Mixed Topics

An elevated serum level of cholesterol has been recognized as a risk factor for atherosclerotic cardiovascular disease (ASCVD) since the publication of the Framingham Study in 1961.¹ Although clinical outcomes related to ASCVD have improved in recent decades, ASCVD remains the leading cause of morbidity and mortality across the globe and remains, in the United States, the leading cause of death among most racial and ethnic groups. Much of this persistent disease burden can be attributed to inadequate control of ­ASCVD risk factors and suboptimal implementation of prevention strategies in the general population.²

Copyright KO Studios

Much of the persistent disease burden can be attributed to inadequate control of ASCVD risk factors and suboptimal implementation of prevention strategies in the general population.

The most recent (2019) iteration of the American College of Cardiology/American Heart Association (ACC/AHA) Guideline on the Primary Prevention of Cardiovascular Disease emphasizes a comprehensive, patient-centered, team-based approach to the management of ASCVD risk factors.² In this article, I review how, first, medication to reduce ASCVD risk should be considered only when a patient’s risk is sufficiently high and, second, shared decision-making and social determinants of health should, in all cases, guide and inform optimal implementation of treatment.²

Estimating risk for ASCVDby ascertaining LDL-C

The Friedewald equation. Traditionally, low-density lipoprotein cholesterol (LDL-C) is estimated using the Friedewald equation^a applied to a fasting lipid profile. In patients who have a low level of LDL-C (< 70 mg/dL), however, the Friedewald equation becomes less accurate; in patients with hypertriglyceridemia (TG ≥ 400 mg/dL), estimation of LDL-C is invalid.

The Martin–Hopkins equation offers a validated estimation of LDL-C when the LDL-C value is < 70 mg/dL.³ This equation—in which the fixed factor of 5 used in the Friedewald equation to estimate very-low-density lipoprotein cholesterol is replaced by an adjustable factor that is based on the patient’s non-HDL-C (ie, TC – HDL-C) and TG values—is preferred by the ACC/AHA Task Force on Clinical Practice Guidelines in this clinical circumstance.⁴

National Institutes of Health equation. This newer equation provides an accurate estimate of the LDL-C level in patients whose TG value is ≤ 800 mg/dL. The equation has not been fully validated for clinical use, however.⁵

Direct measurement obviates the need for an equation to estimate LDL-C, but the test is not available in all health care settings.

For adults ≥ 20 years of age who are not receiving lipid-lowering therapy, a nonfasting lipid profile can be used to estimate ­ASCVD risk and document the baseline LDL-C level. If the TG level is ≥ 400 mg/dL, the test should be administered in the fasting state.⁴

Continue to: Apolipoprotein B

Apolipoprotein B. Alternatively, apolipoprotein B (apoB) can be measured. Because each LDL-C particle contains 1 apoB molecule, the apoB level describes the ­LDL-C level more accurately than a calculation of LDL-C. Many patients with type 2 diabetes and metabolic syndrome have a relatively low calculated LDL-C (thereby falsely reassuring the testing clinician) but have an elevated apoB level. An apoB level ≥ 130 mg/dL corresponds to an LDL-C level >160 mg/dL.⁴

Calculation of non-HDL-C. Because the nonfasting state does not have a significant impact on a patient’s TC and HDL-C levels, the non-HDL-C level also can be calculated from the results of a nonfasting lipid profile.

Non-HDL-C and apoB are equivalent predictors of ASCVD risk. These 2 assessments might offer better risk estimation than other available tools in patients who have type 2 diabetes and metabolic syndrome.⁶

Applying the estimate of 10-year ASCVD risk

Your recommendation for preventive intervention, such as lipid-lowering therapy, should be based on the estimated 10-year risk for ASCVD. Although multiple validated risk assessment tools are available, ACC/AHA recommends the pooled cohort risk equations (PCE), introduced in the 2013 ACC/AHA cholesterol treatment guidelines. The Framingham Heart Study now recommends the ACC/AHA PCE for risk assessment as well.⁷

The PCE, developed from 5 large cohorts, is based on hard atherosclerotic events: nonfatal myocardial infarction, death from coronary artery disease, and stroke. The ACC/AHA PCE is the only risk assessment tool developed using a significant percentage of patients who self-identify as Black.⁸ Alternatives to the ACC/AHA PCE include:

• Multi-ethnic Study of Atherosclerosis (MESA) 10-year ASCVD risk calculator, which incorporates the coronary artery calcium (CAC) score.
• Reynolds Risk Score, which incorporates high-sensitivity C-reactive protein measurement and a family history of premature ASCVD.⁹

Continue to: How much does lifestyle modification actually matter?

 

 

How much does lifestyle modification actually matter?

The absolute impact of diet and exercise on lipid parameters is relatively modest. No studies have demonstrated a reduction in adverse cardiovascular outcomes with specific interventions regarding diet or activity.

Diet. Nevertheless, ACC/AHA recommends that at-risk patients follow a dietary pattern that (1) emphasizes vegetables, fruits, and whole grains and (2) limits sweets, sugar-sweetened beverages, and red meat.

For adults ≥ 20 years of age who are not receiving lipid-lowering therapy, a nonfasting lipid profile can be used to estimate ASCVD risk and document the baseline LDL-C level.

Saturated fat should constitute no more than 5% or 6% of total calories. In controlled-feeding trials,¹⁰ for every 1% of calories from saturated fat that are replaced with carbohydrate or monounsaturated or polyunsaturated fat, the LDL-C level was found to decline by as much as 1.8 mg/dL. Evidence is insufficient to assert that lowering dietary cholesterol reduces LDL-C.¹¹

Activity. Trials of aerobic physical activity, compared with a more sedentary activity pattern, have demonstrated a reduction in the LDL-C level of as much as 6 mg/dL. All adult patients should be counseled to engage in aerobic physical activity of moderate or vigorous intensity—averaging ≥ 40 minutes per session, 3 or 4 sessions per week.¹¹

Primary prevention:Stratification by age

40 to 75 years. ACC/AHA recommends that you routinely assess traditional cardiovascular risk factors for these patients and calculate their 10-year risk for ASCVD using the PCE. Statin therapy as primary prevention is indicated for 3 major groups (TABLE 1).⁴ The US Preventive Services Task Force ­(USPSTF) recommends a 10-year ASCVD risk ≥ 10%, in conjunction with 1 or more additional CVD risk factors (dyslipidemia, diabetes, hypertension, smoking), as the threshold for initiating low- or moderate-intensity statin therapy in this age group.¹²

Continue to: In adults at borderline risk...

In adults at borderline risk (5% to < 7.5% 10-year ASCVD risk) or intermediate risk (≥ 7.5% to < 20% 10-year ASCVD risk), consider risk-enhancing factors to better inform your recommendation for preventive interventions. In these 2 groups, the presence of risk-enhancing factors might justify ­moderate-intensity statin therapy (TABLE 2⁴).

If your decision regarding preventive intervention remains uncertain, measuring CAC might further guide your discussion with the patient.⁴ When the CAC score is:

• 0 Agatston units and higher-risk conditions (eg, diabetes, family history of premature coronary artery disease, smoking) are absent, statin therapy can be withheld; reassess ASCVD risk in 5 to 10 years.
• 1-99 Agatston units, statin therapy can be started, especially for patients ≥ 55 years of age.
• ≥ 100 Agatston units or ≥ 75th percentile, statin therapy is indicated for all patients, regardless of additional risk factors.⁴

Because statins promote progression from unstable, inflammatory atherosclerotic plaque to more stable, calcified plaque, CAC scoring is not valid in patients already on statin therapy.¹³

In primary prevention, patients who have been classified as having low or intermediate risk, based on ASCVD risk scoring, with a CAC score of 0 Agatston units, have an annual all-cause mortality < 1%, regardless of age and gender. Patients classified as being at high risk, based on ASCVD risk scoring, with a CAC score of 0 Agatston units, have a significantly lower annual mortality than low- or intermediate-risk patients with a CAC score > 0 Agatston units.¹⁴

20 to 39 years. Focus on evaluation of lifetime ASCVD risk, rather than short-term (10-year) risk. Lifestyle modification is the primary intervention for younger patients; for those with moderate hypercholesterolemia (LDL-C, 160-189 mg/dL) and a family history of premature ASCVD, however, consider statin therapy. For patients with LDL-C ≥ 190 mg/dL, lifetime ASCVD risk is markedly increased, and high-intensity statin therapy is recommended, regardless of age. In this group, reassess ASCVD risk factors every 4 to 6 years.⁴

Continue to: > 75 years, without ASCVD

> 75 years, without ASCVD. In this group, the ­benefit of statin therapy is less clear and might be lessened by an increased potential for adverse effects. A meta-analysis of 28 trials demonstrated that people ages > 75 years had a 24% relative reduction in major coronary events for every 38.7 mg/dL (1.0 mmol/L) reduction in LDL-C, which is comparable to the risk reduction seen in people ages 40 to 75 years.¹⁵

A meta-analysis of 28 trials demonstrated that people > 75 years of age had a 24% relative reduction in major coronary events for every 38.7 mg/dL (1.0 mmol/L) reduction in LDL-C.

With increasing age, however, the relative reduction in major coronary events with statin therapy decreased,¹⁵ although other trials have not demonstrated age heterogeneity.¹⁶ Because people > 75 years of age have a significantly higher ASCVD event rate, a comparable relative rate reduction with statin therapy results in a larger absolute rate reduction (ARR) and, therefore, a smaller number needed to treat (NNT) to prevent an event, compared to the NNT in younger people.

Secondary prevention

ACC/AHA guidelines define clinical ASCVD as a history of:

• acute coronary syndrome
• myocardial infarction
• coronary or other arterial revascularization
• cerebrovascular event
• symptomatic peripheral artery disease, including aortic aneurysm.

High-intensity statin therapy is indicated for all patients ≤ 75 years who have clinical ­ASCVD. In patients > 75 years, consider a taper to moderate-intensity statin therapy. An upper age limit for seeing benefit from statin therapy in secondary prevention has not been identified.⁴

Base a recommendation for preventive intervention, such as lipidlowering therapy, on the estimated 10-year risk for ASCVD.

In high-risk patients, if LDL-C remains ≥ 70 mg/dL despite maximally tolerated statin therapy, ezetimibe (discussed in the next section) can be added. In very-high-risk patients, if LDL-C remains ≥ 70 mg/dL despite maximally tolerated statin therapy plus ezetimibe, a proprotein convertase subtilisin/­kexin type 9 (PCSK9) inhibitor (also discussed next) can be added. Always precede initiation of a PCSK9 inhibitor with a discussion of the net benefit, safety, and cost with the patient.⁴

Continue to: Options for lipid-lowering pharmacotherapy

 

 

Options for lipid-lowering pharmacotherapy

Statins (formally, hydroxymethylglutaryl-coenzyme A reductase inhibitors) offer the most predictable reduction in ASCVD risk of any lipid-lowering therapy. The evidence report that accompanied the 2016 USPSTF guidelines on statins for the prevention of cardiovascular disease (CVD) stated that low- or moderate-dosage statin therapy is associated with approximately a 30% relative risk reduction (RRR) in CVD events and CVD deaths and a 10% to 15% RRR in all-cause mortality.¹⁷

High-intensity statin therapy reduces LDL-C by ≥ 50%. Moderate-intensity statin therapy reduces LDL-C by 30% to 49% (TABLE 3).⁴

Statins are not without risk: A 2016 report¹⁸ estimated that treating 10,000 patients with a statin for 5 years would cause 1 case of rhabdomyolysis, 5 cases of myopathy, 75 new cases of diabetes, and 7 cases of hemorrhagic stroke. The same treatment would, however, avert approximately 1000 CVD events among patients with preexisting disease and approximately 500 CVD events among patients at elevated risk but without preexisting disease.¹⁸

Ezetimibe, a selective cholesterol-­absorption inhibitor, lowers LDL-C by 13% to 20% and typically is well tolerated. The use of ezetimibe in ASCVD risk reduction is supported by a single randomized controlled trial of more than 18,000 patients with recent acute coronary syndrome. Adding ezetimibe to simvastatin 40 mg resulted in a 2% absolute reduction in major adverse cardiovascular events over a median follow-up of 6 years (NNT = 50), compared to simvastatin alone.¹⁹ ACC/AHA guidelines recommend adding ezetimibe to maximally tolerated statin therapy in patients with clinical ASCVD who do not reach their goal LDL reduction with a statin alone. Ezetimibe also can be considered a statin alternative in patients who are statin intolerant.⁴

PCSK9 inhibitors. When added to statin therapy, evolocumab and alirocumab—monoclonal antibodies that inhibit PCSK9—offer an incremental decrease in LDL-C of approximately 60%.^20-22 In a meta-analysis of 35 trials evaluating the incremental benefit of PCSK9 inhibitor therapy, a significant reduction in cardiovascular events, including myocardial infarction (ARR = 1.3%; NNT = 77), stroke (ARR = 0.4%; NNT = 250), and coronary revascularization (ARR = 1.6%; NNT = 63) was reported. No significant difference was observed in all-cause or cardiovascular mortality.^21,23

Continue to: Inclisiran

Inclisiran, an injectable small-­interfering RNA that inhibits PCSK9 synthesis, provides an incremental decrease in LDL-C of > 50% in patients already receiving statin therapy. Meta-analysis of 3 small cardiovascular outcomes trials revealed no significant difference in the rate of myocardial infarction, stroke, or cardiovascular mortality with inclisiran compared to placebo. Larger outcomes trials are underway and might offer additional insight into this agent’s role in ASCVD risk management.²⁴

Omega-3 fatty acids. Multiple trials have demonstrated that adding omega-3 fatty acids to usual lipid-lowering therapy does not offer a consistent reduction in adverse cardiovascular outcomes, despite providing a significant reduction in TG levels. In a high-risk population with persistently elevated TG despite statin therapy, icosapent ethyl, a purified eicosapentaenoic acid ethyl ester, reduced major ASCVD outcomes by 25% over a median 4.9 years (ARR = 4.8%; NNT = 21), and cardiovascular death by 20% (ARR = 0.9%; NNT = 111), compared with a mineral oil placebo.²⁵ Subsequent trials, using a corn oil placebo, failed to duplicate these data²⁶—raising concern that the mineral oil comparator might have altered results of the eicosapentaenoic acid ethyl ester study.^27,28

Bempedoic acid is a small-molecule ­inhibitor of ATP citrate lyase that increases LDL uptake by the liver. Pooled data from studies of bempedoic acid show, on average, a 15% reduction in TC, a 23% reduction in LDL-C, and a 6% increase in HDL-C, without a significant change in TG.²⁹ In statin-­intolerant patients, bempedoic acid reduced major ASCVD outcomes by 13% over a median 40 months (ARR = 1.6%; NNT = 63), with no significant reduction in cardiovascular death.³⁰

Niacin. Two large trials failed to demonstrate improvement in major cardiovascular events or other clinical benefit when niacin is added to moderate-intensity statin therapy, despite a significant increase in the HDL-C level (on average, 6 mg/dL) and a decrease in the LDL-C level (10-12 mg/dL) and TG (42 mg/dL).^31,32

Fenofibrate lowers TG and increases HDL-C but does not consistently improve cardiovascular outcomes.³³ In a trial of patients with type 2 diabetes and persistent dyslipidemia (serum TG > 204 mg/dL; ­HDL-C < 34 mg/dL) despite statin therapy, adding fenofibrate reduced CVD outcomes by 4.9%—although this absolute difference did not reach statistical significance.³⁴

Neither niacin nor fenofibrate is considered useful for reducing ASCVD risk across broad populations.

Neither niacin nor fenofibrate is considered useful for reducing ASCVD risk across broad populations.⁴

Follow-up to assess progress toward goals

At-risk patients should follow a dietary pattern that emphasizes vegetables, fruits, and whole grains and limits sweets, sugarsweetened beverages, and red meat.

Recheck the lipid profile 4 to 12 weeks after starting lipid-lowering therapy to verify adherence to medication and assess response. The primary goal is the percentage reduction in LDL-C based on ASCVD risk. An additional goal for very-high-risk patients is an LDL-C value ≤ 70 mg/dL. If the reduction in LDL-C is less than desired and adherence is assured, consider titrating the statin dosage or augmenting statin therapy with a nonstatin drug (eg, ezetimibe), or both.⁴

CORRESPONDENCE
Jonathon M. Firnhaber, MD, MAEd, MBA, East Carolina University, Family Medicine Center, 101 Heart Drive, Greenville, NC 27834; [email protected]

An elevated serum level of cholesterol has been recognized as a risk factor for atherosclerotic cardiovascular disease (ASCVD) since the publication of the Framingham Study in 1961.¹ Although clinical outcomes related to ASCVD have improved in recent decades, ASCVD remains the leading cause of morbidity and mortality across the globe and remains, in the United States, the leading cause of death among most racial and ethnic groups. Much of this persistent disease burden can be attributed to inadequate control of ­ASCVD risk factors and suboptimal implementation of prevention strategies in the general population.²

Copyright KO Studios

Much of the persistent disease burden can be attributed to inadequate control of ASCVD risk factors and suboptimal implementation of prevention strategies in the general population.

The most recent (2019) iteration of the American College of Cardiology/American Heart Association (ACC/AHA) Guideline on the Primary Prevention of Cardiovascular Disease emphasizes a comprehensive, patient-centered, team-based approach to the management of ASCVD risk factors.² In this article, I review how, first, medication to reduce ASCVD risk should be considered only when a patient’s risk is sufficiently high and, second, shared decision-making and social determinants of health should, in all cases, guide and inform optimal implementation of treatment.²

Estimating risk for ASCVDby ascertaining LDL-C

The Friedewald equation. Traditionally, low-density lipoprotein cholesterol (LDL-C) is estimated using the Friedewald equation^a applied to a fasting lipid profile. In patients who have a low level of LDL-C (< 70 mg/dL), however, the Friedewald equation becomes less accurate; in patients with hypertriglyceridemia (TG ≥ 400 mg/dL), estimation of LDL-C is invalid.

The Martin–Hopkins equation offers a validated estimation of LDL-C when the LDL-C value is < 70 mg/dL.³ This equation—in which the fixed factor of 5 used in the Friedewald equation to estimate very-low-density lipoprotein cholesterol is replaced by an adjustable factor that is based on the patient’s non-HDL-C (ie, TC – HDL-C) and TG values—is preferred by the ACC/AHA Task Force on Clinical Practice Guidelines in this clinical circumstance.⁴

National Institutes of Health equation. This newer equation provides an accurate estimate of the LDL-C level in patients whose TG value is ≤ 800 mg/dL. The equation has not been fully validated for clinical use, however.⁵

Direct measurement obviates the need for an equation to estimate LDL-C, but the test is not available in all health care settings.

For adults ≥ 20 years of age who are not receiving lipid-lowering therapy, a nonfasting lipid profile can be used to estimate ­ASCVD risk and document the baseline LDL-C level. If the TG level is ≥ 400 mg/dL, the test should be administered in the fasting state.⁴

Continue to: Apolipoprotein B

Apolipoprotein B. Alternatively, apolipoprotein B (apoB) can be measured. Because each LDL-C particle contains 1 apoB molecule, the apoB level describes the ­LDL-C level more accurately than a calculation of LDL-C. Many patients with type 2 diabetes and metabolic syndrome have a relatively low calculated LDL-C (thereby falsely reassuring the testing clinician) but have an elevated apoB level. An apoB level ≥ 130 mg/dL corresponds to an LDL-C level >160 mg/dL.⁴

Calculation of non-HDL-C. Because the nonfasting state does not have a significant impact on a patient’s TC and HDL-C levels, the non-HDL-C level also can be calculated from the results of a nonfasting lipid profile.

Non-HDL-C and apoB are equivalent predictors of ASCVD risk. These 2 assessments might offer better risk estimation than other available tools in patients who have type 2 diabetes and metabolic syndrome.⁶

Applying the estimate of 10-year ASCVD risk

Your recommendation for preventive intervention, such as lipid-lowering therapy, should be based on the estimated 10-year risk for ASCVD. Although multiple validated risk assessment tools are available, ACC/AHA recommends the pooled cohort risk equations (PCE), introduced in the 2013 ACC/AHA cholesterol treatment guidelines. The Framingham Heart Study now recommends the ACC/AHA PCE for risk assessment as well.⁷

The PCE, developed from 5 large cohorts, is based on hard atherosclerotic events: nonfatal myocardial infarction, death from coronary artery disease, and stroke. The ACC/AHA PCE is the only risk assessment tool developed using a significant percentage of patients who self-identify as Black.⁸ Alternatives to the ACC/AHA PCE include:

• Multi-ethnic Study of Atherosclerosis (MESA) 10-year ASCVD risk calculator, which incorporates the coronary artery calcium (CAC) score.
• Reynolds Risk Score, which incorporates high-sensitivity C-reactive protein measurement and a family history of premature ASCVD.⁹

Continue to: How much does lifestyle modification actually matter?

