualitatively between ET and EPT. Regarding use of MHT, consideration should be given to the full range of effects, along with patients’ values and preferences. The overall quality of existing systematic reviews is moderate to poor. Clinicians should evaluate their scientific strength before considering applying their results in clinical practice. Regarding use of any hormone therapy regimen, consideration should be given to the full range of risk and benefits and should involve shared decisionmaking with the patient. It should be recognized that risk-benefit balance is altered by factors such as age, time from menopause, oophorectomy status, and prior hysterectomy and that some outcomes persist and there is some attenuation after stopping use.

This article was translated from Univadis Italy.

A version of the article appeared on Medscape.com.

It is projected that by 2050, 1.6 billion women in the world will have reached menopause or the postmenopausal period, a significant increase, compared with a billion women in 2020. Of all menopausal women, around 75% are affected by troublesome menopause symptoms, such as hot flashes and night sweats.

Around 84% of postmenopausal women experience genitourinary symptoms, such as vulvovaginal atrophy and incontinence.

Menopausal hormone therapy (MHT) is the most effective treatment for managing these symptoms; however, its effects on numerous aspects of female health remain uncertain, in particular with regard to breast cancer. The influence of MHT on breast cancer remains unsettled, with discordant findings from observational studies and randomized clinical trials, a factor that affects the decisions made by doctors concerning hormone therapy in menopausal women.
 

Background

Conjugated equine estrogens (CEEs) were introduced into clinical practice in the 1940s. For decades, MHT was the main treatment in conventional medicine for the symptoms of menopause. MHT was used in Western countries for about 600 million women starting from 1970, and it progressively increased during the 1990s. Professional organizations recommended MHT for the prevention of osteoporosis and chronic heart disease (CHD), and a third of prescriptions were for women older than 60 years.

Against this background, the National Institutes of Health launched randomized trials of MHT through the Women’s Health Initiative (WHI) to test whether the association with reduced risk for CHD found in observational studies was real and to obtain reliable information on the overall risks and benefits regarding the prevention of chronic disease for postmenopausal women aged 50-79 years.

The WHI trials tested standard-dose oral CEEs with and without standard-dose continuous medroxyprogesterone acetate (EPT). In 2002, the results of the WHI studies raised a series of concerns about the long-term safety of MHT, in particular the finding of an increased risk of breast cancer for women undergoing therapy. That risk exceeded the benefits from reductions in hip fractures and colorectal cancer.

The WHI findings received wide attention. Prescriptions for MHT dropped precipitously after 2002 and continued to decline in subsequent years. Declines were most marked for standard-dose EPT and in older women. The results of the CEE study were less negative, compared with those for EPT, as they showed no effect on CHD, a nonsignificant reduction in the risk of breast cancer, and a more favorable risk-benefit ratio for younger women, compared with older women. A decade later, it had become widely accepted that MHT should not be used for the prevention of chronic disease in older women; however, short-term use for treatment of vasomotor symptoms remains an accepted indication.
 

Risks and outcomes

Emerging from a series of WHI reports are complex models on the effect of hormonal therapy on the risk and outcome of breast cancer. In one study, women with an intact uterus received CEEs plus medroxyprogesterone acetate (MPA). An increase in the risk of breast cancer was observed over a median of 5.6 years of treatment, followed by a moderate reduction, with the risk increasing after 13 years of cumulative follow-up. For women treated with CEE alone, the reduction in risk observed over an average of 7.2 years of treatment was maintained for 13 years of follow-up.

Results from observational studies contrast with those from randomized controlled trials, particularly those concerning the use of estrogens only. A meta-analysis by the Collaborative Group on Hormonal Factors in Breast Cancer showed that both EPT and CEE were associated with a higher risk of breast neoplasia. Results of the Million Women Study showed a higher death rate.
 

Treatment methods and duration

Information from prospective studies on the effects of commencing MHT at various ages between 40 and 59 years show that for women who commenced treatment at any time within this age range, the relative risk was similar and was highly significant for all ages. Few women had started MHT treatment well after menopause at ages 60-69 years, and their excess risks during years 5-14 of current use were significant for estrogen-progestogen but not for estrogen-only MHT.