 

 

How much does lifestyle modification actually matter?

The absolute impact of diet and exercise on lipid parameters is relatively modest. No studies have demonstrated a reduction in adverse cardiovascular outcomes with specific interventions regarding diet or activity.

Diet. Nevertheless, ACC/AHA recommends that at-risk patients follow a dietary pattern that (1) emphasizes vegetables, fruits, and whole grains and (2) limits sweets, sugar-sweetened beverages, and red meat.

For adults ≥ 20 years of age who are not receiving lipid-lowering therapy, a nonfasting lipid profile can be used to estimate ASCVD risk and document the baseline LDL-C level.

Saturated fat should constitute no more than 5% or 6% of total calories. In controlled-feeding trials,¹⁰ for every 1% of calories from saturated fat that are replaced with carbohydrate or monounsaturated or polyunsaturated fat, the LDL-C level was found to decline by as much as 1.8 mg/dL. Evidence is insufficient to assert that lowering dietary cholesterol reduces LDL-C.¹¹

Activity. Trials of aerobic physical activity, compared with a more sedentary activity pattern, have demonstrated a reduction in the LDL-C level of as much as 6 mg/dL. All adult patients should be counseled to engage in aerobic physical activity of moderate or vigorous intensity—averaging ≥ 40 minutes per session, 3 or 4 sessions per week.¹¹

Primary prevention:Stratification by age

40 to 75 years. ACC/AHA recommends that you routinely assess traditional cardiovascular risk factors for these patients and calculate their 10-year risk for ASCVD using the PCE. Statin therapy as primary prevention is indicated for 3 major groups (TABLE 1).⁴ The US Preventive Services Task Force ­(USPSTF) recommends a 10-year ASCVD risk ≥ 10%, in conjunction with 1 or more additional CVD risk factors (dyslipidemia, diabetes, hypertension, smoking), as the threshold for initiating low- or moderate-intensity statin therapy in this age group.¹²

Continue to: In adults at borderline risk...

In adults at borderline risk (5% to < 7.5% 10-year ASCVD risk) or intermediate risk (≥ 7.5% to < 20% 10-year ASCVD risk), consider risk-enhancing factors to better inform your recommendation for preventive interventions. In these 2 groups, the presence of risk-enhancing factors might justify ­moderate-intensity statin therapy (TABLE 2⁴).

If your decision regarding preventive intervention remains uncertain, measuring CAC might further guide your discussion with the patient.⁴ When the CAC score is:

• 0 Agatston units and higher-risk conditions (eg, diabetes, family history of premature coronary artery disease, smoking) are absent, statin therapy can be withheld; reassess ASCVD risk in 5 to 10 years.
• 1-99 Agatston units, statin therapy can be started, especially for patients ≥ 55 years of age.
• ≥ 100 Agatston units or ≥ 75th percentile, statin therapy is indicated for all patients, regardless of additional risk factors.⁴

Because statins promote progression from unstable, inflammatory atherosclerotic plaque to more stable, calcified plaque, CAC scoring is not valid in patients already on statin therapy.¹³

In primary prevention, patients who have been classified as having low or intermediate risk, based on ASCVD risk scoring, with a CAC score of 0 Agatston units, have an annual all-cause mortality < 1%, regardless of age and gender. Patients classified as being at high risk, based on ASCVD risk scoring, with a CAC score of 0 Agatston units, have a significantly lower annual mortality than low- or intermediate-risk patients with a CAC score > 0 Agatston units.¹⁴

20 to 39 years. Focus on evaluation of lifetime ASCVD risk, rather than short-term (10-year) risk. Lifestyle modification is the primary intervention for younger patients; for those with moderate hypercholesterolemia (LDL-C, 160-189 mg/dL) and a family history of premature ASCVD, however, consider statin therapy. For patients with LDL-C ≥ 190 mg/dL, lifetime ASCVD risk is markedly increased, and high-intensity statin therapy is recommended, regardless of age. In this group, reassess ASCVD risk factors every 4 to 6 years.⁴

Continue to: > 75 years, without ASCVD

> 75 years, without ASCVD. In this group, the ­benefit of statin therapy is less clear and might be lessened by an increased potential for adverse effects. A meta-analysis of 28 trials demonstrated that people ages > 75 years had a 24% relative reduction in major coronary events for every 38.7 mg/dL (1.0 mmol/L) reduction in LDL-C, which is comparable to the risk reduction seen in people ages 40 to 75 years.¹⁵

A meta-analysis of 28 trials demonstrated that people > 75 years of age had a 24% relative reduction in major coronary events for every 38.7 mg/dL (1.0 mmol/L) reduction in LDL-C.

With increasing age, however, the relative reduction in major coronary events with statin therapy decreased,¹⁵ although other trials have not demonstrated age heterogeneity.¹⁶ Because people > 75 years of age have a significantly higher ASCVD event rate, a comparable relative rate reduction with statin therapy results in a larger absolute rate reduction (ARR) and, therefore, a smaller number needed to treat (NNT) to prevent an event, compared to the NNT in younger people.

Secondary prevention

ACC/AHA guidelines define clinical ASCVD as a history of:

• acute coronary syndrome
• myocardial infarction
• coronary or other arterial revascularization
• cerebrovascular event
• symptomatic peripheral artery disease, including aortic aneurysm.

High-intensity statin therapy is indicated for all patients ≤ 75 years who have clinical ­ASCVD. In patients > 75 years, consider a taper to moderate-intensity statin therapy. An upper age limit for seeing benefit from statin therapy in secondary prevention has not been identified.⁴

Base a recommendation for preventive intervention, such as lipidlowering therapy, on the estimated 10-year risk for ASCVD.

In high-risk patients, if LDL-C remains ≥ 70 mg/dL despite maximally tolerated statin therapy, ezetimibe (discussed in the next section) can be added. In very-high-risk patients, if LDL-C remains ≥ 70 mg/dL despite maximally tolerated statin therapy plus ezetimibe, a proprotein convertase subtilisin/­kexin type 9 (PCSK9) inhibitor (also discussed next) can be added. Always precede initiation of a PCSK9 inhibitor with a discussion of the net benefit, safety, and cost with the patient.⁴

Continue to: Options for lipid-lowering pharmacotherapy

 

 

Options for lipid-lowering pharmacotherapy

Statins (formally, hydroxymethylglutaryl-coenzyme A reductase inhibitors) offer the most predictable reduction in ASCVD risk of any lipid-lowering therapy. The evidence report that accompanied the 2016 USPSTF guidelines on statins for the prevention of cardiovascular disease (CVD) stated that low- or moderate-dosage statin therapy is associated with approximately a 30% relative risk reduction (RRR) in CVD events and CVD deaths and a 10% to 15% RRR in all-cause mortality.¹⁷

High-intensity statin therapy reduces LDL-C by ≥ 50%. Moderate-intensity statin therapy reduces LDL-C by 30% to 49% (TABLE 3).⁴

Statins are not without risk: A 2016 report¹⁸ estimated that treating 10,000 patients with a statin for 5 years would cause 1 case of rhabdomyolysis, 5 cases of myopathy, 75 new cases of diabetes, and 7 cases of hemorrhagic stroke. The same treatment would, however, avert approximately 1000 CVD events among patients with preexisting disease and approximately 500 CVD events among patients at elevated risk but without preexisting disease.¹⁸

Ezetimibe, a selective cholesterol-­absorption inhibitor, lowers LDL-C by 13% to 20% and typically is well tolerated. The use of ezetimibe in ASCVD risk reduction is supported by a single randomized controlled trial of more than 18,000 patients with recent acute coronary syndrome. Adding ezetimibe to simvastatin 40 mg resulted in a 2% absolute reduction in major adverse cardiovascular events over a median follow-up of 6 years (NNT = 50), compared to simvastatin alone.¹⁹ ACC/AHA guidelines recommend adding ezetimibe to maximally tolerated statin therapy in patients with clinical ASCVD who do not reach their goal LDL reduction with a statin alone. Ezetimibe also can be considered a statin alternative in patients who are statin intolerant.⁴

PCSK9 inhibitors. When added to statin therapy, evolocumab and alirocumab—monoclonal antibodies that inhibit PCSK9—offer an incremental decrease in LDL-C of approximately 60%.^20-22 In a meta-analysis of 35 trials evaluating the incremental benefit of PCSK9 inhibitor therapy, a significant reduction in cardiovascular events, including myocardial infarction (ARR = 1.3%; NNT = 77), stroke (ARR = 0.4%; NNT = 250), and coronary revascularization (ARR = 1.6%; NNT = 63) was reported. No significant difference was observed in all-cause or cardiovascular mortality.^21,23

Continue to: Inclisiran

Inclisiran, an injectable small-­interfering RNA that inhibits PCSK9 synthesis, provides an incremental decrease in LDL-C of > 50% in patients already receiving statin therapy. Meta-analysis of 3 small cardiovascular outcomes trials revealed no significant difference in the rate of myocardial infarction, stroke, or cardiovascular mortality with inclisiran compared to placebo. Larger outcomes trials are underway and might offer additional insight into this agent’s role in ASCVD risk management.²⁴

Omega-3 fatty acids. Multiple trials have demonstrated that adding omega-3 fatty acids to usual lipid-lowering therapy does not offer a consistent reduction in adverse cardiovascular outcomes, despite providing a significant reduction in TG levels. In a high-risk population with persistently elevated TG despite statin therapy, icosapent ethyl, a purified eicosapentaenoic acid ethyl ester, reduced major ASCVD outcomes by 25% over a median 4.9 years (ARR = 4.8%; NNT = 21), and cardiovascular death by 20% (ARR = 0.9%; NNT = 111), compared with a mineral oil placebo.²⁵ Subsequent trials, using a corn oil placebo, failed to duplicate these data²⁶—raising concern that the mineral oil comparator might have altered results of the eicosapentaenoic acid ethyl ester study.^27,28

Bempedoic acid is a small-molecule ­inhibitor of ATP citrate lyase that increases LDL uptake by the liver. Pooled data from studies of bempedoic acid show, on average, a 15% reduction in TC, a 23% reduction in LDL-C, and a 6% increase in HDL-C, without a significant change in TG.²⁹ In statin-­intolerant patients, bempedoic acid reduced major ASCVD outcomes by 13% over a median 40 months (ARR = 1.6%; NNT = 63), with no significant reduction in cardiovascular death.³⁰

Niacin. Two large trials failed to demonstrate improvement in major cardiovascular events or other clinical benefit when niacin is added to moderate-intensity statin therapy, despite a significant increase in the HDL-C level (on average, 6 mg/dL) and a decrease in the LDL-C level (10-12 mg/dL) and TG (42 mg/dL).^31,32

Fenofibrate lowers TG and increases HDL-C but does not consistently improve cardiovascular outcomes.³³ In a trial of patients with type 2 diabetes and persistent dyslipidemia (serum TG > 204 mg/dL; ­HDL-C < 34 mg/dL) despite statin therapy, adding fenofibrate reduced CVD outcomes by 4.9%—although this absolute difference did not reach statistical significance.³⁴

Neither niacin nor fenofibrate is considered useful for reducing ASCVD risk across broad populations.

Neither niacin nor fenofibrate is considered useful for reducing ASCVD risk across broad populations.⁴

Follow-up to assess progress toward goals

At-risk patients should follow a dietary pattern that emphasizes vegetables, fruits, and whole grains and limits sweets, sugarsweetened beverages, and red meat.

Recheck the lipid profile 4 to 12 weeks after starting lipid-lowering therapy to verify adherence to medication and assess response. The primary goal is the percentage reduction in LDL-C based on ASCVD risk. An additional goal for very-high-risk patients is an LDL-C value ≤ 70 mg/dL. If the reduction in LDL-C is less than desired and adherence is assured, consider titrating the statin dosage or augmenting statin therapy with a nonstatin drug (eg, ezetimibe), or both.⁴

CORRESPONDENCE
Jonathon M. Firnhaber, MD, MAEd, MBA, East Carolina University, Family Medicine Center, 101 Heart Drive, Greenville, NC 27834; [email protected]

An elevated serum level of cholesterol has been recognized as a risk factor for atherosclerotic cardiovascular disease (ASCVD) since the publication of the Framingham Study in 1961.¹ Although clinical outcomes related to ASCVD have improved in recent decades, ASCVD remains the leading cause of morbidity and mortality across the globe and remains, in the United States, the leading cause of death among most racial and ethnic groups. Much of this persistent disease burden can be attributed to inadequate control of ­ASCVD risk factors and suboptimal implementation of prevention strategies in the general population.²

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Much of the persistent disease burden can be attributed to inadequate control of ASCVD risk factors and suboptimal implementation of prevention strategies in the general population.

The most recent (2019) iteration of the American College of Cardiology/American Heart Association (ACC/AHA) Guideline on the Primary Prevention of Cardiovascular Disease emphasizes a comprehensive, patient-centered, team-based approach to the management of ASCVD risk factors.² In this article, I review how, first, medication to reduce ASCVD risk should be considered only when a patient’s risk is sufficiently high and, second, shared decision-making and social determinants of health should, in all cases, guide and inform optimal implementation of treatment.²

Estimating risk for ASCVDby ascertaining LDL-C

The Friedewald equation. Traditionally, low-density lipoprotein cholesterol (LDL-C) is estimated using the Friedewald equation^a applied to a fasting lipid profile. In patients who have a low level of LDL-C (< 70 mg/dL), however, the Friedewald equation becomes less accurate; in patients with hypertriglyceridemia (TG ≥ 400 mg/dL), estimation of LDL-C is invalid.

The Martin–Hopkins equation offers a validated estimation of LDL-C when the LDL-C value is < 70 mg/dL.³ This equation—in which the fixed factor of 5 used in the Friedewald equation to estimate very-low-density lipoprotein cholesterol is replaced by an adjustable factor that is based on the patient’s non-HDL-C (ie, TC – HDL-C) and TG values—is preferred by the ACC/AHA Task Force on Clinical Practice Guidelines in this clinical circumstance.⁴

National Institutes of Health equation. This newer equation provides an accurate estimate of the LDL-C level in patients whose TG value is ≤ 800 mg/dL. The equation has not been fully validated for clinical use, however.⁵

Direct measurement obviates the need for an equation to estimate LDL-C, but the test is not available in all health care settings.

For adults ≥ 20 years of age who are not receiving lipid-lowering therapy, a nonfasting lipid profile can be used to estimate ­ASCVD risk and document the baseline LDL-C level. If the TG level is ≥ 400 mg/dL, the test should be administered in the fasting state.⁴

Continue to: Apolipoprotein B

Apolipoprotein B. Alternatively, apolipoprotein B (apoB) can be measured. Because each LDL-C particle contains 1 apoB molecule, the apoB level describes the ­LDL-C level more accurately than a calculation of LDL-C. Many patients with type 2 diabetes and metabolic syndrome have a relatively low calculated LDL-C (thereby falsely reassuring the testing clinician) but have an elevated apoB level. An apoB level ≥ 130 mg/dL corresponds to an LDL-C level >160 mg/dL.⁴

Calculation of non-HDL-C. Because the nonfasting state does not have a significant impact on a patient’s TC and HDL-C levels, the non-HDL-C level also can be calculated from the results of a nonfasting lipid profile.

Non-HDL-C and apoB are equivalent predictors of ASCVD risk. These 2 assessments might offer better risk estimation than other available tools in patients who have type 2 diabetes and metabolic syndrome.⁶

Applying the estimate of 10-year ASCVD risk

Your recommendation for preventive intervention, such as lipid-lowering therapy, should be based on the estimated 10-year risk for ASCVD. Although multiple validated risk assessment tools are available, ACC/AHA recommends the pooled cohort risk equations (PCE), introduced in the 2013 ACC/AHA cholesterol treatment guidelines. The Framingham Heart Study now recommends the ACC/AHA PCE for risk assessment as well.⁷

The PCE, developed from 5 large cohorts, is based on hard atherosclerotic events: nonfatal myocardial infarction, death from coronary artery disease, and stroke. The ACC/AHA PCE is the only risk assessment tool developed using a significant percentage of patients who self-identify as Black.⁸ Alternatives to the ACC/AHA PCE include:

• Multi-ethnic Study of Atherosclerosis (MESA) 10-year ASCVD risk calculator, which incorporates the coronary artery calcium (CAC) score.
• Reynolds Risk Score, which incorporates high-sensitivity C-reactive protein measurement and a family history of premature ASCVD.⁹

Continue to: How much does lifestyle modification actually matter?

 

 

How much does lifestyle modification actually matter?

The absolute impact of diet and exercise on lipid parameters is relatively modest. No studies have demonstrated a reduction in adverse cardiovascular outcomes with specific interventions regarding diet or activity.

Diet. Nevertheless, ACC/AHA recommends that at-risk patients follow a dietary pattern that (1) emphasizes vegetables, fruits, and whole grains and (2) limits sweets, sugar-sweetened beverages, and red meat.

For adults ≥ 20 years of age who are not receiving lipid-lowering therapy, a nonfasting lipid profile can be used to estimate ASCVD risk and document the baseline LDL-C level.

Saturated fat should constitute no more than 5% or 6% of total calories. In controlled-feeding trials,¹⁰ for every 1% of calories from saturated fat that are replaced with carbohydrate or monounsaturated or polyunsaturated fat, the LDL-C level was found to decline by as much as 1.8 mg/dL. Evidence is insufficient to assert that lowering dietary cholesterol reduces LDL-C.¹¹

Activity. Trials of aerobic physical activity, compared with a more sedentary activity pattern, have demonstrated a reduction in the LDL-C level of as much as 6 mg/dL. All adult patients should be counseled to engage in aerobic physical activity of moderate or vigorous intensity—averaging ≥ 40 minutes per session, 3 or 4 sessions per week.¹¹

Primary prevention:Stratification by age

40 to 75 years. ACC/AHA recommends that you routinely assess traditional cardiovascular risk factors for these patients and calculate their 10-year risk for ASCVD using the PCE. Statin therapy as primary prevention is indicated for 3 major groups (TABLE 1).⁴ The US Preventive Services Task Force ­(USPSTF) recommends a 10-year ASCVD risk ≥ 10%, in conjunction with 1 or more additional CVD risk factors (dyslipidemia, diabetes, hypertension, smoking), as the threshold for initiating low- or moderate-intensity statin therapy in this age group.¹²

Continue to: In adults at borderline risk...

In adults at borderline risk (5% to < 7.5% 10-year ASCVD risk) or intermediate risk (≥ 7.5% to < 20% 10-year ASCVD risk), consider risk-enhancing factors to better inform your recommendation for preventive interventions. In these 2 groups, the presence of risk-enhancing factors might justify ­moderate-intensity statin therapy (TABLE 2⁴).

If your decision regarding preventive intervention remains uncertain, measuring CAC might further guide your discussion with the patient.⁴ When the CAC score is:

• 0 Agatston units and higher-risk conditions (eg, diabetes, family history of premature coronary artery disease, smoking) are absent, statin therapy can be withheld; reassess ASCVD risk in 5 to 10 years.
• 1-99 Agatston units, statin therapy can be started, especially for patients ≥ 55 years of age.
• ≥ 100 Agatston units or ≥ 75th percentile, statin therapy is indicated for all patients, regardless of additional risk factors.⁴

Because statins promote progression from unstable, inflammatory atherosclerotic plaque to more stable, calcified plaque, CAC scoring is not valid in patients already on statin therapy.¹³

In primary prevention, patients who have been classified as having low or intermediate risk, based on ASCVD risk scoring, with a CAC score of 0 Agatston units, have an annual all-cause mortality < 1%, regardless of age and gender. Patients classified as being at high risk, based on ASCVD risk scoring, with a CAC score of 0 Agatston units, have a significantly lower annual mortality than low- or intermediate-risk patients with a CAC score > 0 Agatston units.¹⁴

20 to 39 years. Focus on evaluation of lifetime ASCVD risk, rather than short-term (10-year) risk. Lifestyle modification is the primary intervention for younger patients; for those with moderate hypercholesterolemia (LDL-C, 160-189 mg/dL) and a family history of premature ASCVD, however, consider statin therapy. For patients with LDL-C ≥ 190 mg/dL, lifetime ASCVD risk is markedly increased, and high-intensity statin therapy is recommended, regardless of age. In this group, reassess ASCVD risk factors every 4 to 6 years.⁴

Continue to: > 75 years, without ASCVD

> 75 years, without ASCVD. In this group, the ­benefit of statin therapy is less clear and might be lessened by an increased potential for adverse effects. A meta-analysis of 28 trials demonstrated that people ages > 75 years had a 24% relative reduction in major coronary events for every 38.7 mg/dL (1.0 mmol/L) reduction in LDL-C, which is comparable to the risk reduction seen in people ages 40 to 75 years.¹⁵

A meta-analysis of 28 trials demonstrated that people > 75 years of age had a 24% relative reduction in major coronary events for every 38.7 mg/dL (1.0 mmol/L) reduction in LDL-C.

With increasing age, however, the relative reduction in major coronary events with statin therapy decreased,¹⁵ although other trials have not demonstrated age heterogeneity.¹⁶ Because people > 75 years of age have a significantly higher ASCVD event rate, a comparable relative rate reduction with statin therapy results in a larger absolute rate reduction (ARR) and, therefore, a smaller number needed to treat (NNT) to prevent an event, compared to the NNT in younger people.

Secondary prevention

ACC/AHA guidelines define clinical ASCVD as a history of:

• acute coronary syndrome
• myocardial infarction
• coronary or other arterial revascularization
• cerebrovascular event
• symptomatic peripheral artery disease, including aortic aneurysm.

High-intensity statin therapy is indicated for all patients ≤ 75 years who have clinical ­ASCVD. In patients > 75 years, consider a taper to moderate-intensity statin therapy. An upper age limit for seeing benefit from statin therapy in secondary prevention has not been identified.⁴

Base a recommendation for preventive intervention, such as lipidlowering therapy, on the estimated 10-year risk for ASCVD.

In high-risk patients, if LDL-C remains ≥ 70 mg/dL despite maximally tolerated statin therapy, ezetimibe (discussed in the next section) can be added. In very-high-risk patients, if LDL-C remains ≥ 70 mg/dL despite maximally tolerated statin therapy plus ezetimibe, a proprotein convertase subtilisin/­kexin type 9 (PCSK9) inhibitor (also discussed next) can be added. Always precede initiation of a PCSK9 inhibitor with a discussion of the net benefit, safety, and cost with the patient.⁴

Continue to: Options for lipid-lowering pharmacotherapy

 

 

Options for lipid-lowering pharmacotherapy

Statins (formally, hydroxymethylglutaryl-coenzyme A reductase inhibitors) offer the most predictable reduction in ASCVD risk of any lipid-lowering therapy. The evidence report that accompanied the 2016 USPSTF guidelines on statins for the prevention of cardiovascular disease (CVD) stated that low- or moderate-dosage statin therapy is associated with approximately a 30% relative risk reduction (RRR) in CVD events and CVD deaths and a 10% to 15% RRR in all-cause mortality.¹⁷

High-intensity statin therapy reduces LDL-C by ≥ 50%. Moderate-intensity statin therapy reduces LDL-C by 30% to 49% (TABLE 3).⁴

Statins are not without risk: A 2016 report¹⁸ estimated that treating 10,000 patients with a statin for 5 years would cause 1 case of rhabdomyolysis, 5 cases of myopathy, 75 new cases of diabetes, and 7 cases of hemorrhagic stroke. The same treatment would, however, avert approximately 1000 CVD events among patients with preexisting disease and approximately 500 CVD events among patients at elevated risk but without preexisting disease.¹⁸

Ezetimibe, a selective cholesterol-­absorption inhibitor, lowers LDL-C by 13% to 20% and typically is well tolerated. The use of ezetimibe in ASCVD risk reduction is supported by a single randomized controlled trial of more than 18,000 patients with recent acute coronary syndrome. Adding ezetimibe to simvastatin 40 mg resulted in a 2% absolute reduction in major adverse cardiovascular events over a median follow-up of 6 years (NNT = 50), compared to simvastatin alone.¹⁹ ACC/AHA guidelines recommend adding ezetimibe to maximally tolerated statin therapy in patients with clinical ASCVD who do not reach their goal LDL reduction with a statin alone. Ezetimibe also can be considered a statin alternative in patients who are statin intolerant.⁴

PCSK9 inhibitors. When added to statin therapy, evolocumab and alirocumab—monoclonal antibodies that inhibit PCSK9—offer an incremental decrease in LDL-C of approximately 60%.^20-22 In a meta-analysis of 35 trials evaluating the incremental benefit of PCSK9 inhibitor therapy, a significant reduction in cardiovascular events, including myocardial infarction (ARR = 1.3%; NNT = 77), stroke (ARR = 0.4%; NNT = 250), and coronary revascularization (ARR = 1.6%; NNT = 63) was reported. No significant difference was observed in all-cause or cardiovascular mortality.^21,23

Continue to: Inclisiran

Inclisiran, an injectable small-­interfering RNA that inhibits PCSK9 synthesis, provides an incremental decrease in LDL-C of > 50% in patients already receiving statin therapy. Meta-analysis of 3 small cardiovascular outcomes trials revealed no significant difference in the rate of myocardial infarction, stroke, or cardiovascular mortality with inclisiran compared to placebo. Larger outcomes trials are underway and might offer additional insight into this agent’s role in ASCVD risk management.²⁴

Omega-3 fatty acids. Multiple trials have demonstrated that adding omega-3 fatty acids to usual lipid-lowering therapy does not offer a consistent reduction in adverse cardiovascular outcomes, despite providing a significant reduction in TG levels. In a high-risk population with persistently elevated TG despite statin therapy, icosapent ethyl, a purified eicosapentaenoic acid ethyl ester, reduced major ASCVD outcomes by 25% over a median 4.9 years (ARR = 4.8%; NNT = 21), and cardiovascular death by 20% (ARR = 0.9%; NNT = 111), compared with a mineral oil placebo.²⁵ Subsequent trials, using a corn oil placebo, failed to duplicate these data²⁶—raising concern that the mineral oil comparator might have altered results of the eicosapentaenoic acid ethyl ester study.^27,28

Bempedoic acid is a small-molecule ­inhibitor of ATP citrate lyase that increases LDL uptake by the liver. Pooled data from studies of bempedoic acid show, on average, a 15% reduction in TC, a 23% reduction in LDL-C, and a 6% increase in HDL-C, without a significant change in TG.²⁹ In statin-­intolerant patients, bempedoic acid reduced major ASCVD outcomes by 13% over a median 40 months (ARR = 1.6%; NNT = 63), with no significant reduction in cardiovascular death.³⁰

Niacin. Two large trials failed to demonstrate improvement in major cardiovascular events or other clinical benefit when niacin is added to moderate-intensity statin therapy, despite a significant increase in the HDL-C level (on average, 6 mg/dL) and a decrease in the LDL-C level (10-12 mg/dL) and TG (42 mg/dL).^31,32

Fenofibrate lowers TG and increases HDL-C but does not consistently improve cardiovascular outcomes.³³ In a trial of patients with type 2 diabetes and persistent dyslipidemia (serum TG > 204 mg/dL; ­HDL-C < 34 mg/dL) despite statin therapy, adding fenofibrate reduced CVD outcomes by 4.9%—although this absolute difference did not reach statistical significance.³⁴

Neither niacin nor fenofibrate is considered useful for reducing ASCVD risk across broad populations.

Neither niacin nor fenofibrate is considered useful for reducing ASCVD risk across broad populations.⁴

Follow-up to assess progress toward goals

At-risk patients should follow a dietary pattern that emphasizes vegetables, fruits, and whole grains and limits sweets, sugarsweetened beverages, and red meat.

Recheck the lipid profile 4 to 12 weeks after starting lipid-lowering therapy to verify adherence to medication and assess response. The primary goal is the percentage reduction in LDL-C based on ASCVD risk. An additional goal for very-high-risk patients is an LDL-C value ≤ 70 mg/dL. If the reduction in LDL-C is less than desired and adherence is assured, consider titrating the statin dosage or augmenting statin therapy with a nonstatin drug (eg, ezetimibe), or both.⁴

CORRESPONDENCE
Jonathon M. Firnhaber, MD, MAEd, MBA, East Carolina University, Family Medicine Center, 101 Heart Drive, Greenville, NC 27834; [email protected]

Results of a study recently published in Nature Communications suggests that radiation from ultraviolet nail polish dryers could induce cell death and trigger molecular changes linked to cancer in human cells. According to two experts, these findings raise concerns regarding the safety of frequent use of these nail dryers.

In the study, human and mouse cells were exposed to radiation from UV nail dryers. Exposing human and mice skin cells to UVA light for 20 minutes resulted in the death of 20%-30% of cells; three consecutive 20-minute sessions resulted in the death of 65%-70% of cells. Additionally, surviving cells suffered oxidative damage to their DNA and mitochondria, with mutational patterns similar to those seen in skin cancer, study investigator Maria Zhivagui, PhD, of the University of California, San Diego, and associates reported.  

“This study showed that irradiation of human and mouse cell lines using UV nail polish dryers resulted in DNA damage and genome mutations,” Shari Lipner, MD, PhD, director of the nail division at New York–Presbyterian Hospital/Weill Cornell Medicine, New York, said in an interview. The study “ties together exposure to UV light from nail polish dryers and genetic mutations that are associated with skin cancers,” added Dr. Lipner, who was not involved with the study.

UV nail lamps are commonly used to dry and harden gel nail polish formulas. Often referred to as “mini tanning beds,” these devices emit UVA radiation, classified as a Group 1 Carcinogen by the International Agency for Research on Cancer.

“Both UVA and UVB are main drivers of both melanoma and keratinocyte carcinomas (basal cell carcinoma and squamous cell carcinoma),” said Anthony Rossi, MD, a dermatologic surgeon at Memorial Sloan Kettering Cancer Center, New York, who was also not a study investigator. UV irradiance “produces DNA mutations that are specific to forming types of skin cancer,” he said in an interview.

UVA wavelengths commonly used in nail dryers can penetrate all layers of the epidermis, the top layer of the skin, potentially affecting stem cells in the skin, according to the study.

Dr. Lipner noted that “there have been several case reports of patients with histories of gel manicures using UV nail polish dryers who later developed squamous cell carcinomas on the dorsal hands, fingers, and nails, and articles describing high UV emissions from nail polish dryers, but the direct connection between UV dryers and skin cancer development was tenuous.” The first of its kind, the new study investigated the impact of UV nail drying devices at a cellular level.

The results of this study, in combination with previous case reports suggesting the development of skin cancers following UVA dryer use, raise concern regarding the safety of these commonly used devices. The study, the authors wrote, “does not provide direct evidence for an increased cancer risk in human beings,” but their findings and “prior evidence strongly suggest that radiation emitted by UV nail polish dryers may cause cancers of the hand and that UV nail polish dryers, similar to tanning beds, may increase the risk of early onset skin cancer.”

Courtesy MSKCC

Dr. Rossi said that, “while this study shows that the UV exposure does affect human cells and causes mutations, the study was not done in vivo in human beings, so further studies are needed to know at what dose and frequency gel manicures would be needed to cause detrimental effects.” However, for people who regularly receive gel manicures involving UV nail dryers, both Dr. Lipner and Dr. Rossi recommend applying a broad-spectrum sunscreen to protect the dorsal hands, fingertips, and skin surrounding the nails, or wearing UV-protective gloves.

The study was supported by an Alfred B. Sloan Research Fellowship to one of the authors and grants from the National Institutes of Health to two authors. One author reported being a compensated consultant and having an equity interest in io9. Dr. Lipner and Dr. Rossi reported no relevant financial relationships.

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

Results of a study recently published in Nature Communications suggests that radiation from ultraviolet nail polish dryers could induce cell death and trigger molecular changes linked to cancer in human cells. According to two experts, these findings raise concerns regarding the safety of frequent use of these nail dryers.

In the study, human and mouse cells were exposed to radiation from UV nail dryers. Exposing human and mice skin cells to UVA light for 20 minutes resulted in the death of 20%-30% of cells; three consecutive 20-minute sessions resulted in the death of 65%-70% of cells. Additionally, surviving cells suffered oxidative damage to their DNA and mitochondria, with mutational patterns similar to those seen in skin cancer, study investigator Maria Zhivagui, PhD, of the University of California, San Diego, and associates reported.  

“This study showed that irradiation of human and mouse cell lines using UV nail polish dryers resulted in DNA damage and genome mutations,” Shari Lipner, MD, PhD, director of the nail division at New York–Presbyterian Hospital/Weill Cornell Medicine, New York, said in an interview. The study “ties together exposure to UV light from nail polish dryers and genetic mutations that are associated with skin cancers,” added Dr. Lipner, who was not involved with the study.

UV nail lamps are commonly used to dry and harden gel nail polish formulas. Often referred to as “mini tanning beds,” these devices emit UVA radiation, classified as a Group 1 Carcinogen by the International Agency for Research on Cancer.

“Both UVA and UVB are main drivers of both melanoma and keratinocyte carcinomas (basal cell carcinoma and squamous cell carcinoma),” said Anthony Rossi, MD, a dermatologic surgeon at Memorial Sloan Kettering Cancer Center, New York, who was also not a study investigator. UV irradiance “produces DNA mutations that are specific to forming types of skin cancer,” he said in an interview.

UVA wavelengths commonly used in nail dryers can penetrate all layers of the epidermis, the top layer of the skin, potentially affecting stem cells in the skin, according to the study.

Dr. Lipner noted that “there have been several case reports of patients with histories of gel manicures using UV nail polish dryers who later developed squamous cell carcinomas on the dorsal hands, fingers, and nails, and articles describing high UV emissions from nail polish dryers, but the direct connection between UV dryers and skin cancer development was tenuous.” The first of its kind, the new study investigated the impact of UV nail drying devices at a cellular level.

The results of this study, in combination with previous case reports suggesting the development of skin cancers following UVA dryer use, raise concern regarding the safety of these commonly used devices. The study, the authors wrote, “does not provide direct evidence for an increased cancer risk in human beings,” but their findings and “prior evidence strongly suggest that radiation emitted by UV nail polish dryers may cause cancers of the hand and that UV nail polish dryers, similar to tanning beds, may increase the risk of early onset skin cancer.”

Courtesy MSKCC

Dr. Rossi said that, “while this study shows that the UV exposure does affect human cells and causes mutations, the study was not done in vivo in human beings, so further studies are needed to know at what dose and frequency gel manicures would be needed to cause detrimental effects.” However, for people who regularly receive gel manicures involving UV nail dryers, both Dr. Lipner and Dr. Rossi recommend applying a broad-spectrum sunscreen to protect the dorsal hands, fingertips, and skin surrounding the nails, or wearing UV-protective gloves.

The study was supported by an Alfred B. Sloan Research Fellowship to one of the authors and grants from the National Institutes of Health to two authors. One author reported being a compensated consultant and having an equity interest in io9. Dr. Lipner and Dr. Rossi reported no relevant financial relationships.

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

Results of a study recently published in Nature Communications suggests that radiation from ultraviolet nail polish dryers could induce cell death and trigger molecular changes linked to cancer in human cells. According to two experts, these findings raise concerns regarding the safety of frequent use of these nail dryers.

In the study, human and mouse cells were exposed to radiation from UV nail dryers. Exposing human and mice skin cells to UVA light for 20 minutes resulted in the death of 20%-30% of cells; three consecutive 20-minute sessions resulted in the death of 65%-70% of cells. Additionally, surviving cells suffered oxidative damage to their DNA and mitochondria, with mutational patterns similar to those seen in skin cancer, study investigator Maria Zhivagui, PhD, of the University of California, San Diego, and associates reported.  

“This study showed that irradiation of human and mouse cell lines using UV nail polish dryers resulted in DNA damage and genome mutations,” Shari Lipner, MD, PhD, director of the nail division at New York–Presbyterian Hospital/Weill Cornell Medicine, New York, said in an interview. The study “ties together exposure to UV light from nail polish dryers and genetic mutations that are associated with skin cancers,” added Dr. Lipner, who was not involved with the study.

UV nail lamps are commonly used to dry and harden gel nail polish formulas. Often referred to as “mini tanning beds,” these devices emit UVA radiation, classified as a Group 1 Carcinogen by the International Agency for Research on Cancer.

“Both UVA and UVB are main drivers of both melanoma and keratinocyte carcinomas (basal cell carcinoma and squamous cell carcinoma),” said Anthony Rossi, MD, a dermatologic surgeon at Memorial Sloan Kettering Cancer Center, New York, who was also not a study investigator. UV irradiance “produces DNA mutations that are specific to forming types of skin cancer,” he said in an interview.

UVA wavelengths commonly used in nail dryers can penetrate all layers of the epidermis, the top layer of the skin, potentially affecting stem cells in the skin, according to the study.

Dr. Lipner noted that “there have been several case reports of patients with histories of gel manicures using UV nail polish dryers who later developed squamous cell carcinomas on the dorsal hands, fingers, and nails, and articles describing high UV emissions from nail polish dryers, but the direct connection between UV dryers and skin cancer development was tenuous.” The first of its kind, the new study investigated the impact of UV nail drying devices at a cellular level.

The results of this study, in combination with previous case reports suggesting the development of skin cancers following UVA dryer use, raise concern regarding the safety of these commonly used devices. The study, the authors wrote, “does not provide direct evidence for an increased cancer risk in human beings,” but their findings and “prior evidence strongly suggest that radiation emitted by UV nail polish dryers may cause cancers of the hand and that UV nail polish dryers, similar to tanning beds, may increase the risk of early onset skin cancer.”

Courtesy MSKCC

Dr. Rossi said that, “while this study shows that the UV exposure does affect human cells and causes mutations, the study was not done in vivo in human beings, so further studies are needed to know at what dose and frequency gel manicures would be needed to cause detrimental effects.” However, for people who regularly receive gel manicures involving UV nail dryers, both Dr. Lipner and Dr. Rossi recommend applying a broad-spectrum sunscreen to protect the dorsal hands, fingertips, and skin surrounding the nails, or wearing UV-protective gloves.

The study was supported by an Alfred B. Sloan Research Fellowship to one of the authors and grants from the National Institutes of Health to two authors. One author reported being a compensated consultant and having an equity interest in io9. Dr. Lipner and Dr. Rossi reported no relevant financial relationships.

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

Alpha-gal syndrome is an increasingly common cause of gastrointestinal issues that remains underrecognized by the medical community, according to an American Gastroenterological Association clinical practice update.

Although the allergic response is best known for a combination of anaphylaxis, skin changes, and gastrointestinal symptoms that occurs within hours of consuming mammalian-derived food products, health care providers should know that many patients experience gastrointestinal distress in the absence of other clinical signs, lead author Sarah K. McGill, MD, MSc, of the University of North Carolina at Chapel Hill, and colleagues reported.

“It is important for gastroenterologists to be aware of this condition and to be capable of diagnosing and treating it in a timely manner,” the investigators wrote in Clinical Gastroenterology and Hepatology.

To this end, Dr. McGill and colleagues drafted the present clinical practice update, covering pathogenesis, clinical manifestations, diagnosis, and management.

“The allergy in alpha-gal syndrome is to galactose alpha-1,3-galactose, an oligosaccharide on the cells of all nonprimate mammals,” the investigators wrote. “Surprisingly, sensitization to alpha-gal, that is, the process by which human beings develop IgE antibodies to the sugar, is understood to occur after the bite of a tick or parasitic infection. In the United States, the Lone Star tick, an ectoparasite whose principal host is deer, is strongly implicated.”

Gastrointestinal focused clinical research is scarce, the investigators noted, citing two observational studies involving 375 patients positive for alpha-gal IgE. Almost half of these patients (40.7%) had gastrointestinal symptoms alone. Across the entire population, the most common gastrointestinal symptoms were abdominal pain (71%) and vomiting (22%). About three out of four patients reported improvement on an alpha-gal avoidance diet.

“Clinicians should consider alpha-gal syndrome in the differential diagnosis of patients with unexplained gastrointestinal symptoms of abdominal pain, diarrhea, nausea, and vomiting, particularly those who live or have lived in an alpha-gal–prevalent area,” the investigators wrote.

In the United States, these areas span the domain of the Lone Star tick, including most of the East Coast, the central Midwest, the South, and all of Texas. Overseas, alpha-gal syndrome has been reported in Japan, Australia, Western Europe, and South Africa.

Clinical suspicion should be increased in patients with a history of tick bite, engagement in outdoor activities, and awakening in the night with gastrointestinal distress (because of the delay between allergen ingestion and symptom onset). Workup should include serum testing for alpha-gal IgE antibodies, according to the update. Serum positivity alone, however, is not sufficient for diagnosis. Alpha-gal syndrome must be confirmed by symptom resolution or improvement upon adherence to an alpha-gal avoidance diet for at least a month.

“During this time, patients may want to avoid eating at restaurants, which can easily cross-contaminate food, and processed food, which may contain alpha-gal in additives,” Dr. McGill and colleagues wrote.

Patients with alpha-gal syndrome who accidentally consume alpha-gal should take 25-50 mg of diphenhydramine and ensure access to a self-injectable epinephrine if symptoms progress, particularly if respiratory compromise occurs, they added.