If these associations are largely causal, then for women of average weight in developed countries, 5 years of MHT, starting at age 50 years, would increase breast cancer incidence at ages 50-69 years by about 1 in every 50 users of estrogen plus daily progestogen preparations; 1 in every 70 users of estrogen plus intermittent progestogen preparations; and 1 in every 200 users of estrogen-only preparations. The corresponding excesses from 10 years of MHT would be about twice as great.

During 5-14 years of MHT use, the RRs were similarly increased if MHT use had started at ages 40-44 years, 45-49 years, 50-54 years, and 55-59 years; RRs appeared to be attenuated if MHT use had started after age 60 years. They were also attenuated by adiposity, particularly for estrogen-only MHT (which had little effect in obese women). After MHT use ceased, some excess risk of breast cancer persisted for more than a decade; this is directly correlated with the duration of treatment.

Therefore, it can be expected that the effects of MHT may vary between participants on the basis of age or time since menopause, as well as treatments (MHT type, dose, formulation, duration of use, and route of administration). Regarding formulation effects on the risk of breast cancer, new evidence shows an increased risk of 28%. Progestogens appeared to be differentially associated with breast cancer (micronized progesterone: odds ratio, 0.99; 95% confidence interval 0.55-1.79; synthetic progestin: OR, 1.28; 95% CI, 1.22-1.35). When prescribing MHT, micronized progesterone may be the safer progestogen to use.

In conclusion, MHT has a complex balance of benefits and risk on various health outcomes. Some effects differ qualitatively between ET and EPT. Regarding use of MHT, consideration should be given to the full range of effects, along with patients’ values and preferences. The overall quality of existing systematic reviews is moderate to poor. Clinicians should evaluate their scientific strength before considering applying their results in clinical practice. Regarding use of any hormone therapy regimen, consideration should be given to the full range of risk and benefits and should involve shared decisionmaking with the patient. It should be recognized that risk-benefit balance is altered by factors such as age, time from menopause, oophorectomy status, and prior hysterectomy and that some outcomes persist and there is some attenuation after stopping use.

This article was translated from Univadis Italy.

A version of the article appeared on Medscape.com.

It is projected that by 2050, 1.6 billion women in the world will have reached menopause or the postmenopausal period, a significant increase, compared with a billion women in 2020. Of all menopausal women, around 75% are affected by troublesome menopause symptoms, such as hot flashes and night sweats.

Around 84% of postmenopausal women experience genitourinary symptoms, such as vulvovaginal atrophy and incontinence.

Menopausal hormone therapy (MHT) is the most effective treatment for managing these symptoms; however, its effects on numerous aspects of female health remain uncertain, in particular with regard to breast cancer. The influence of MHT on breast cancer remains unsettled, with discordant findings from observational studies and randomized clinical trials, a factor that affects the decisions made by doctors concerning hormone therapy in menopausal women.
 

Background

Conjugated equine estrogens (CEEs) were introduced into clinical practice in the 1940s. For decades, MHT was the main treatment in conventional medicine for the symptoms of menopause. MHT was used in Western countries for about 600 million women starting from 1970, and it progressively increased during the 1990s. Professional organizations recommended MHT for the prevention of osteoporosis and chronic heart disease (CHD), and a third of prescriptions were for women older than 60 years.

Against this background, the National Institutes of Health launched randomized trials of MHT through the Women’s Health Initiative (WHI) to test whether the association with reduced risk for CHD found in observational studies was real and to obtain reliable information on the overall risks and benefits regarding the prevention of chronic disease for postmenopausal women aged 50-79 years.

The WHI trials tested standard-dose oral CEEs with and without standard-dose continuous medroxyprogesterone acetate (EPT). In 2002, the results of the WHI studies raised a series of concerns about the long-term safety of MHT, in particular the finding of an increased risk of breast cancer for women undergoing therapy. That risk exceeded the benefits from reductions in hip fractures and colorectal cancer.