The coauthors are Jana G. Hasash, MD, and Thomas A. Platts-Mills, MD, PhD.

The investigators disclosed relationships with Olympus America, Exact Sciences, Guardant Health, Finch Therapeutics, and others.

Alpha-gal syndrome is an increasingly common cause of gastrointestinal issues that remains underrecognized by the medical community, according to an American Gastroenterological Association clinical practice update.

Although the allergic response is best known for a combination of anaphylaxis, skin changes, and gastrointestinal symptoms that occurs within hours of consuming mammalian-derived food products, health care providers should know that many patients experience gastrointestinal distress in the absence of other clinical signs, lead author Sarah K. McGill, MD, MSc, of the University of North Carolina at Chapel Hill, and colleagues reported.

“It is important for gastroenterologists to be aware of this condition and to be capable of diagnosing and treating it in a timely manner,” the investigators wrote in Clinical Gastroenterology and Hepatology.

To this end, Dr. McGill and colleagues drafted the present clinical practice update, covering pathogenesis, clinical manifestations, diagnosis, and management.

“The allergy in alpha-gal syndrome is to galactose alpha-1,3-galactose, an oligosaccharide on the cells of all nonprimate mammals,” the investigators wrote. “Surprisingly, sensitization to alpha-gal, that is, the process by which human beings develop IgE antibodies to the sugar, is understood to occur after the bite of a tick or parasitic infection. In the United States, the Lone Star tick, an ectoparasite whose principal host is deer, is strongly implicated.”

Gastrointestinal focused clinical research is scarce, the investigators noted, citing two observational studies involving 375 patients positive for alpha-gal IgE. Almost half of these patients (40.7%) had gastrointestinal symptoms alone. Across the entire population, the most common gastrointestinal symptoms were abdominal pain (71%) and vomiting (22%). About three out of four patients reported improvement on an alpha-gal avoidance diet.

“Clinicians should consider alpha-gal syndrome in the differential diagnosis of patients with unexplained gastrointestinal symptoms of abdominal pain, diarrhea, nausea, and vomiting, particularly those who live or have lived in an alpha-gal–prevalent area,” the investigators wrote.

In the United States, these areas span the domain of the Lone Star tick, including most of the East Coast, the central Midwest, the South, and all of Texas. Overseas, alpha-gal syndrome has been reported in Japan, Australia, Western Europe, and South Africa.

Clinical suspicion should be increased in patients with a history of tick bite, engagement in outdoor activities, and awakening in the night with gastrointestinal distress (because of the delay between allergen ingestion and symptom onset). Workup should include serum testing for alpha-gal IgE antibodies, according to the update. Serum positivity alone, however, is not sufficient for diagnosis. Alpha-gal syndrome must be confirmed by symptom resolution or improvement upon adherence to an alpha-gal avoidance diet for at least a month.

“During this time, patients may want to avoid eating at restaurants, which can easily cross-contaminate food, and processed food, which may contain alpha-gal in additives,” Dr. McGill and colleagues wrote.

Patients with alpha-gal syndrome who accidentally consume alpha-gal should take 25-50 mg of diphenhydramine and ensure access to a self-injectable epinephrine if symptoms progress, particularly if respiratory compromise occurs, they added.

The coauthors are Jana G. Hasash, MD, and Thomas A. Platts-Mills, MD, PhD.

The investigators disclosed relationships with Olympus America, Exact Sciences, Guardant Health, Finch Therapeutics, and others.

Alpha-gal syndrome is an increasingly common cause of gastrointestinal issues that remains underrecognized by the medical community, according to an American Gastroenterological Association clinical practice update.

Although the allergic response is best known for a combination of anaphylaxis, skin changes, and gastrointestinal symptoms that occurs within hours of consuming mammalian-derived food products, health care providers should know that many patients experience gastrointestinal distress in the absence of other clinical signs, lead author Sarah K. McGill, MD, MSc, of the University of North Carolina at Chapel Hill, and colleagues reported.

“It is important for gastroenterologists to be aware of this condition and to be capable of diagnosing and treating it in a timely manner,” the investigators wrote in Clinical Gastroenterology and Hepatology.

To this end, Dr. McGill and colleagues drafted the present clinical practice update, covering pathogenesis, clinical manifestations, diagnosis, and management.

“The allergy in alpha-gal syndrome is to galactose alpha-1,3-galactose, an oligosaccharide on the cells of all nonprimate mammals,” the investigators wrote. “Surprisingly, sensitization to alpha-gal, that is, the process by which human beings develop IgE antibodies to the sugar, is understood to occur after the bite of a tick or parasitic infection. In the United States, the Lone Star tick, an ectoparasite whose principal host is deer, is strongly implicated.”

Gastrointestinal focused clinical research is scarce, the investigators noted, citing two observational studies involving 375 patients positive for alpha-gal IgE. Almost half of these patients (40.7%) had gastrointestinal symptoms alone. Across the entire population, the most common gastrointestinal symptoms were abdominal pain (71%) and vomiting (22%). About three out of four patients reported improvement on an alpha-gal avoidance diet.

“Clinicians should consider alpha-gal syndrome in the differential diagnosis of patients with unexplained gastrointestinal symptoms of abdominal pain, diarrhea, nausea, and vomiting, particularly those who live or have lived in an alpha-gal–prevalent area,” the investigators wrote.

In the United States, these areas span the domain of the Lone Star tick, including most of the East Coast, the central Midwest, the South, and all of Texas. Overseas, alpha-gal syndrome has been reported in Japan, Australia, Western Europe, and South Africa.

Clinical suspicion should be increased in patients with a history of tick bite, engagement in outdoor activities, and awakening in the night with gastrointestinal distress (because of the delay between allergen ingestion and symptom onset). Workup should include serum testing for alpha-gal IgE antibodies, according to the update. Serum positivity alone, however, is not sufficient for diagnosis. Alpha-gal syndrome must be confirmed by symptom resolution or improvement upon adherence to an alpha-gal avoidance diet for at least a month.

“During this time, patients may want to avoid eating at restaurants, which can easily cross-contaminate food, and processed food, which may contain alpha-gal in additives,” Dr. McGill and colleagues wrote.

Patients with alpha-gal syndrome who accidentally consume alpha-gal should take 25-50 mg of diphenhydramine and ensure access to a self-injectable epinephrine if symptoms progress, particularly if respiratory compromise occurs, they added.

The coauthors are Jana G. Hasash, MD, and Thomas A. Platts-Mills, MD, PhD.

The investigators disclosed relationships with Olympus America, Exact Sciences, Guardant Health, Finch Therapeutics, and others.

A whole new, tiny level of hangry

Ever been so hungry that everything just got on your nerves? Maybe you feel a little snappy right now? Like you’ll just lash out unless you get something to eat? Been there. And so have bacteria.

New research shows that some bacteria go into a full-on Hulk smash if they’re not getting the nutrients they need by releasing toxins into the body. Sounds like a bacterial temper tantrum.

Rosenthal et al.

Even though two cells may be genetically identical, they don’t always behave the same in a bacterial community. Some do their job and stay in line, but some evil twins rage out and make people sick by releasing toxins into the environment, Adam Rosenthal, PhD, of the University of North Carolina and his colleagues discovered.

To figure out why some cells were all business as usual while others were not, the investigators looked at Clostridium perfringens, a bacterium found in the intestines of humans and other vertebrates. When the C. perfringens cells were fed a little acetate to munch on, the hangry cells calmed down faster than a kid with a bag of fruit snacks, reducing toxin levels. Some cells even disappeared, falling in line with their model-citizen counterparts.

So what does this really mean? More research, duh. Now that we know nutrients play a role in toxicity, it may open the door to finding a way to fight against antibiotic resistance in humans and reduce antibiotic use in the food industry.

So think to yourself. Are you bothered for no reason? Getting a little testy with your friends and coworkers? Maybe you just haven’t eaten in a while. You’re literally not alone. Even a single-cell organism can behave based on its hunger levels.

Now go have a snack. Your bacteria are getting restless.
 

The very hangry iguana?

Imagine yourself on a warm, sunny tropical beach. You are enjoying a piece of cake as you take in the slow beat of the waves lapping against the shore. Life is as good as it could be.

Then you feel a presence nearby. Hostility. Hunger. A set of feral, covetous eyes in the nearby jungle. A reptilian beast stalks you, and its all-encompassing sweet tooth desires your cake.

Wait, hold on, what?

As an unfortunate 3-year-old on vacation in Costa Rica found out, there’s at least one iguana in the world out there with a taste for sugar (better than a taste for blood, we suppose).

Ulrike Mai/Pixabay

While out on the beach, the lizard darted out of nowhere, bit the girl on the back of the hand, and stole her cake. Still not the worst party guest ever. The child was taken to a local clinic, where the wound was cleaned and a 5-day antibiotic treatment (lizards carry salmonella) was provided. Things seemed fine, and the girl returned home without incident.

But of course, that’s not the end of the story. Five months later, the girl’s parents noticed a red bump at the wound site. Over the next 3 months, the surrounding skin grew red and painful. A trip to the hospital in California revealed that she had a ganglion cyst and a discharge of pus. Turns out our cake-obsessed lizard friend did give the little girl a gift: the first known human case of Mycobacterium marinum infection following an iguana bite on record.

M. marinum, which causes a disease similar to tuberculosis, typically infects fish but can infect humans if skin wounds are exposed to contaminated water. It’s also resistant to most antibiotics, which is why the first round didn’t clear up the infection. A second round of more-potent antibiotics seems to be working well.

So, to sum up, this poor child got bitten by a lizard, had her cake stolen, and contracted a rare illness in exchange. For a 3-year-old, that’s gotta be in the top-10 worst days ever. Unless, of course, we’re actually living in the Marvel universe (sorry, multiverse at this point). Then we’re totally going to see the emergence of the new superhero Iguana Girl in 15 years or so. Keep your eyes open.
 

No allergies? Let them give up cake

Allergy season is already here – starting earlier every year, it seems – and many people are not happy about it. So unhappy, actually, that there’s a list of things they would be willing to give up for a year to get rid of their of allergies, according to a survey conducted by OnePoll on behalf of Flonase.

nicoletaionescu/Getty Images

Nearly 40% of 2,000 respondents with allergies would go a year without eating cake or chocolate or playing video games in exchange for allergy-free status, the survey results show. Almost as many would forgo coffee (38%) or pizza (37%) for a year, while 36% would stay off social media and 31% would take a pay cut or give up their smartphones, the Independent reported.

More than half of the allergic Americans – 54%, to be exact – who were polled this past winter – Feb. 24 to March 1, to be exact – consider allergy symptoms to be the most frustrating part of the spring. Annoying things that were less frustrating to the group included mosquitoes (41%), filing tax returns (38%), and daylight savings time (37%).

The Trump arraignment circus, of course, occurred too late to make the list, as did the big “We’re going back to the office! No wait, we’re closing the office forever!” email extravaganza and emotional roller coaster. That second one, however, did not get nearly as much media coverage.

A whole new, tiny level of hangry

Ever been so hungry that everything just got on your nerves? Maybe you feel a little snappy right now? Like you’ll just lash out unless you get something to eat? Been there. And so have bacteria.

New research shows that some bacteria go into a full-on Hulk smash if they’re not getting the nutrients they need by releasing toxins into the body. Sounds like a bacterial temper tantrum.

Rosenthal et al.

Even though two cells may be genetically identical, they don’t always behave the same in a bacterial community. Some do their job and stay in line, but some evil twins rage out and make people sick by releasing toxins into the environment, Adam Rosenthal, PhD, of the University of North Carolina and his colleagues discovered.

To figure out why some cells were all business as usual while others were not, the investigators looked at Clostridium perfringens, a bacterium found in the intestines of humans and other vertebrates. When the C. perfringens cells were fed a little acetate to munch on, the hangry cells calmed down faster than a kid with a bag of fruit snacks, reducing toxin levels. Some cells even disappeared, falling in line with their model-citizen counterparts.

So what does this really mean? More research, duh. Now that we know nutrients play a role in toxicity, it may open the door to finding a way to fight against antibiotic resistance in humans and reduce antibiotic use in the food industry.

So think to yourself. Are you bothered for no reason? Getting a little testy with your friends and coworkers? Maybe you just haven’t eaten in a while. You’re literally not alone. Even a single-cell organism can behave based on its hunger levels.

Now go have a snack. Your bacteria are getting restless.
 

The very hangry iguana?

Imagine yourself on a warm, sunny tropical beach. You are enjoying a piece of cake as you take in the slow beat of the waves lapping against the shore. Life is as good as it could be.

Then you feel a presence nearby. Hostility. Hunger. A set of feral, covetous eyes in the nearby jungle. A reptilian beast stalks you, and its all-encompassing sweet tooth desires your cake.

Wait, hold on, what?

As an unfortunate 3-year-old on vacation in Costa Rica found out, there’s at least one iguana in the world out there with a taste for sugar (better than a taste for blood, we suppose).

Ulrike Mai/Pixabay

While out on the beach, the lizard darted out of nowhere, bit the girl on the back of the hand, and stole her cake. Still not the worst party guest ever. The child was taken to a local clinic, where the wound was cleaned and a 5-day antibiotic treatment (lizards carry salmonella) was provided. Things seemed fine, and the girl returned home without incident.

But of course, that’s not the end of the story. Five months later, the girl’s parents noticed a red bump at the wound site. Over the next 3 months, the surrounding skin grew red and painful. A trip to the hospital in California revealed that she had a ganglion cyst and a discharge of pus. Turns out our cake-obsessed lizard friend did give the little girl a gift: the first known human case of Mycobacterium marinum infection following an iguana bite on record.

M. marinum, which causes a disease similar to tuberculosis, typically infects fish but can infect humans if skin wounds are exposed to contaminated water. It’s also resistant to most antibiotics, which is why the first round didn’t clear up the infection. A second round of more-potent antibiotics seems to be working well.

So, to sum up, this poor child got bitten by a lizard, had her cake stolen, and contracted a rare illness in exchange. For a 3-year-old, that’s gotta be in the top-10 worst days ever. Unless, of course, we’re actually living in the Marvel universe (sorry, multiverse at this point). Then we’re totally going to see the emergence of the new superhero Iguana Girl in 15 years or so. Keep your eyes open.
 

No allergies? Let them give up cake

Allergy season is already here – starting earlier every year, it seems – and many people are not happy about it. So unhappy, actually, that there’s a list of things they would be willing to give up for a year to get rid of their of allergies, according to a survey conducted by OnePoll on behalf of Flonase.

nicoletaionescu/Getty Images

Nearly 40% of 2,000 respondents with allergies would go a year without eating cake or chocolate or playing video games in exchange for allergy-free status, the survey results show. Almost as many would forgo coffee (38%) or pizza (37%) for a year, while 36% would stay off social media and 31% would take a pay cut or give up their smartphones, the Independent reported.

More than half of the allergic Americans – 54%, to be exact – who were polled this past winter – Feb. 24 to March 1, to be exact – consider allergy symptoms to be the most frustrating part of the spring. Annoying things that were less frustrating to the group included mosquitoes (41%), filing tax returns (38%), and daylight savings time (37%).

The Trump arraignment circus, of course, occurred too late to make the list, as did the big “We’re going back to the office! No wait, we’re closing the office forever!” email extravaganza and emotional roller coaster. That second one, however, did not get nearly as much media coverage.

A whole new, tiny level of hangry

Ever been so hungry that everything just got on your nerves? Maybe you feel a little snappy right now? Like you’ll just lash out unless you get something to eat? Been there. And so have bacteria.

New research shows that some bacteria go into a full-on Hulk smash if they’re not getting the nutrients they need by releasing toxins into the body. Sounds like a bacterial temper tantrum.

Rosenthal et al.

Even though two cells may be genetically identical, they don’t always behave the same in a bacterial community. Some do their job and stay in line, but some evil twins rage out and make people sick by releasing toxins into the environment, Adam Rosenthal, PhD, of the University of North Carolina and his colleagues discovered.

To figure out why some cells were all business as usual while others were not, the investigators looked at Clostridium perfringens, a bacterium found in the intestines of humans and other vertebrates. When the C. perfringens cells were fed a little acetate to munch on, the hangry cells calmed down faster than a kid with a bag of fruit snacks, reducing toxin levels. Some cells even disappeared, falling in line with their model-citizen counterparts.

So what does this really mean? More research, duh. Now that we know nutrients play a role in toxicity, it may open the door to finding a way to fight against antibiotic resistance in humans and reduce antibiotic use in the food industry.

So think to yourself. Are you bothered for no reason? Getting a little testy with your friends and coworkers? Maybe you just haven’t eaten in a while. You’re literally not alone. Even a single-cell organism can behave based on its hunger levels.

Now go have a snack. Your bacteria are getting restless.
 

The very hangry iguana?

Imagine yourself on a warm, sunny tropical beach. You are enjoying a piece of cake as you take in the slow beat of the waves lapping against the shore. Life is as good as it could be.

Then you feel a presence nearby. Hostility. Hunger. A set of feral, covetous eyes in the nearby jungle. A reptilian beast stalks you, and its all-encompassing sweet tooth desires your cake.

Wait, hold on, what?

As an unfortunate 3-year-old on vacation in Costa Rica found out, there’s at least one iguana in the world out there with a taste for sugar (better than a taste for blood, we suppose).

Ulrike Mai/Pixabay

While out on the beach, the lizard darted out of nowhere, bit the girl on the back of the hand, and stole her cake. Still not the worst party guest ever. The child was taken to a local clinic, where the wound was cleaned and a 5-day antibiotic treatment (lizards carry salmonella) was provided. Things seemed fine, and the girl returned home without incident.

But of course, that’s not the end of the story. Five months later, the girl’s parents noticed a red bump at the wound site. Over the next 3 months, the surrounding skin grew red and painful. A trip to the hospital in California revealed that she had a ganglion cyst and a discharge of pus. Turns out our cake-obsessed lizard friend did give the little girl a gift: the first known human case of Mycobacterium marinum infection following an iguana bite on record.

M. marinum, which causes a disease similar to tuberculosis, typically infects fish but can infect humans if skin wounds are exposed to contaminated water. It’s also resistant to most antibiotics, which is why the first round didn’t clear up the infection. A second round of more-potent antibiotics seems to be working well.

So, to sum up, this poor child got bitten by a lizard, had her cake stolen, and contracted a rare illness in exchange. For a 3-year-old, that’s gotta be in the top-10 worst days ever. Unless, of course, we’re actually living in the Marvel universe (sorry, multiverse at this point). Then we’re totally going to see the emergence of the new superhero Iguana Girl in 15 years or so. Keep your eyes open.
 

No allergies? Let them give up cake

Allergy season is already here – starting earlier every year, it seems – and many people are not happy about it. So unhappy, actually, that there’s a list of things they would be willing to give up for a year to get rid of their of allergies, according to a survey conducted by OnePoll on behalf of Flonase.

nicoletaionescu/Getty Images

Nearly 40% of 2,000 respondents with allergies would go a year without eating cake or chocolate or playing video games in exchange for allergy-free status, the survey results show. Almost as many would forgo coffee (38%) or pizza (37%) for a year, while 36% would stay off social media and 31% would take a pay cut or give up their smartphones, the Independent reported.

More than half of the allergic Americans – 54%, to be exact – who were polled this past winter – Feb. 24 to March 1, to be exact – consider allergy symptoms to be the most frustrating part of the spring. Annoying things that were less frustrating to the group included mosquitoes (41%), filing tax returns (38%), and daylight savings time (37%).

The Trump arraignment circus, of course, occurred too late to make the list, as did the big “We’re going back to the office! No wait, we’re closing the office forever!” email extravaganza and emotional roller coaster. That second one, however, did not get nearly as much media coverage.

Psychiatrists practice in a wide array of ways. We approach our work and our patients with beliefs and preconceptions that develop over time. Our training has significant influence, though our own personalities and biases also affect our understanding.

Psychiatrists have philosophical lenses through which they see patients. We can reflect and see some standard archetypes. We are familiar with the reductionistic pharmacologist, the somatic treatment specialist, the psychodynamic ‘guru,’ and the medicolegally paralyzed practitioner. It is without judgment that we lay these out, for our very point is that we have these constituent parts within our own clinical identities. The intensity with which we subscribe to these clinical sensibilities could contribute to a biased orthodoxy.

Orthodoxy can be defined as an accepted theory that stems from an authoritative entity. This is a well-known phenomenon that continues to be visible. For example, one can quickly peruse psychodynamic literature to find one school of thought criticizing another. It is not without some confrontation and even interpersonal rifts that the lineage of psychoanalytic theory has evolved. This has always been of interest to us. A core facet of psychoanalysis is empathy, truly knowing the inner state of a different person. And yet, the very bastions of this clinical sensibility frequently resort to veiled attacks on those in their field who have opposing views. It then begs the question: If even enlightened institutions fail at a nonjudgmental approach toward their colleagues, what hope is there for the rest of us clinicians, mired in the thick of day-to-day clinical practice?