The WHI findings received wide attention. Prescriptions for MHT dropped precipitously after 2002 and continued to decline in subsequent years. Declines were most marked for standard-dose EPT and in older women. The results of the CEE study were less negative, compared with those for EPT, as they showed no effect on CHD, a nonsignificant reduction in the risk of breast cancer, and a more favorable risk-benefit ratio for younger women, compared with older women. A decade later, it had become widely accepted that MHT should not be used for the prevention of chronic disease in older women; however, short-term use for treatment of vasomotor symptoms remains an accepted indication.
 

Risks and outcomes

Emerging from a series of WHI reports are complex models on the effect of hormonal therapy on the risk and outcome of breast cancer. In one study, women with an intact uterus received CEEs plus medroxyprogesterone acetate (MPA). An increase in the risk of breast cancer was observed over a median of 5.6 years of treatment, followed by a moderate reduction, with the risk increasing after 13 years of cumulative follow-up. For women treated with CEE alone, the reduction in risk observed over an average of 7.2 years of treatment was maintained for 13 years of follow-up.

Results from observational studies contrast with those from randomized controlled trials, particularly those concerning the use of estrogens only. A meta-analysis by the Collaborative Group on Hormonal Factors in Breast Cancer showed that both EPT and CEE were associated with a higher risk of breast neoplasia. Results of the Million Women Study showed a higher death rate.
 

Treatment methods and duration

Information from prospective studies on the effects of commencing MHT at various ages between 40 and 59 years show that for women who commenced treatment at any time within this age range, the relative risk was similar and was highly significant for all ages. Few women had started MHT treatment well after menopause at ages 60-69 years, and their excess risks during years 5-14 of current use were significant for estrogen-progestogen but not for estrogen-only MHT.

If these associations are largely causal, then for women of average weight in developed countries, 5 years of MHT, starting at age 50 years, would increase breast cancer incidence at ages 50-69 years by about 1 in every 50 users of estrogen plus daily progestogen preparations; 1 in every 70 users of estrogen plus intermittent progestogen preparations; and 1 in every 200 users of estrogen-only preparations. The corresponding excesses from 10 years of MHT would be about twice as great.

During 5-14 years of MHT use, the RRs were similarly increased if MHT use had started at ages 40-44 years, 45-49 years, 50-54 years, and 55-59 years; RRs appeared to be attenuated if MHT use had started after age 60 years. They were also attenuated by adiposity, particularly for estrogen-only MHT (which had little effect in obese women). After MHT use ceased, some excess risk of breast cancer persisted for more than a decade; this is directly correlated with the duration of treatment.

Therefore, it can be expected that the effects of MHT may vary between participants on the basis of age or time since menopause, as well as treatments (MHT type, dose, formulation, duration of use, and route of administration). Regarding formulation effects on the risk of breast cancer, new evidence shows an increased risk of 28%. Progestogens appeared to be differentially associated with breast cancer (micronized progesterone: odds ratio, 0.99; 95% confidence interval 0.55-1.79; synthetic progestin: OR, 1.28; 95% CI, 1.22-1.35). When prescribing MHT, micronized progesterone may be the safer progestogen to use.

In conclusion, MHT has a complex balance of benefits and risk on various health outcomes. Some effects differ qualitatively between ET and EPT. Regarding use of MHT, consideration should be given to the full range of effects, along with patients’ values and preferences. The overall quality of existing systematic reviews is moderate to poor. Clinicians should evaluate their scientific strength before considering applying their results in clinical practice. Regarding use of any hormone therapy regimen, consideration should be given to the full range of risk and benefits and should involve shared decisionmaking with the patient. It should be recognized that risk-benefit balance is altered by factors such as age, time from menopause, oophorectomy status, and prior hysterectomy and that some outcomes persist and there is some attenuation after stopping use.

This article was translated from Univadis Italy.

A version of the article appeared on Medscape.com.