It is our contention that the odds are against us. Even the aforementioned critique of psychoanalytic orthodoxy is just another example of how we humans organize our experience. Even as we write an article in argument against unbridled critique, we find it difficult to do so without engaging in it. For to criticize another is to help shore up our own personal identities. This is especially the case when clinicians deal with issues that we feel strongly about. The human psyche has a need to organize its experience, as “our experience of ourselves is fundamental to how we operate in the world. Our subjective experience is the phenomenology of all that one might be aware of.”¹

In this vein, we would like to cite attribution theory. This is a view of human behavior within social psychology. The Austrian psychologist Fritz Heider, PhD, investigated “the domain of social interactions, wondering how people perceive each other in interaction and especially how they make sense of each other’s behavior.”² Attribution theory suggests that as humans organize our social interactions, we may make two basic assumptions. One is that our own behavior is highly affected by an environment that is beyond our control. The second is that when judging the behavior of others, we are more likely to attribute it to internal traits that they have. A classic example is automobile traffic. When we see someone driving erratically, we are more likely to blame them for being an inherently bad driver. However, if attention is called to our own driving, we are more likely to cite external factors such as rush hour, a bad driver around us, or a faulty vehicle.

We would like to reference one last model of human behavior. It has become customary within the field of neuroscience to view the brain as a predictive organ: “Theories of prediction in perception, action, and learning suggest that the brain serves to reduce the discrepancies between expectation and actual experience, i.e., by reducing the prediction error.”³ Perception itself has recently been described as a controlled hallucination, where the brain makes predictions of what it thinks it is about to see based on past experiences. Visual stimulus ultimately takes time to enter our eyes and be processed in the brain – “predictions would need to preactivate neural representations that would typically be driven by sensory input, before the actual arrival of that input.”⁴ It thus seems to be an inherent method of the brain to anticipate visual and even social events to help human beings sustain themselves.

Having spoken of a psychoanalytic conceptualization of self-organization, the theory of attribution, and research into social neuroscience, we turn our attention back to the central question that this article would like to address. Can we, as clinicians, truly put ourselves into the mindset of our colleagues and appreciate, and even agree with, the philosophies and methodologies of our fellow psychiatrists?

When we find ourselves busy in rote clinical practice, we believe the likelihood of intercollegiate mentalization is low; our ability to relate to our peers becomes strained. We ultimately do not practice in a vacuum. Psychiatrists, even those in a solo private practice, are ultimately part of a community of providers who, more or less, follow some emergent ‘standard of care.’ This can be a vague concept; but one that takes on a concrete form in the minds of certain clinicians and certainly in the setting of a medicolegal court. Yet, the psychiatrists that we know all have very stereotyped ways of practice. And at the heart of it, we all think that we are right.

We can use polypharmacy as an example. Imagine that you have a new patient intake, who tells you that they are transferring care from another psychiatrist. They inform you of their medication regimen. This patient presents on eight or more psychotropics. Many of us may have a visceral reaction at this point and, following the aforementioned attribution theory, we may ask ourselves what ‘quack’ of a doctor would do this. Yet some among us would think that a very competent psychopharmacologist was daring enough to use the full armamentarium of psychopharmacology to help this patient, who must be treatment refractory.

When speaking with such a patient, we would be quick to reflect on our own parsimonious use of medications. We would tell ourselves that we are responsible providers and would be quick to recommend discontinuation of medications. This would help us feel better about ourselves, and would of course assuage the ever-present medicolegal ‘big brother’ in our minds. It is through this very process that we affirm our self-identities. For if this patient’s previous physician was a bad psychiatrist, then we are a good psychiatrist. It is through this process that our clinical selves find confirmation.

We do not mean to reduce the complexities of human behavior to quick stereotypes. However, it is our belief that when confronted with clinical or philosophical disputes with our colleagues, the basic rules of human behavior will attempt to dissolve and override efforts at mentalization, collegiality, or interpersonal sensitivity. For to accept a clinical practice view that is different from ours would be akin to giving up the essence of our clinical identities. It could be compared to the fragmentation process of a vulnerable psyche when confronted with a reality that is at odds with preconceived notions and experiences.

While we may be able to appreciate the nuances and sensibilities of another provider, we believe it would be particularly difficult for most of us to actually attempt to practice in a fashion that is not congruent with our own organizers of experience. Whether or not our practice style is ‘perfect,’ it has worked for us. Social neuroscience and our understanding of the organization of the self would predict that we would hold onto our way of practice with all the mind’s defenses. Externalization, denial, and projection could all be called into action in this battle against existential fragmentation.

Do we seek to portray a clinical world where there is no hope for genuine modeling of clinical sensibilities to other psychiatrists? That is not our intention. Yet it seems that many of the theoretical frameworks that we subscribe to argue against this possibility. We would be hypocritical if we did not here state that our own theoretical frameworks are yet other examples of “organizers of experience.” Attribution theory, intersubjectivity, and social neuroscience are simply our ways of organizing the chaos of perceptions, ideas, and intricacies of human behavior.

If we accept that psychiatrists, like all human beings, are trapped in a subjective experience, then we can be more playful and flexible when interacting with our colleagues. We do not have to be as defensive of our practices and accusatory of others. If we practice daily according to some orthodoxy, then we color our experiences of the patient and of our colleagues’ ways of practice. We automatically start off on the wrong foot. And yet, to give up this orthodoxy would, by definition, be disorganizing and fragmenting to us. For as Nietzsche said, “truth is an illusion without which a certain species could not survive.”⁵

Dr. Khalafian practices full time as a general outpatient psychiatrist. He trained at the University of California, San Diego, for his psychiatric residency and currently works as a telepsychiatrist, serving an outpatient clinic population in northern California. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Khalafian have no conflicts of interest.

References

1. Buirski P and Haglund P. Making sense together: The intersubjective approach to psychotherapy. Northvale, NJ: Jason Aronson; 2001.

2. Malle BF. Attribution theories: How people make sense of behavior. In Chadee D (ed.), Theories in social psychology. pp. 72-95. Wiley-Blackwell; 2011.

3. Brown EC and Brune M. The role of prediction in social neuroscience. Front Hum Neurosci. 2012 May 24;6:147. doi: 10.3389/fnhum.2012.00147.

4. Blom T et al. Predictions drive neural representations of visual events ahead of incoming sensory information. Proc Natl Acad Sci USA. 2020 Mar 31;117(13):7510-7515. doi: 10.1073/pnas.1917777117.

5. Yalom I. The Gift of Therapy. Harper Perennial; 2002.

Psychiatrists practice in a wide array of ways. We approach our work and our patients with beliefs and preconceptions that develop over time. Our training has significant influence, though our own personalities and biases also affect our understanding.

Psychiatrists have philosophical lenses through which they see patients. We can reflect and see some standard archetypes. We are familiar with the reductionistic pharmacologist, the somatic treatment specialist, the psychodynamic ‘guru,’ and the medicolegally paralyzed practitioner. It is without judgment that we lay these out, for our very point is that we have these constituent parts within our own clinical identities. The intensity with which we subscribe to these clinical sensibilities could contribute to a biased orthodoxy.

Orthodoxy can be defined as an accepted theory that stems from an authoritative entity. This is a well-known phenomenon that continues to be visible. For example, one can quickly peruse psychodynamic literature to find one school of thought criticizing another. It is not without some confrontation and even interpersonal rifts that the lineage of psychoanalytic theory has evolved. This has always been of interest to us. A core facet of psychoanalysis is empathy, truly knowing the inner state of a different person. And yet, the very bastions of this clinical sensibility frequently resort to veiled attacks on those in their field who have opposing views. It then begs the question: If even enlightened institutions fail at a nonjudgmental approach toward their colleagues, what hope is there for the rest of us clinicians, mired in the thick of day-to-day clinical practice?

It is our contention that the odds are against us. Even the aforementioned critique of psychoanalytic orthodoxy is just another example of how we humans organize our experience. Even as we write an article in argument against unbridled critique, we find it difficult to do so without engaging in it. For to criticize another is to help shore up our own personal identities. This is especially the case when clinicians deal with issues that we feel strongly about. The human psyche has a need to organize its experience, as “our experience of ourselves is fundamental to how we operate in the world. Our subjective experience is the phenomenology of all that one might be aware of.”¹

In this vein, we would like to cite attribution theory. This is a view of human behavior within social psychology. The Austrian psychologist Fritz Heider, PhD, investigated “the domain of social interactions, wondering how people perceive each other in interaction and especially how they make sense of each other’s behavior.”² Attribution theory suggests that as humans organize our social interactions, we may make two basic assumptions. One is that our own behavior is highly affected by an environment that is beyond our control. The second is that when judging the behavior of others, we are more likely to attribute it to internal traits that they have. A classic example is automobile traffic. When we see someone driving erratically, we are more likely to blame them for being an inherently bad driver. However, if attention is called to our own driving, we are more likely to cite external factors such as rush hour, a bad driver around us, or a faulty vehicle.

We would like to reference one last model of human behavior. It has become customary within the field of neuroscience to view the brain as a predictive organ: “Theories of prediction in perception, action, and learning suggest that the brain serves to reduce the discrepancies between expectation and actual experience, i.e., by reducing the prediction error.”³ Perception itself has recently been described as a controlled hallucination, where the brain makes predictions of what it thinks it is about to see based on past experiences. Visual stimulus ultimately takes time to enter our eyes and be processed in the brain – “predictions would need to preactivate neural representations that would typically be driven by sensory input, before the actual arrival of that input.”⁴ It thus seems to be an inherent method of the brain to anticipate visual and even social events to help human beings sustain themselves.

Having spoken of a psychoanalytic conceptualization of self-organization, the theory of attribution, and research into social neuroscience, we turn our attention back to the central question that this article would like to address. Can we, as clinicians, truly put ourselves into the mindset of our colleagues and appreciate, and even agree with, the philosophies and methodologies of our fellow psychiatrists?

When we find ourselves busy in rote clinical practice, we believe the likelihood of intercollegiate mentalization is low; our ability to relate to our peers becomes strained. We ultimately do not practice in a vacuum. Psychiatrists, even those in a solo private practice, are ultimately part of a community of providers who, more or less, follow some emergent ‘standard of care.’ This can be a vague concept; but one that takes on a concrete form in the minds of certain clinicians and certainly in the setting of a medicolegal court. Yet, the psychiatrists that we know all have very stereotyped ways of practice. And at the heart of it, we all think that we are right.

We can use polypharmacy as an example. Imagine that you have a new patient intake, who tells you that they are transferring care from another psychiatrist. They inform you of their medication regimen. This patient presents on eight or more psychotropics. Many of us may have a visceral reaction at this point and, following the aforementioned attribution theory, we may ask ourselves what ‘quack’ of a doctor would do this. Yet some among us would think that a very competent psychopharmacologist was daring enough to use the full armamentarium of psychopharmacology to help this patient, who must be treatment refractory.

When speaking with such a patient, we would be quick to reflect on our own parsimonious use of medications. We would tell ourselves that we are responsible providers and would be quick to recommend discontinuation of medications. This would help us feel better about ourselves, and would of course assuage the ever-present medicolegal ‘big brother’ in our minds. It is through this very process that we affirm our self-identities. For if this patient’s previous physician was a bad psychiatrist, then we are a good psychiatrist. It is through this process that our clinical selves find confirmation.

We do not mean to reduce the complexities of human behavior to quick stereotypes. However, it is our belief that when confronted with clinical or philosophical disputes with our colleagues, the basic rules of human behavior will attempt to dissolve and override efforts at mentalization, collegiality, or interpersonal sensitivity. For to accept a clinical practice view that is different from ours would be akin to giving up the essence of our clinical identities. It could be compared to the fragmentation process of a vulnerable psyche when confronted with a reality that is at odds with preconceived notions and experiences.

While we may be able to appreciate the nuances and sensibilities of another provider, we believe it would be particularly difficult for most of us to actually attempt to practice in a fashion that is not congruent with our own organizers of experience. Whether or not our practice style is ‘perfect,’ it has worked for us. Social neuroscience and our understanding of the organization of the self would predict that we would hold onto our way of practice with all the mind’s defenses. Externalization, denial, and projection could all be called into action in this battle against existential fragmentation.

Do we seek to portray a clinical world where there is no hope for genuine modeling of clinical sensibilities to other psychiatrists? That is not our intention. Yet it seems that many of the theoretical frameworks that we subscribe to argue against this possibility. We would be hypocritical if we did not here state that our own theoretical frameworks are yet other examples of “organizers of experience.” Attribution theory, intersubjectivity, and social neuroscience are simply our ways of organizing the chaos of perceptions, ideas, and intricacies of human behavior.

If we accept that psychiatrists, like all human beings, are trapped in a subjective experience, then we can be more playful and flexible when interacting with our colleagues. We do not have to be as defensive of our practices and accusatory of others. If we practice daily according to some orthodoxy, then we color our experiences of the patient and of our colleagues’ ways of practice. We automatically start off on the wrong foot. And yet, to give up this orthodoxy would, by definition, be disorganizing and fragmenting to us. For as Nietzsche said, “truth is an illusion without which a certain species could not survive.”⁵

Dr. Khalafian practices full time as a general outpatient psychiatrist. He trained at the University of California, San Diego, for his psychiatric residency and currently works as a telepsychiatrist, serving an outpatient clinic population in northern California. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Khalafian have no conflicts of interest.

References

1. Buirski P and Haglund P. Making sense together: The intersubjective approach to psychotherapy. Northvale, NJ: Jason Aronson; 2001.

2. Malle BF. Attribution theories: How people make sense of behavior. In Chadee D (ed.), Theories in social psychology. pp. 72-95. Wiley-Blackwell; 2011.

3. Brown EC and Brune M. The role of prediction in social neuroscience. Front Hum Neurosci. 2012 May 24;6:147. doi: 10.3389/fnhum.2012.00147.

4. Blom T et al. Predictions drive neural representations of visual events ahead of incoming sensory information. Proc Natl Acad Sci USA. 2020 Mar 31;117(13):7510-7515. doi: 10.1073/pnas.1917777117.

5. Yalom I. The Gift of Therapy. Harper Perennial; 2002.

Psychiatrists practice in a wide array of ways. We approach our work and our patients with beliefs and preconceptions that develop over time. Our training has significant influence, though our own personalities and biases also affect our understanding.

Psychiatrists have philosophical lenses through which they see patients. We can reflect and see some standard archetypes. We are familiar with the reductionistic pharmacologist, the somatic treatment specialist, the psychodynamic ‘guru,’ and the medicolegally paralyzed practitioner. It is without judgment that we lay these out, for our very point is that we have these constituent parts within our own clinical identities. The intensity with which we subscribe to these clinical sensibilities could contribute to a biased orthodoxy.

Orthodoxy can be defined as an accepted theory that stems from an authoritative entity. This is a well-known phenomenon that continues to be visible. For example, one can quickly peruse psychodynamic literature to find one school of thought criticizing another. It is not without some confrontation and even interpersonal rifts that the lineage of psychoanalytic theory has evolved. This has always been of interest to us. A core facet of psychoanalysis is empathy, truly knowing the inner state of a different person. And yet, the very bastions of this clinical sensibility frequently resort to veiled attacks on those in their field who have opposing views. It then begs the question: If even enlightened institutions fail at a nonjudgmental approach toward their colleagues, what hope is there for the rest of us clinicians, mired in the thick of day-to-day clinical practice?

It is our contention that the odds are against us. Even the aforementioned critique of psychoanalytic orthodoxy is just another example of how we humans organize our experience. Even as we write an article in argument against unbridled critique, we find it difficult to do so without engaging in it. For to criticize another is to help shore up our own personal identities. This is especially the case when clinicians deal with issues that we feel strongly about. The human psyche has a need to organize its experience, as “our experience of ourselves is fundamental to how we operate in the world. Our subjective experience is the phenomenology of all that one might be aware of.”¹

In this vein, we would like to cite attribution theory. This is a view of human behavior within social psychology. The Austrian psychologist Fritz Heider, PhD, investigated “the domain of social interactions, wondering how people perceive each other in interaction and especially how they make sense of each other’s behavior.”² Attribution theory suggests that as humans organize our social interactions, we may make two basic assumptions. One is that our own behavior is highly affected by an environment that is beyond our control. The second is that when judging the behavior of others, we are more likely to attribute it to internal traits that they have. A classic example is automobile traffic. When we see someone driving erratically, we are more likely to blame them for being an inherently bad driver. However, if attention is called to our own driving, we are more likely to cite external factors such as rush hour, a bad driver around us, or a faulty vehicle.

We would like to reference one last model of human behavior. It has become customary within the field of neuroscience to view the brain as a predictive organ: “Theories of prediction in perception, action, and learning suggest that the brain serves to reduce the discrepancies between expectation and actual experience, i.e., by reducing the prediction error.”³ Perception itself has recently been described as a controlled hallucination, where the brain makes predictions of what it thinks it is about to see based on past experiences. Visual stimulus ultimately takes time to enter our eyes and be processed in the brain – “predictions would need to preactivate neural representations that would typically be driven by sensory input, before the actual arrival of that input.”⁴ It thus seems to be an inherent method of the brain to anticipate visual and even social events to help human beings sustain themselves.

Having spoken of a psychoanalytic conceptualization of self-organization, the theory of attribution, and research into social neuroscience, we turn our attention back to the central question that this article would like to address. Can we, as clinicians, truly put ourselves into the mindset of our colleagues and appreciate, and even agree with, the philosophies and methodologies of our fellow psychiatrists?

When we find ourselves busy in rote clinical practice, we believe the likelihood of intercollegiate mentalization is low; our ability to relate to our peers becomes strained. We ultimately do not practice in a vacuum. Psychiatrists, even those in a solo private practice, are ultimately part of a community of providers who, more or less, follow some emergent ‘standard of care.’ This can be a vague concept; but one that takes on a concrete form in the minds of certain clinicians and certainly in the setting of a medicolegal court. Yet, the psychiatrists that we know all have very stereotyped ways of practice. And at the heart of it, we all think that we are right.

We can use polypharmacy as an example. Imagine that you have a new patient intake, who tells you that they are transferring care from another psychiatrist. They inform you of their medication regimen. This patient presents on eight or more psychotropics. Many of us may have a visceral reaction at this point and, following the aforementioned attribution theory, we may ask ourselves what ‘quack’ of a doctor would do this. Yet some among us would think that a very competent psychopharmacologist was daring enough to use the full armamentarium of psychopharmacology to help this patient, who must be treatment refractory.

When speaking with such a patient, we would be quick to reflect on our own parsimonious use of medications. We would tell ourselves that we are responsible providers and would be quick to recommend discontinuation of medications. This would help us feel better about ourselves, and would of course assuage the ever-present medicolegal ‘big brother’ in our minds. It is through this very process that we affirm our self-identities. For if this patient’s previous physician was a bad psychiatrist, then we are a good psychiatrist. It is through this process that our clinical selves find confirmation.

We do not mean to reduce the complexities of human behavior to quick stereotypes. However, it is our belief that when confronted with clinical or philosophical disputes with our colleagues, the basic rules of human behavior will attempt to dissolve and override efforts at mentalization, collegiality, or interpersonal sensitivity. For to accept a clinical practice view that is different from ours would be akin to giving up the essence of our clinical identities. It could be compared to the fragmentation process of a vulnerable psyche when confronted with a reality that is at odds with preconceived notions and experiences.

While we may be able to appreciate the nuances and sensibilities of another provider, we believe it would be particularly difficult for most of us to actually attempt to practice in a fashion that is not congruent with our own organizers of experience. Whether or not our practice style is ‘perfect,’ it has worked for us. Social neuroscience and our understanding of the organization of the self would predict that we would hold onto our way of practice with all the mind’s defenses. Externalization, denial, and projection could all be called into action in this battle against existential fragmentation.

Do we seek to portray a clinical world where there is no hope for genuine modeling of clinical sensibilities to other psychiatrists? That is not our intention. Yet it seems that many of the theoretical frameworks that we subscribe to argue against this possibility. We would be hypocritical if we did not here state that our own theoretical frameworks are yet other examples of “organizers of experience.” Attribution theory, intersubjectivity, and social neuroscience are simply our ways of organizing the chaos of perceptions, ideas, and intricacies of human behavior.

If we accept that psychiatrists, like all human beings, are trapped in a subjective experience, then we can be more playful and flexible when interacting with our colleagues. We do not have to be as defensive of our practices and accusatory of others. If we practice daily according to some orthodoxy, then we color our experiences of the patient and of our colleagues’ ways of practice. We automatically start off on the wrong foot. And yet, to give up this orthodoxy would, by definition, be disorganizing and fragmenting to us. For as Nietzsche said, “truth is an illusion without which a certain species could not survive.”⁵

Dr. Khalafian practices full time as a general outpatient psychiatrist. He trained at the University of California, San Diego, for his psychiatric residency and currently works as a telepsychiatrist, serving an outpatient clinic population in northern California. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Khalafian have no conflicts of interest.

References

1. Buirski P and Haglund P. Making sense together: The intersubjective approach to psychotherapy. Northvale, NJ: Jason Aronson; 2001.

2. Malle BF. Attribution theories: How people make sense of behavior. In Chadee D (ed.), Theories in social psychology. pp. 72-95. Wiley-Blackwell; 2011.

3. Brown EC and Brune M. The role of prediction in social neuroscience. Front Hum Neurosci. 2012 May 24;6:147. doi: 10.3389/fnhum.2012.00147.

4. Blom T et al. Predictions drive neural representations of visual events ahead of incoming sensory information. Proc Natl Acad Sci USA. 2020 Mar 31;117(13):7510-7515. doi: 10.1073/pnas.1917777117.

5. Yalom I. The Gift of Therapy. Harper Perennial; 2002.

Contaminated, deadly, and blindness-causing eyedrops that were recalled earlier this year were made in India at a factory not inspected by the U.S. Food and Drug Administration, according to a new report. 

Scientists are concerned that the once-rare treatment-resistant bacteria found in the eyedrops can spread person-to-person, posing a risk of becoming a recurrent problem in the United States, The New York Times reported.

In January, EzriCare and Delsam Pharma artificial tears and ointment products were recalled after being linked to the bacterium P. aeruginosa. The bacteria have caused at least 68 infections, including three deaths and at least eight cases of blindness. The eyedrops were imported to the United States from India, and many of the cases occurred after the bacteria spread person-to-person at a long-term care facility in Connecticut, according to the Times, which cited FDA and Centers for Disease Control and Prevention lead investigator Maroya Walters, PhD.

Dr. Walters said the cases that caused death or blindness were traced to the EzriCare artificial tears product.

“It’s very hard to get rid of,” University of North Carolina at Chapel Hill infectious disease specialist David van Duin, MD, PhD, told the Times, noting that the bacteria cling to sink drains, water faucets, and other moist places. 

The FDA said it had halted the import of the recalled products and has since visited the plant in India where they were made, which is owned by Global Pharma Healthcare. In a citation to the company dated March 2, the FDA listed nearly a dozen problems, such as dirty equipment and the absence of safety procedures and tests. 

A version of this article originally appeared on WebMD.com.

Contaminated, deadly, and blindness-causing eyedrops that were recalled earlier this year were made in India at a factory not inspected by the U.S. Food and Drug Administration, according to a new report. 

Scientists are concerned that the once-rare treatment-resistant bacteria found in the eyedrops can spread person-to-person, posing a risk of becoming a recurrent problem in the United States, The New York Times reported.

In January, EzriCare and Delsam Pharma artificial tears and ointment products were recalled after being linked to the bacterium P. aeruginosa. The bacteria have caused at least 68 infections, including three deaths and at least eight cases of blindness. The eyedrops were imported to the United States from India, and many of the cases occurred after the bacteria spread person-to-person at a long-term care facility in Connecticut, according to the Times, which cited FDA and Centers for Disease Control and Prevention lead investigator Maroya Walters, PhD.

Dr. Walters said the cases that caused death or blindness were traced to the EzriCare artificial tears product.

“It’s very hard to get rid of,” University of North Carolina at Chapel Hill infectious disease specialist David van Duin, MD, PhD, told the Times, noting that the bacteria cling to sink drains, water faucets, and other moist places. 

The FDA said it had halted the import of the recalled products and has since visited the plant in India where they were made, which is owned by Global Pharma Healthcare. In a citation to the company dated March 2, the FDA listed nearly a dozen problems, such as dirty equipment and the absence of safety procedures and tests. 

A version of this article originally appeared on WebMD.com.

Contaminated, deadly, and blindness-causing eyedrops that were recalled earlier this year were made in India at a factory not inspected by the U.S. Food and Drug Administration, according to a new report. 

Scientists are concerned that the once-rare treatment-resistant bacteria found in the eyedrops can spread person-to-person, posing a risk of becoming a recurrent problem in the United States, The New York Times reported.

In January, EzriCare and Delsam Pharma artificial tears and ointment products were recalled after being linked to the bacterium P. aeruginosa. The bacteria have caused at least 68 infections, including three deaths and at least eight cases of blindness. The eyedrops were imported to the United States from India, and many of the cases occurred after the bacteria spread person-to-person at a long-term care facility in Connecticut, according to the Times, which cited FDA and Centers for Disease Control and Prevention lead investigator Maroya Walters, PhD.

Dr. Walters said the cases that caused death or blindness were traced to the EzriCare artificial tears product.

“It’s very hard to get rid of,” University of North Carolina at Chapel Hill infectious disease specialist David van Duin, MD, PhD, told the Times, noting that the bacteria cling to sink drains, water faucets, and other moist places. 

The FDA said it had halted the import of the recalled products and has since visited the plant in India where they were made, which is owned by Global Pharma Healthcare. In a citation to the company dated March 2, the FDA listed nearly a dozen problems, such as dirty equipment and the absence of safety procedures and tests. 

A version of this article originally appeared on WebMD.com.

I started taking care of Jim, a 68-year-old man with metastatic renal cell carcinoma back in the fall of 2018. Jim lived far from our clinic in the rural western Sierra Mountains and had a hard time getting to Santa Monica, but needed ongoing pain and symptom management, as well as follow-up visits with oncology and discussions with our teams about preparing for the end of life.

Luckily for Jim, the Centers for Medicare & Medicaid Services had relaxed the rules around telehealth because of the public health emergency, and we were easily able to provide telemedicine visits throughout the pandemic ensuring that Jim retained access to the care team that had managed his cancer for several years at that point. This would not have been possible without the use of telemedicine – at least not without great effort and expense by Jim to make frequent trips to our Santa Monica clinic.

So, you can imagine my apprehension when I received an email the other day from our billing department, informing billing providers like myself that “telehealth visits are still covered through the end of the year.” While this initially seemed like reassuring news, it immediately begged the question – what happens at the end of the year? What will care look like for patients like Jim who live at a significant distance from their providers?

The end of the COVID-19 public health emergency on May 11 has prompted states to reevaluate the future of telehealth for Medicaid and Medicare recipients. Most states plan to make some telehealth services permanent, particularly in rural areas. While other telehealth services have been extended through Dec. 31, 2024, under the Consolidated Appropriations Act of 2023.

But still, I worry about the end of the telemedicine era because telehealth (or, “video visits”) has revolutionized outpatient palliative care delivery. We can now see very ill patients in their own homes without imposing an undue burden on them to come in for yet another office visit. Prior to the public health emergency, our embedded palliative care program would see patients only when they were in the oncology clinic so as to not burden them with having to travel to yet another clinic. This made our palliative providers less efficient since patients were being seen by multiple providers in the same space, which led to some time spent waiting around. It also frequently tied up our clinic exam rooms for long periods of time, delaying care for patients sitting in the waiting room.

Telehealth changed that virtually overnight. With the widespread availability of smartphones and tablets, patients could stay at home and speak more comfortably in their own surroundings – especially about the difficult topics we tend to dig into in palliative care – such as fears, suffering, grief, loss, legacy, regret, trauma, gratitude, dying – without the impersonal, aseptic environment of a clinic. We could visit with their family/caregivers, kids, and their pets. We could tour their living space and see how they were managing from a functional standpoint. We could get to know aspects of our patients’ lives that we’d never have seen in the clinic that could help us understand their goals and values better and help care for them more fully.

The benefit to the institution was also measurable. We could see our patients faster – the time from referral to consult dropped dramatically because patients could be scheduled for next-day virtual visits instead of having to wait for them to come back to an oncology visit. We could do quick symptom-focused visits that prior to telehealth would have been conducted by phone without the ability to perform at the very least an observational physical exam of the patient, which is important when prescribing medications to medically frail populations.
 

If telemedicine goes, how will it affect outpatient palliative care?

If that goes away, I do not know what will happen to outpatient palliative care. I can tell you we will be much less efficient in terms of when we see patients. There will probably be a higher clinic burden to patients, as well as higher financial toxicity to patients (Parking in the structure attached to my office building is $22 per day). And, what about the uncaptured costs associated with transportation for those whose illness prevents them from driving themselves? This can range from Uber costs to the time cost for a patient’s family member to take off work and arrange for childcare in order to drive the patient to a clinic for a visit.

In February, I received emails from the Drug Enforcement Agency suggesting that they, too, may roll back providers’ ability to prescribe controlled substances to patients who are mainly receiving telehealth services. While I understand and fully support the need to curb inappropriate overprescribing of controlled medications, I am concerned about the unintended consequences to cancer patients who live at a remote distance from their oncologists and palliative care providers. I remain hopeful that DEA will consider a carveout exception for those patients who have cancer, are receiving palliative care services, or are deemed to be at the end of life, much like the chronic opioid guidelines developed by the Centers for Disease Control and Prevention have done.
 

Telemedicine in essential care

Back to Jim. Using telehealth and electronic prescribing, our oncology and palliative care programs were able to keep Jim comfortable and at home through the end of his life. He did not have to travel 3 hours each way to get care. He did not have to spend money on parking and gas, and his daughter did not have to take days off work and arrange for a babysitter in order to drive him to our clinic. We partnered with a local pharmacy that was willing to special order medications for Jim when his pain became worse and he required a long-acting opioid. We partnered with a local home health company that kept a close eye on Jim and let us know when he seemed to be declining further, prompting discussions about transitioning to hospice.

I’m proud of the fact that our group helped Jim stay in comfortable surroundings and out of the clinic and hospital over the last 6 months of his life, but that would never have happened without the safe and thoughtful use of telehealth by our team.

Ironically, because of a public health emergency, we were able to provide efficient and high-quality palliative care at the right time, to the right person, in the right place, satisfying CMS goals to provide better care for patients and whole populations at lower costs.

Ms. D’Ambruoso is a hospice and palliative care nurse practitioner for UCLA Health Cancer Care, Santa Monica, Calif.

I started taking care of Jim, a 68-year-old man with metastatic renal cell carcinoma back in the fall of 2018. Jim lived far from our clinic in the rural western Sierra Mountains and had a hard time getting to Santa Monica, but needed ongoing pain and symptom management, as well as follow-up visits with oncology and discussions with our teams about preparing for the end of life.

Luckily for Jim, the Centers for Medicare & Medicaid Services had relaxed the rules around telehealth because of the public health emergency, and we were easily able to provide telemedicine visits throughout the pandemic ensuring that Jim retained access to the care team that had managed his cancer for several years at that point. This would not have been possible without the use of telemedicine – at least not without great effort and expense by Jim to make frequent trips to our Santa Monica clinic.

So, you can imagine my apprehension when I received an email the other day from our billing department, informing billing providers like myself that “telehealth visits are still covered through the end of the year.” While this initially seemed like reassuring news, it immediately begged the question – what happens at the end of the year? What will care look like for patients like Jim who live at a significant distance from their providers?

The end of the COVID-19 public health emergency on May 11 has prompted states to reevaluate the future of telehealth for Medicaid and Medicare recipients. Most states plan to make some telehealth services permanent, particularly in rural areas. While other telehealth services have been extended through Dec. 31, 2024, under the Consolidated Appropriations Act of 2023.

But still, I worry about the end of the telemedicine era because telehealth (or, “video visits”) has revolutionized outpatient palliative care delivery. We can now see very ill patients in their own homes without imposing an undue burden on them to come in for yet another office visit. Prior to the public health emergency, our embedded palliative care program would see patients only when they were in the oncology clinic so as to not burden them with having to travel to yet another clinic. This made our palliative providers less efficient since patients were being seen by multiple providers in the same space, which led to some time spent waiting around. It also frequently tied up our clinic exam rooms for long periods of time, delaying care for patients sitting in the waiting room.

Telehealth changed that virtually overnight. With the widespread availability of smartphones and tablets, patients could stay at home and speak more comfortably in their own surroundings – especially about the difficult topics we tend to dig into in palliative care – such as fears, suffering, grief, loss, legacy, regret, trauma, gratitude, dying – without the impersonal, aseptic environment of a clinic. We could visit with their family/caregivers, kids, and their pets. We could tour their living space and see how they were managing from a functional standpoint. We could get to know aspects of our patients’ lives that we’d never have seen in the clinic that could help us understand their goals and values better and help care for them more fully.

The benefit to the institution was also measurable. We could see our patients faster – the time from referral to consult dropped dramatically because patients could be scheduled for next-day virtual visits instead of having to wait for them to come back to an oncology visit. We could do quick symptom-focused visits that prior to telehealth would have been conducted by phone without the ability to perform at the very least an observational physical exam of the patient, which is important when prescribing medications to medically frail populations.
 

If telemedicine goes, how will it affect outpatient palliative care?

If that goes away, I do not know what will happen to outpatient palliative care. I can tell you we will be much less efficient in terms of when we see patients. There will probably be a higher clinic burden to patients, as well as higher financial toxicity to patients (Parking in the structure attached to my office building is $22 per day). And, what about the uncaptured costs associated with transportation for those whose illness prevents them from driving themselves? This can range from Uber costs to the time cost for a patient’s family member to take off work and arrange for childcare in order to drive the patient to a clinic for a visit.

In February, I received emails from the Drug Enforcement Agency suggesting that they, too, may roll back providers’ ability to prescribe controlled substances to patients who are mainly receiving telehealth services. While I understand and fully support the need to curb inappropriate overprescribing of controlled medications, I am concerned about the unintended consequences to cancer patients who live at a remote distance from their oncologists and palliative care providers. I remain hopeful that DEA will consider a carveout exception for those patients who have cancer, are receiving palliative care services, or are deemed to be at the end of life, much like the chronic opioid guidelines developed by the Centers for Disease Control and Prevention have done.
 

Telemedicine in essential care

Back to Jim. Using telehealth and electronic prescribing, our oncology and palliative care programs were able to keep Jim comfortable and at home through the end of his life. He did not have to travel 3 hours each way to get care. He did not have to spend money on parking and gas, and his daughter did not have to take days off work and arrange for a babysitter in order to drive him to our clinic. We partnered with a local pharmacy that was willing to special order medications for Jim when his pain became worse and he required a long-acting opioid. We partnered with a local home health company that kept a close eye on Jim and let us know when he seemed to be declining further, prompting discussions about transitioning to hospice.

I’m proud of the fact that our group helped Jim stay in comfortable surroundings and out of the clinic and hospital over the last 6 months of his life, but that would never have happened without the safe and thoughtful use of telehealth by our team.

Ironically, because of a public health emergency, we were able to provide efficient and high-quality palliative care at the right time, to the right person, in the right place, satisfying CMS goals to provide better care for patients and whole populations at lower costs.

Ms. D’Ambruoso is a hospice and palliative care nurse practitioner for UCLA Health Cancer Care, Santa Monica, Calif.

I started taking care of Jim, a 68-year-old man with metastatic renal cell carcinoma back in the fall of 2018. Jim lived far from our clinic in the rural western Sierra Mountains and had a hard time getting to Santa Monica, but needed ongoing pain and symptom management, as well as follow-up visits with oncology and discussions with our teams about preparing for the end of life.

Luckily for Jim, the Centers for Medicare & Medicaid Services had relaxed the rules around telehealth because of the public health emergency, and we were easily able to provide telemedicine visits throughout the pandemic ensuring that Jim retained access to the care team that had managed his cancer for several years at that point. This would not have been possible without the use of telemedicine – at least not without great effort and expense by Jim to make frequent trips to our Santa Monica clinic.

So, you can imagine my apprehension when I received an email the other day from our billing department, informing billing providers like myself that “telehealth visits are still covered through the end of the year.” While this initially seemed like reassuring news, it immediately begged the question – what happens at the end of the year? What will care look like for patients like Jim who live at a significant distance from their providers?

The end of the COVID-19 public health emergency on May 11 has prompted states to reevaluate the future of telehealth for Medicaid and Medicare recipients. Most states plan to make some telehealth services permanent, particularly in rural areas. While other telehealth services have been extended through Dec. 31, 2024, under the Consolidated Appropriations Act of 2023.

But still, I worry about the end of the telemedicine era because telehealth (or, “video visits”) has revolutionized outpatient palliative care delivery. We can now see very ill patients in their own homes without imposing an undue burden on them to come in for yet another office visit. Prior to the public health emergency, our embedded palliative care program would see patients only when they were in the oncology clinic so as to not burden them with having to travel to yet another clinic. This made our palliative providers less efficient since patients were being seen by multiple providers in the same space, which led to some time spent waiting around. It also frequently tied up our clinic exam rooms for long periods of time, delaying care for patients sitting in the waiting room.

Telehealth changed that virtually overnight. With the widespread availability of smartphones and tablets, patients could stay at home and speak more comfortably in their own surroundings – especially about the difficult topics we tend to dig into in palliative care – such as fears, suffering, grief, loss, legacy, regret, trauma, gratitude, dying – without the impersonal, aseptic environment of a clinic. We could visit with their family/caregivers, kids, and their pets. We could tour their living space and see how they were managing from a functional standpoint. We could get to know aspects of our patients’ lives that we’d never have seen in the clinic that could help us understand their goals and values better and help care for them more fully.

The benefit to the institution was also measurable. We could see our patients faster – the time from referral to consult dropped dramatically because patients could be scheduled for next-day virtual visits instead of having to wait for them to come back to an oncology visit. We could do quick symptom-focused visits that prior to telehealth would have been conducted by phone without the ability to perform at the very least an observational physical exam of the patient, which is important when prescribing medications to medically frail populations.
 

If telemedicine goes, how will it affect outpatient palliative care?

If that goes away, I do not know what will happen to outpatient palliative care. I can tell you we will be much less efficient in terms of when we see patients. There will probably be a higher clinic burden to patients, as well as higher financial toxicity to patients (Parking in the structure attached to my office building is $22 per day). And, what about the uncaptured costs associated with transportation for those whose illness prevents them from driving themselves? This can range from Uber costs to the time cost for a patient’s family member to take off work and arrange for childcare in order to drive the patient to a clinic for a visit.

In February, I received emails from the Drug Enforcement Agency suggesting that they, too, may roll back providers’ ability to prescribe controlled substances to patients who are mainly receiving telehealth services. While I understand and fully support the need to curb inappropriate overprescribing of controlled medications, I am concerned about the unintended consequences to cancer patients who live at a remote distance from their oncologists and palliative care providers. I remain hopeful that DEA will consider a carveout exception for those patients who have cancer, are receiving palliative care services, or are deemed to be at the end of life, much like the chronic opioid guidelines developed by the Centers for Disease Control and Prevention have done.
 

Telemedicine in essential care

Back to Jim. Using telehealth and electronic prescribing, our oncology and palliative care programs were able to keep Jim comfortable and at home through the end of his life. He did not have to travel 3 hours each way to get care. He did not have to spend money on parking and gas, and his daughter did not have to take days off work and arrange for a babysitter in order to drive him to our clinic. We partnered with a local pharmacy that was willing to special order medications for Jim when his pain became worse and he required a long-acting opioid. We partnered with a local home health company that kept a close eye on Jim and let us know when he seemed to be declining further, prompting discussions about transitioning to hospice.

I’m proud of the fact that our group helped Jim stay in comfortable surroundings and out of the clinic and hospital over the last 6 months of his life, but that would never have happened without the safe and thoughtful use of telehealth by our team.

Ironically, because of a public health emergency, we were able to provide efficient and high-quality palliative care at the right time, to the right person, in the right place, satisfying CMS goals to provide better care for patients and whole populations at lower costs.

Ms. D’Ambruoso is a hospice and palliative care nurse practitioner for UCLA Health Cancer Care, Santa Monica, Calif.

People’s perception of time is subjective and based not only on their emotional state but also on heartbeat and heart rate (HR), two new studies suggest.

Researchers studied young adults with an electrocardiogram (ECG), measuring electrical activity at millisecond resolution while participants listened to tones that varied in duration. Participants were asked to report whether certain tones were longer or shorter, in relation to others.

The researchers found that the momentary perception of time was not continuous but rather expanded or contracted with each heartbeat. When the heartbeat preceding a tone was shorter, participants regarded the tone as longer in duration; but when the preceding heartbeat was longer, the participants experienced the tone as shorter.

“Our findings suggest that there is a unique role that cardiac dynamics play in the momentary experience of time,” lead author Saeedah Sadeghi, MSc, a doctoral candidate in the department of psychology at Cornell University, Ithaca, N.Y., said in an interview.

The study was published online  in Psychophysiology.

In a second study, published in the journal Current Biology, a separate team of researchers asked participants to judge whether a brief event – the presentation of a tone or an image – was shorter or longer than a reference duration. ECG was used to track systole and diastole when participants were presented with these events.

The researchers found that the durations were underestimated during systole and overestimated during diastole, suggesting that time seemed to “speed up” or “slow down,” based on cardiac contraction and relaxation. When participants rated the events as more arousing, their perceived durations contracted, even during diastole.

“In our new paper, we show that our heart shapes the perceived duration of events, so time passes quicker when the heart contracts but slower when the heart relaxes,” lead author Irena Arslanova, PhD, postdoctoral researcher in cognitive neuroscience, Royal Holloway University of London, told this news organization.
 

Temporal ‘wrinkles’

“Subjective time is malleable,” observed Ms. Sadeghi and colleagues in their report. “Rather than being a uniform dimension, perceived duration has ‘wrinkles,’ with certain intervals appearing to dilate or contract relative to objective time” – a phenomenon sometimes referred to as “distortion.”

“We have known that people aren’t always consistent in how they perceive time, and objective duration doesn’t always explain subjective perception of time,” Ms. Sadeghi said.

Although the potential role of the heart in the experience of time has been hypothesized, research into the heart-time connection has been limited, with previous studies focusing primarily on estimating the average cardiac measures on longer time scales over seconds to minutes.

The current study sought to investigate “the beat-by-beat fluctuations of the heart period on the experience of brief moments in time” because, compared with longer time scales, subsecond temporal perception “has different underlying mechanisms” and a subsecond stimulus can be a “small fraction of a heartbeat.”

To home in on this small fraction, the researchers studied 45 participants (aged 18-21), who listened to 210 tones ranging in duration from 80 ms (short) to 188 ms (long). The tones were linearly spaced at 18-ms increments (80, 98, 116, 134, 152, 170, 188).

Participants were asked to categorize each tone as “short” or “long.” All tones were randomly assigned to be synchronized either with the systolic or diastolic phase of the cardiac cycle (50% each). The tones were triggered by participants’ heartbeats.

In addition, participants engaged in a heartbeat-counting activity, in which they were asked not to touch their pulse but to count their heartbeats by tuning in to their bodily sensations at intervals of 25, 35, and 45 seconds.
 

‘Classical’ response

“Participants exhibited an increased heart period after tone onset, which returned to baseline following an average canonical bell shape,” the authors reported.

The researchers performed regression analyses to determine how, on average, the heart rate before the tone was related to perceived duration or how the amount of change after the tone was related to perceived duration.

They found that when the heart rate was higher before the tone, participants tended to be more accurate in their time perception. When the heartbeat preceding a tone was shorter, participants experienced the tone as longer; conversely, when the heartbeat was longer, they experienced the duration of the identical sound as shorter.

When participants focused their attention on the sounds, their heart rate was affected such that their orienting responses actually changed their heart rate and, in turn, their temporal perception.

“The orienting response is classical,” Ms. Sadeghi said. “When you attend to something unpredictable or novel, the act of orienting attention decreases the HR.”

She explained that the heartbeats are “noise to the brain.” When people need to perceive external events, “a decrease in HR facilitates the intake of things from outside and facilitates sensory intake.”

A lower HR “makes it easier for the person to take in the tone and perceive it, so it feels as though they perceive more of the tone and the duration seems longer – similarly, when the HR decreases.”

It is unknown whether this is a causal relationship, she cautioned, “but it seems as though the decrease in HR somehow makes it easier to ‘get’ more of the tone, which then appears to have longer duration.”
 

Bidirectional relationship

“We know that experienced time can be distorted,” said Dr. Arslanova. “Time flies by when we’re busy or having fun but drags on when we’re bored or waiting for something, yet we still don’t know how the brain gives rise to such elastic experience of time.”

The brain controls the heart in response to the information the heart provides about the state of the body, she noted, “but we have begun to see more research showing that the heart–brain relationship is bidirectional.”

This means that the heart plays a role in shaping “how we process information and experience emotions.” In this analysis, Dr. Arslanova and colleagues “wanted to study whether the heart also shapes the experience of time.”

To do so, they conducted two experiments.

In the first, participants (n = 28) were presented with brief events during systole or during diastole. The events took the form of an emotionally neutral visual shape or auditory tone, shown for durations of 200 to 400 ms.

Participants were asked whether these events were of longer or shorter duration, compared with a reference duration.

The researchers found significant main effect of cardiac phase systole (F(1,27) = 8.1, P =.01), with stimuli presented at diastole regarded, on average, as 7 ms longer than those presented at systole.

They also found a significant main effect of modality (F(1,27) = 5.7, P = .02), with tones judged, on average, as 13 ms longer than visual stimuli.

“This means that time ‘sped up’ during the heart’s contraction and ‘slowed down’ during the heart’s relaxation,” Dr. Arslanova said.

The effect of cardiac phase on duration perception was independent of changes in HR, the authors noted.

In the second experiment, participants performed a similar task, but this time, it involved the images of faces containing emotional expressions. The researchers again observed a similar pattern of time appearing to speed up during systole and slow down during diastole, with stimuli present at diastole regarded as being an average 9 ms longer than those presented at systole.

These opposing effects of systole and diastole on time perception were present only for low and average arousal ratings (b = 14.4 [SE 3.2], P < .001 and b = 9.2 [2.3], P <.001, respectively). However, this effect disappeared when arousal ratings increased (b = 4.1 [3.2] P =.21).

“Interestingly, when participants rated the events as more arousing, their perceived durations contracted, even during the heart’s relaxation,” Dr. Arslanova observed. “This means that in a nonaroused state, the two cardiac phases pull the experienced duration in opposite directions – time contracts, then expands.”

The findings “also predict that increasing HR would speed up passing time, making events seem shorter, because there will be a stronger influence from the heart’s contractions,” she said.

She described the relationship between time perception and emotion as complex, noting that the findings are important because they show “that the way we experience time cannot be examined in isolation from our body,” she said.
 

Converging evidence

Martin Wiener, PhD, assistant professor, George Mason University, Fairfax, Va., said both papers “provide converging evidence on the role of the heart in our perception of time.”

Together, “the results share that our sense of time – that is, our incoming sensory perception of the present ‘moment’ – is adjusted or ‘gated’ by both our HR and cardiac phase,” said Dr. Wiener, executive director of the Timing Research Forum.

The studies “provide a link between the body and the brain, in terms of our perception, and that we cannot study one without the context of the other,” said Dr. Wiener, who was not involved with the current study.

“All of this opens up a new avenue of research, and so it is very exciting to see,” Dr. Wiener stated.

No source of funding was listed for the study by Ms. Sadeghi and coauthors. They declared no relevant financial relationships.

Dr. Arslanova and coauthors declared no competing interests. Senior author Manos Tsakiris, PhD, receives funding from the European Research Council Consolidator Grant. Dr. Wiener declared no relevant financial relationships.
 

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

People’s perception of time is subjective and based not only on their emotional state but also on heartbeat and heart rate (HR), two new studies suggest.

Researchers studied young adults with an electrocardiogram (ECG), measuring electrical activity at millisecond resolution while participants listened to tones that varied in duration. Participants were asked to report whether certain tones were longer or shorter, in relation to others.

The researchers found that the momentary perception of time was not continuous but rather expanded or contracted with each heartbeat. When the heartbeat preceding a tone was shorter, participants regarded the tone as longer in duration; but when the preceding heartbeat was longer, the participants experienced the tone as shorter.

“Our findings suggest that there is a unique role that cardiac dynamics play in the momentary experience of time,” lead author Saeedah Sadeghi, MSc, a doctoral candidate in the department of psychology at Cornell University, Ithaca, N.Y., said in an interview.

The study was published online  in Psychophysiology.

In a second study, published in the journal Current Biology, a separate team of researchers asked participants to judge whether a brief event – the presentation of a tone or an image – was shorter or longer than a reference duration. ECG was used to track systole and diastole when participants were presented with these events.

The researchers found that the durations were underestimated during systole and overestimated during diastole, suggesting that time seemed to “speed up” or “slow down,” based on cardiac contraction and relaxation. When participants rated the events as more arousing, their perceived durations contracted, even during diastole.

“In our new paper, we show that our heart shapes the perceived duration of events, so time passes quicker when the heart contracts but slower when the heart relaxes,” lead author Irena Arslanova, PhD, postdoctoral researcher in cognitive neuroscience, Royal Holloway University of London, told this news organization.
 

Temporal ‘wrinkles’

“Subjective time is malleable,” observed Ms. Sadeghi and colleagues in their report. “Rather than being a uniform dimension, perceived duration has ‘wrinkles,’ with certain intervals appearing to dilate or contract relative to objective time” – a phenomenon sometimes referred to as “distortion.”

“We have known that people aren’t always consistent in how they perceive time, and objective duration doesn’t always explain subjective perception of time,” Ms. Sadeghi said.

Although the potential role of the heart in the experience of time has been hypothesized, research into the heart-time connection has been limited, with previous studies focusing primarily on estimating the average cardiac measures on longer time scales over seconds to minutes.

The current study sought to investigate “the beat-by-beat fluctuations of the heart period on the experience of brief moments in time” because, compared with longer time scales, subsecond temporal perception “has different underlying mechanisms” and a subsecond stimulus can be a “small fraction of a heartbeat.”

To home in on this small fraction, the researchers studied 45 participants (aged 18-21), who listened to 210 tones ranging in duration from 80 ms (short) to 188 ms (long). The tones were linearly spaced at 18-ms increments (80, 98, 116, 134, 152, 170, 188).

Participants were asked to categorize each tone as “short” or “long.” All tones were randomly assigned to be synchronized either with the systolic or diastolic phase of the cardiac cycle (50% each). The tones were triggered by participants’ heartbeats.

In addition, participants engaged in a heartbeat-counting activity, in which they were asked not to touch their pulse but to count their heartbeats by tuning in to their bodily sensations at intervals of 25, 35, and 45 seconds.
 

‘Classical’ response

“Participants exhibited an increased heart period after tone onset, which returned to baseline following an average canonical bell shape,” the authors reported.

The researchers performed regression analyses to determine how, on average, the heart rate before the tone was related to perceived duration or how the amount of change after the tone was related to perceived duration.

They found that when the heart rate was higher before the tone, participants tended to be more accurate in their time perception. When the heartbeat preceding a tone was shorter, participants experienced the tone as longer; conversely, when the heartbeat was longer, they experienced the duration of the identical sound as shorter.

When participants focused their attention on the sounds, their heart rate was affected such that their orienting responses actually changed their heart rate and, in turn, their temporal perception.

“The orienting response is classical,” Ms. Sadeghi said. “When you attend to something unpredictable or novel, the act of orienting attention decreases the HR.”

She explained that the heartbeats are “noise to the brain.” When people need to perceive external events, “a decrease in HR facilitates the intake of things from outside and facilitates sensory intake.”

A lower HR “makes it easier for the person to take in the tone and perceive it, so it feels as though they perceive more of the tone and the duration seems longer – similarly, when the HR decreases.”

It is unknown whether this is a causal relationship, she cautioned, “but it seems as though the decrease in HR somehow makes it easier to ‘get’ more of the tone, which then appears to have longer duration.”
 

Bidirectional relationship

“We know that experienced time can be distorted,” said Dr. Arslanova. “Time flies by when we’re busy or having fun but drags on when we’re bored or waiting for something, yet we still don’t know how the brain gives rise to such elastic experience of time.”

The brain controls the heart in response to the information the heart provides about the state of the body, she noted, “but we have begun to see more research showing that the heart–brain relationship is bidirectional.”

This means that the heart plays a role in shaping “how we process information and experience emotions.” In this analysis, Dr. Arslanova and colleagues “wanted to study whether the heart also shapes the experience of time.”

To do so, they conducted two experiments.

In the first, participants (n = 28) were presented with brief events during systole or during diastole. The events took the form of an emotionally neutral visual shape or auditory tone, shown for durations of 200 to 400 ms.

Participants were asked whether these events were of longer or shorter duration, compared with a reference duration.

The researchers found significant main effect of cardiac phase systole (F(1,27) = 8.1, P =.01), with stimuli presented at diastole regarded, on average, as 7 ms longer than those presented at systole.

They also found a significant main effect of modality (F(1,27) = 5.7, P = .02), with tones judged, on average, as 13 ms longer than visual stimuli.

“This means that time ‘sped up’ during the heart’s contraction and ‘slowed down’ during the heart’s relaxation,” Dr. Arslanova said.

The effect of cardiac phase on duration perception was independent of changes in HR, the authors noted.

In the second experiment, participants performed a similar task, but this time, it involved the images of faces containing emotional expressions. The researchers again observed a similar pattern of time appearing to speed up during systole and slow down during diastole, with stimuli present at diastole regarded as being an average 9 ms longer than those presented at systole.

These opposing effects of systole and diastole on time perception were present only for low and average arousal ratings (b = 14.4 [SE 3.2], P < .001 and b = 9.2 [2.3], P <.001, respectively). However, this effect disappeared when arousal ratings increased (b = 4.1 [3.2] P =.21).

“Interestingly, when participants rated the events as more arousing, their perceived durations contracted, even during the heart’s relaxation,” Dr. Arslanova observed. “This means that in a nonaroused state, the two cardiac phases pull the experienced duration in opposite directions – time contracts, then expands.”

The findings “also predict that increasing HR would speed up passing time, making events seem shorter, because there will be a stronger influence from the heart’s contractions,” she said.

She described the relationship between time perception and emotion as complex, noting that the findings are important because they show “that the way we experience time cannot be examined in isolation from our body,” she said.
 

Converging evidence

Martin Wiener, PhD, assistant professor, George Mason University, Fairfax, Va., said both papers “provide converging evidence on the role of the heart in our perception of time.”

Together, “the results share that our sense of time – that is, our incoming sensory perception of the present ‘moment’ – is adjusted or ‘gated’ by both our HR and cardiac phase,” said Dr. Wiener, executive director of the Timing Research Forum.

The studies “provide a link between the body and the brain, in terms of our perception, and that we cannot study one without the context of the other,” said Dr. Wiener, who was not involved with the current study.

“All of this opens up a new avenue of research, and so it is very exciting to see,” Dr. Wiener stated.

No source of funding was listed for the study by Ms. Sadeghi and coauthors. They declared no relevant financial relationships.

Dr. Arslanova and coauthors declared no competing interests. Senior author Manos Tsakiris, PhD, receives funding from the European Research Council Consolidator Grant. Dr. Wiener declared no relevant financial relationships.
 

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

People’s perception of time is subjective and based not only on their emotional state but also on heartbeat and heart rate (HR), two new studies suggest.

Researchers studied young adults with an electrocardiogram (ECG), measuring electrical activity at millisecond resolution while participants listened to tones that varied in duration. Participants were asked to report whether certain tones were longer or shorter, in relation to others.

The researchers found that the momentary perception of time was not continuous but rather expanded or contracted with each heartbeat. When the heartbeat preceding a tone was shorter, participants regarded the tone as longer in duration; but when the preceding heartbeat was longer, the participants experienced the tone as shorter.

“Our findings suggest that there is a unique role that cardiac dynamics play in the momentary experience of time,” lead author Saeedah Sadeghi, MSc, a doctoral candidate in the department of psychology at Cornell University, Ithaca, N.Y., said in an interview.

The study was published online  in Psychophysiology.

In a second study, published in the journal Current Biology, a separate team of researchers asked participants to judge whether a brief event – the presentation of a tone or an image – was shorter or longer than a reference duration. ECG was used to track systole and diastole when participants were presented with these events.

The researchers found that the durations were underestimated during systole and overestimated during diastole, suggesting that time seemed to “speed up” or “slow down,” based on cardiac contraction and relaxation. When participants rated the events as more arousing, their perceived durations contracted, even during diastole.

“In our new paper, we show that our heart shapes the perceived duration of events, so time passes quicker when the heart contracts but slower when the heart relaxes,” lead author Irena Arslanova, PhD, postdoctoral researcher in cognitive neuroscience, Royal Holloway University of London, told this news organization.
 

Temporal ‘wrinkles’

“Subjective time is malleable,” observed Ms. Sadeghi and colleagues in their report. “Rather than being a uniform dimension, perceived duration has ‘wrinkles,’ with certain intervals appearing to dilate or contract relative to objective time” – a phenomenon sometimes referred to as “distortion.”

“We have known that people aren’t always consistent in how they perceive time, and objective duration doesn’t always explain subjective perception of time,” Ms. Sadeghi said.

Although the potential role of the heart in the experience of time has been hypothesized, research into the heart-time connection has been limited, with previous studies focusing primarily on estimating the average cardiac measures on longer time scales over seconds to minutes.

The current study sought to investigate “the beat-by-beat fluctuations of the heart period on the experience of brief moments in time” because, compared with longer time scales, subsecond temporal perception “has different underlying mechanisms” and a subsecond stimulus can be a “small fraction of a heartbeat.”

To home in on this small fraction, the researchers studied 45 participants (aged 18-21), who listened to 210 tones ranging in duration from 80 ms (short) to 188 ms (long). The tones were linearly spaced at 18-ms increments (80, 98, 116, 134, 152, 170, 188).

Participants were asked to categorize each tone as “short” or “long.” All tones were randomly assigned to be synchronized either with the systolic or diastolic phase of the cardiac cycle (50% each). The tones were triggered by participants’ heartbeats.

In addition, participants engaged in a heartbeat-counting activity, in which they were asked not to touch their pulse but to count their heartbeats by tuning in to their bodily sensations at intervals of 25, 35, and 45 seconds.
 

‘Classical’ response

“Participants exhibited an increased heart period after tone onset, which returned to baseline following an average canonical bell shape,” the authors reported.

The researchers performed regression analyses to determine how, on average, the heart rate before the tone was related to perceived duration or how the amount of change after the tone was related to perceived duration.

They found that when the heart rate was higher before the tone, participants tended to be more accurate in their time perception. When the heartbeat preceding a tone was shorter, participants experienced the tone as longer; conversely, when the heartbeat was longer, they experienced the duration of the identical sound as shorter.

When participants focused their attention on the sounds, their heart rate was affected such that their orienting responses actually changed their heart rate and, in turn, their temporal perception.

“The orienting response is classical,” Ms. Sadeghi said. “When you attend to something unpredictable or novel, the act of orienting attention decreases the HR.”

She explained that the heartbeats are “noise to the brain.” When people need to perceive external events, “a decrease in HR facilitates the intake of things from outside and facilitates sensory intake.”

A lower HR “makes it easier for the person to take in the tone and perceive it, so it feels as though they perceive more of the tone and the duration seems longer – similarly, when the HR decreases.”

It is unknown whether this is a causal relationship, she cautioned, “but it seems as though the decrease in HR somehow makes it easier to ‘get’ more of the tone, which then appears to have longer duration.”
 

Bidirectional relationship

“We know that experienced time can be distorted,” said Dr. Arslanova. “Time flies by when we’re busy or having fun but drags on when we’re bored or waiting for something, yet we still don’t know how the brain gives rise to such elastic experience of time.”

The brain controls the heart in response to the information the heart provides about the state of the body, she noted, “but we have begun to see more research showing that the heart–brain relationship is bidirectional.”

This means that the heart plays a role in shaping “how we process information and experience emotions.” In this analysis, Dr. Arslanova and colleagues “wanted to study whether the heart also shapes the experience of time.”

To do so, they conducted two experiments.

In the first, participants (n = 28) were presented with brief events during systole or during diastole. The events took the form of an emotionally neutral visual shape or auditory tone, shown for durations of 200 to 400 ms.

Participants were asked whether these events were of longer or shorter duration, compared with a reference duration.

The researchers found significant main effect of cardiac phase systole (F(1,27) = 8.1, P =.01), with stimuli presented at diastole regarded, on average, as 7 ms longer than those presented at systole.

They also found a significant main effect of modality (F(1,27) = 5.7, P = .02), with tones judged, on average, as 13 ms longer than visual stimuli.

“This means that time ‘sped up’ during the heart’s contraction and ‘slowed down’ during the heart’s relaxation,” Dr. Arslanova said.

The effect of cardiac phase on duration perception was independent of changes in HR, the authors noted.

In the second experiment, participants performed a similar task, but this time, it involved the images of faces containing emotional expressions. The researchers again observed a similar pattern of time appearing to speed up during systole and slow down during diastole, with stimuli present at diastole regarded as being an average 9 ms longer than those presented at systole.

These opposing effects of systole and diastole on time perception were present only for low and average arousal ratings (b = 14.4 [SE 3.2], P < .001 and b = 9.2 [2.3], P <.001, respectively). However, this effect disappeared when arousal ratings increased (b = 4.1 [3.2] P =.21).

“Interestingly, when participants rated the events as more arousing, their perceived durations contracted, even during the heart’s relaxation,” Dr. Arslanova observed. “This means that in a nonaroused state, the two cardiac phases pull the experienced duration in opposite directions – time contracts, then expands.”

The findings “also predict that increasing HR would speed up passing time, making events seem shorter, because there will be a stronger influence from the heart’s contractions,” she said.

She described the relationship between time perception and emotion as complex, noting that the findings are important because they show “that the way we experience time cannot be examined in isolation from our body,” she said.
 

Converging evidence

Martin Wiener, PhD, assistant professor, George Mason University, Fairfax, Va., said both papers “provide converging evidence on the role of the heart in our perception of time.”

Together, “the results share that our sense of time – that is, our incoming sensory perception of the present ‘moment’ – is adjusted or ‘gated’ by both our HR and cardiac phase,” said Dr. Wiener, executive director of the Timing Research Forum.

The studies “provide a link between the body and the brain, in terms of our perception, and that we cannot study one without the context of the other,” said Dr. Wiener, who was not involved with the current study.

“All of this opens up a new avenue of research, and so it is very exciting to see,” Dr. Wiener stated.

No source of funding was listed for the study by Ms. Sadeghi and coauthors. They declared no relevant financial relationships.

Dr. Arslanova and coauthors declared no competing interests. Senior author Manos Tsakiris, PhD, receives funding from the European Research Council Consolidator Grant. Dr. Wiener declared no relevant financial relationships.
 

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

A former manager at the Philadelphia Veterans Affairs Medical Center (VAMC) has been sentenced to 6 months in federal prison for his part in a bribery scheme.

Ralph Johnson was convicted of accepting $30,000 in kickbacks and bribes for steering contracts to Earron and Carlicha Starks, who ran Ekno Medical Supply and Collondale Medical Supply from 2009 to 2019. Johnson served as chief of environmental services at the medical center. He admitted to receiving cash in binders and packages mailed to his home between 2018 and 2019.

The Starkses pleaded guilty first to paying kickbacks on $7 million worth of contracts to Florida VA facilities, then participated in a sting that implicated Johnson.

The VA Office of Inspector General began investigating Johnson in 2018 after the Starkses, who were indicted for bribing staff at US Department of Veterans Affairs (VA) hospitals in Miami and West Palm Beach, Florida, said they also paid officials in VA facilities on the East Coast.

According to the Philadelphia Inquirer, the judge credited Johnson’s past military service and his “extensive cooperation” with federal authorities investigating fraud within the VA. Johnson apologized to his former employers: “Throughout these 2 and a half years [since the arrest] there’s not a day I don’t think about the wrongness that I did.”

In addition to the prison sentence, Johnson has been ordered to pay back, at $50 a month, the $440,000-plus he cost the Philadelphia VAMC in fraudulent and bloated contracts.

Johnson is at least the third Philadelphia VAMC employee indicted or sentenced for fraud since 2020.

A former manager at the Philadelphia Veterans Affairs Medical Center (VAMC) has been sentenced to 6 months in federal prison for his part in a bribery scheme.

Ralph Johnson was convicted of accepting $30,000 in kickbacks and bribes for steering contracts to Earron and Carlicha Starks, who ran Ekno Medical Supply and Collondale Medical Supply from 2009 to 2019. Johnson served as chief of environmental services at the medical center. He admitted to receiving cash in binders and packages mailed to his home between 2018 and 2019.

The Starkses pleaded guilty first to paying kickbacks on $7 million worth of contracts to Florida VA facilities, then participated in a sting that implicated Johnson.

The VA Office of Inspector General began investigating Johnson in 2018 after the Starkses, who were indicted for bribing staff at US Department of Veterans Affairs (VA) hospitals in Miami and West Palm Beach, Florida, said they also paid officials in VA facilities on the East Coast.

According to the Philadelphia Inquirer, the judge credited Johnson’s past military service and his “extensive cooperation” with federal authorities investigating fraud within the VA. Johnson apologized to his former employers: “Throughout these 2 and a half years [since the arrest] there’s not a day I don’t think about the wrongness that I did.”

In addition to the prison sentence, Johnson has been ordered to pay back, at $50 a month, the $440,000-plus he cost the Philadelphia VAMC in fraudulent and bloated contracts.

Johnson is at least the third Philadelphia VAMC employee indicted or sentenced for fraud since 2020.

A former manager at the Philadelphia Veterans Affairs Medical Center (VAMC) has been sentenced to 6 months in federal prison for his part in a bribery scheme.

Ralph Johnson was convicted of accepting $30,000 in kickbacks and bribes for steering contracts to Earron and Carlicha Starks, who ran Ekno Medical Supply and Collondale Medical Supply from 2009 to 2019. Johnson served as chief of environmental services at the medical center. He admitted to receiving cash in binders and packages mailed to his home between 2018 and 2019.

The Starkses pleaded guilty first to paying kickbacks on $7 million worth of contracts to Florida VA facilities, then participated in a sting that implicated Johnson.

The VA Office of Inspector General began investigating Johnson in 2018 after the Starkses, who were indicted for bribing staff at US Department of Veterans Affairs (VA) hospitals in Miami and West Palm Beach, Florida, said they also paid officials in VA facilities on the East Coast.

According to the Philadelphia Inquirer, the judge credited Johnson’s past military service and his “extensive cooperation” with federal authorities investigating fraud within the VA. Johnson apologized to his former employers: “Throughout these 2 and a half years [since the arrest] there’s not a day I don’t think about the wrongness that I did.”

In addition to the prison sentence, Johnson has been ordered to pay back, at $50 a month, the $440,000-plus he cost the Philadelphia VAMC in fraudulent and bloated contracts.

Johnson is at least the third Philadelphia VAMC employee indicted or sentenced for fraud since 2020.

If Miley Cyrus has planted “Flowers” in your head, rest assured you’re not alone.

An earworm – a bit of music you can’t shake from your brain – happens to almost everyone. 

The culprit is typically a song you’ve heard repeatedly with a strong rhythm and melody (like Miley’s No. 1 hit this year).

It pops into your head and stays there, unbidden and often unwanted. As you fish for something new on Spotify, there’s always a chance that a catchy hook holds an earworm.

“A catchy tune or melody is the part of a song most likely to get stuck in a person’s head, often a bit from the chorus,” said Elizabeth H. Margulis, PhD, a professor at Princeton (N.J.) University and director of its music cognition lab. The phenomenon, which has been studied since 1885 (way before earbuds), goes by such names as stuck song syndrome, sticky music, musical imagery repetition, intrusive musical imagery, or the semi-official term, involuntary musical imagery, or INMI.

Research confirms how common it is. A 2020 study of American college students found that 97% had experienced an earworm in the past month, similar to findings from a larger Finnish survey done more than 10 years ago.

One in five people had experienced an earworm more than once a day, the study found. The typical length was 10-30 minutes, though 8.5% said theirs lasted more than 3 hours. Levels of “distress and interference” that earworms caused was mostly “mild to moderate.” 

Some 86% said they tried to stop it – most frequently by distraction, like talking to a friend or listening to another song.

If music is important to you, your earworms are more likely to last longer and be harder to control, earlier research found. And women are thought to be more likely to have them.

“Very musical people may have more earworms because it’s easy for them to conjure up a certain tune,” says David Silbersweig, MD, chairman of the department of psychiatry and codirector of the Institute for the Neurosciences at Brigham and Women’s Hospital in Boston.

Moreover, people who lack “psychological flexibility” may find earworms more bothersome. The more they try to avoid or control intrusive thoughts (or songs), the more persistent those thoughts become. 

“This is consistent with OCD (obsessive-compulsive disorder) research on the paradoxical effect of thought suppression,” the authors of the 2020 study wrote. In fact, people who report very annoying or stressful earworms are more likely to have obsessive-compulsive symptoms.

Earworms have been linked to other medical conditions as well, and even harmless earworms can be intrusive and time-consuming. That makes them worth a closer look.

Digging for the source of earworms

Scientists trace earworms to the auditory cortex in the temporal lobe of the brain, which controls how you perceive music, as well as deep temporal lobe areas that are responsible for retrieving memories. Your amygdala and ventral striatum, parts of your brain that involve emotion, also tie into the making of an earworm.

MRI experiments found that “INMI is a common internal experience recruiting brain networks involved in perception, emotions, memory and spontaneous thoughts,” a 2015 paper in  Consciousness and Cognition  reported.

These brain networks work in tandem if you connect a song to an emotional memory – that’s when you’re more likely to experience it as an earworm. The “loop” of music you’ll hear in your head is usually a 20-second snippet.

Think of it as a “cognitive itch,” as researchers from the Netherlands put it. An earworm can be triggered by associating a song with a specific situation or emotion. Trying to suppress it just reminds you it’s there, “scratching” the itch and making it worse. “The more one tries to suppress the songs, the more their impetus increases, a mental process known as ironic process theory,” they wrote. 

“It’s also worth pointing out that earworms don’t always occur right after a song ends,” said Michael K. Scullin, PhD, an associate professor of psychology and neuroscience at Baylor University in Waco, Tex. “Sometimes they only occur many hours later, and sometimes the earworm isn’t the song you were most recently listening to.”

These processes aren’t fully understood, he said, “but they likely represent memory consolidation mechanisms; that is, the brain trying to reactivate and stabilize musical memories.” Kind of like switching “radio stations” in your head. 

When to worry

Earworms are most often harmless. “They’re part of a healthy brain,” said Dr. Silbersweig. But in rare cases, they indicate certain medical conditions. People with OCD, for example, have been shown to have earworms during times of stress. If this is the case, cognitive-behavioral therapy as well as some antidepressants may help.

Take an earworm seriously if it’s linked to other symptoms, said Elaine Jones, MD, a neurologist in Hilton Head, S.C., and a fellow of the American Academy of Neurology. Those symptoms could include “loss of consciousness or confusion, visual loss or changes, speech arrest, tremors of arms or legs,” she said.

“Most worrisome would be a seizure, but other causes could include a migraine aura. In a younger person, less than 20 years old, this kind of earworm could indicate a psychiatric condition like schizophrenia.” Drug toxicity or brain damage can also present with earworms.

Her bottom line: “If an earworm is persistent for more than 24 hours, or if it is associated with the other symptoms mentioned above, it would be important to reach out to your primary care doctor to ensure that nothing more serious is going on,” said Dr. Jones. With no other symptoms, “it is more likely to be just an earworm.”

Japanese research also indicates that an earworm that lasts for several hours in a day can be linked to depression. If a person has symptoms such as low mood, insomnia, and loss of appetite, along with earworms that last several hours a day, treatment may help. 

There’s another category called “musical hallucinations” – where the person thinks they are actually hearing music, which could be a symptom of depression, although scientists don’t know for sure. The drug vortioxetine, which may help boost serotonin in the brain, has shown some promise in reducing earworms. 

Some research has shown that diseases that damage the auditory pathway in the brain have a link to musical hallucinations. 

How to stop a simple earworm

Here are six easy ways to make it stop:

• Mix up your playlist. “Listening to songs repeatedly does increase the likelihood that they’ll get stuck,” said Dr. Margulis. 
• Take breaks from your tunes throughout the day. “Longer listening durations are more likely to lead to earworms,” Dr. Scullin said.
• Use your feet. than the beat of your earworm. This will interrupt your memory of the tempo and can help chase away the earworm.
• Stick with that song. “Listen to a song all the way through,” said Dr. Silbersweig. If you only listen to snippets of a song, the  can take hold. That’s the brain’s tendency to remember things that are interrupted more easily than completed things.
• Distract yourself. Lose yourself in a book, a movie, your work, or a hobby that requires concentration. “Redirecting attention to an absorbing task can be an effective way to dislodge an earworm,” said Dr. Margulis. 
• Chew gum.  shows that the action of doing so interferes with repetitive memories and stops your mind from “scanning” a song. Then enjoy the sound of silence!

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

If Miley Cyrus has planted “Flowers” in your head, rest assured you’re not alone.

An earworm – a bit of music you can’t shake from your brain – happens to almost everyone. 

The culprit is typically a song you’ve heard repeatedly with a strong rhythm and melody (like Miley’s No. 1 hit this year).

It pops into your head and stays there, unbidden and often unwanted. As you fish for something new on Spotify, there’s always a chance that a catchy hook holds an earworm.

“A catchy tune or melody is the part of a song most likely to get stuck in a person’s head, often a bit from the chorus,” said Elizabeth H. Margulis, PhD, a professor at Princeton (N.J.) University and director of its music cognition lab. The phenomenon, which has been studied since 1885 (way before earbuds), goes by such names as stuck song syndrome, sticky music, musical imagery repetition, intrusive musical imagery, or the semi-official term, involuntary musical imagery, or INMI.

Research confirms how common it is. A 2020 study of American college students found that 97% had experienced an earworm in the past month, similar to findings from a larger Finnish survey done more than 10 years ago.

One in five people had experienced an earworm more than once a day, the study found. The typical length was 10-30 minutes, though 8.5% said theirs lasted more than 3 hours. Levels of “distress and interference” that earworms caused was mostly “mild to moderate.” 

Some 86% said they tried to stop it – most frequently by distraction, like talking to a friend or listening to another song.

If music is important to you, your earworms are more likely to last longer and be harder to control, earlier research found. And women are thought to be more likely to have them.

“Very musical people may have more earworms because it’s easy for them to conjure up a certain tune,” says David Silbersweig, MD, chairman of the department of psychiatry and codirector of the Institute for the Neurosciences at Brigham and Women’s Hospital in Boston.

Moreover, people who lack “psychological flexibility” may find earworms more bothersome. The more they try to avoid or control intrusive thoughts (or songs), the more persistent those thoughts become. 

“This is consistent with OCD (obsessive-compulsive disorder) research on the paradoxical effect of thought suppression,” the authors of the 2020 study wrote. In fact, people who report very annoying or stressful earworms are more likely to have obsessive-compulsive symptoms.

Earworms have been linked to other medical conditions as well, and even harmless earworms can be intrusive and time-consuming. That makes them worth a closer look.

Digging for the source of earworms

Scientists trace earworms to the auditory cortex in the temporal lobe of the brain, which controls how you perceive music, as well as deep temporal lobe areas that are responsible for retrieving memories. Your amygdala and ventral striatum, parts of your brain that involve emotion, also tie into the making of an earworm.

MRI experiments found that “INMI is a common internal experience recruiting brain networks involved in perception, emotions, memory and spontaneous thoughts,” a 2015 paper in  Consciousness and Cognition  reported.

These brain networks work in tandem if you connect a song to an emotional memory – that’s when you’re more likely to experience it as an earworm. The “loop” of music you’ll hear in your head is usually a 20-second snippet.

Think of it as a “cognitive itch,” as researchers from the Netherlands put it. An earworm can be triggered by associating a song with a specific situation or emotion. Trying to suppress it just reminds you it’s there, “scratching” the itch and making it worse. “The more one tries to suppress the songs, the more their impetus increases, a mental process known as ironic process theory,” they wrote. 

“It’s also worth pointing out that earworms don’t always occur right after a song ends,” said Michael K. Scullin, PhD, an associate professor of psychology and neuroscience at Baylor University in Waco, Tex. “Sometimes they only occur many hours later, and sometimes the earworm isn’t the song you were most recently listening to.”

These processes aren’t fully understood, he said, “but they likely represent memory consolidation mechanisms; that is, the brain trying to reactivate and stabilize musical memories.” Kind of like switching “radio stations” in your head. 

When to worry

Earworms are most often harmless. “They’re part of a healthy brain,” said Dr. Silbersweig. But in rare cases, they indicate certain medical conditions. People with OCD, for example, have been shown to have earworms during times of stress. If this is the case, cognitive-behavioral therapy as well as some antidepressants may help.

Take an earworm seriously if it’s linked to other symptoms, said Elaine Jones, MD, a neurologist in Hilton Head, S.C., and a fellow of the American Academy of Neurology. Those symptoms could include “loss of consciousness or confusion, visual loss or changes, speech arrest, tremors of arms or legs,” she said.

“Most worrisome would be a seizure, but other causes could include a migraine aura. In a younger person, less than 20 years old, this kind of earworm could indicate a psychiatric condition like schizophrenia.” Drug toxicity or brain damage can also present with earworms.

Her bottom line: “If an earworm is persistent for more than 24 hours, or if it is associated with the other symptoms mentioned above, it would be important to reach out to your primary care doctor to ensure that nothing more serious is going on,” said Dr. Jones. With no other symptoms, “it is more likely to be just an earworm.”

Japanese research also indicates that an earworm that lasts for several hours in a day can be linked to depression. If a person has symptoms such as low mood, insomnia, and loss of appetite, along with earworms that last several hours a day, treatment may help. 

There’s another category called “musical hallucinations” – where the person thinks they are actually hearing music, which could be a symptom of depression, although scientists don’t know for sure. The drug vortioxetine, which may help boost serotonin in the brain, has shown some promise in reducing earworms. 

Some research has shown that diseases that damage the auditory pathway in the brain have a link to musical hallucinations. 

How to stop a simple earworm

Here are six easy ways to make it stop:

• Mix up your playlist. “Listening to songs repeatedly does increase the likelihood that they’ll get stuck,” said Dr. Margulis. 
• Take breaks from your tunes throughout the day. “Longer listening durations are more likely to lead to earworms,” Dr. Scullin said.
• Use your feet. than the beat of your earworm. This will interrupt your memory of the tempo and can help chase away the earworm.
• Stick with that song. “Listen to a song all the way through,” said Dr. Silbersweig. If you only listen to snippets of a song, the  can take hold. That’s the brain’s tendency to remember things that are interrupted more easily than completed things.
• Distract yourself. Lose yourself in a book, a movie, your work, or a hobby that requires concentration. “Redirecting attention to an absorbing task can be an effective way to dislodge an earworm,” said Dr. Margulis. 
• Chew gum.  shows that the action of doing so interferes with repetitive memories and stops your mind from “scanning” a song. Then enjoy the sound of silence!

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

If Miley Cyrus has planted “Flowers” in your head, rest assured you’re not alone.

An earworm – a bit of music you can’t shake from your brain – happens to almost everyone. 

The culprit is typically a song you’ve heard repeatedly with a strong rhythm and melody (like Miley’s No. 1 hit this year).

It pops into your head and stays there, unbidden and often unwanted. As you fish for something new on Spotify, there’s always a chance that a catchy hook holds an earworm.

“A catchy tune or melody is the part of a song most likely to get stuck in a person’s head, often a bit from the chorus,” said Elizabeth H. Margulis, PhD, a professor at Princeton (N.J.) University and director of its music cognition lab. The phenomenon, which has been studied since 1885 (way before earbuds), goes by such names as stuck song syndrome, sticky music, musical imagery repetition, intrusive musical imagery, or the semi-official term, involuntary musical imagery, or INMI.

Research confirms how common it is. A 2020 study of American college students found that 97% had experienced an earworm in the past month, similar to findings from a larger Finnish survey done more than 10 years ago.

One in five people had experienced an earworm more than once a day, the study found. The typical length was 10-30 minutes, though 8.5% said theirs lasted more than 3 hours. Levels of “distress and interference” that earworms caused was mostly “mild to moderate.” 

Some 86% said they tried to stop it – most frequently by distraction, like talking to a friend or listening to another song.

If music is important to you, your earworms are more likely to last longer and be harder to control, earlier research found. And women are thought to be more likely to have them.

“Very musical people may have more earworms because it’s easy for them to conjure up a certain tune,” says David Silbersweig, MD, chairman of the department of psychiatry and codirector of the Institute for the Neurosciences at Brigham and Women’s Hospital in Boston.

Moreover, people who lack “psychological flexibility” may find earworms more bothersome. The more they try to avoid or control intrusive thoughts (or songs), the more persistent those thoughts become. 

“This is consistent with OCD (obsessive-compulsive disorder) research on the paradoxical effect of thought suppression,” the authors of the 2020 study wrote. In fact, people who report very annoying or stressful earworms are more likely to have obsessive-compulsive symptoms.

Earworms have been linked to other medical conditions as well, and even harmless earworms can be intrusive and time-consuming. That makes them worth a closer look.

Digging for the source of earworms

Scientists trace earworms to the auditory cortex in the temporal lobe of the brain, which controls how you perceive music, as well as deep temporal lobe areas that are responsible for retrieving memories. Your amygdala and ventral striatum, parts of your brain that involve emotion, also tie into the making of an earworm.

MRI experiments found that “INMI is a common internal experience recruiting brain networks involved in perception, emotions, memory and spontaneous thoughts,” a 2015 paper in  Consciousness and Cognition  reported.

These brain networks work in tandem if you connect a song to an emotional memory – that’s when you’re more likely to experience it as an earworm. The “loop” of music you’ll hear in your head is usually a 20-second snippet.

Think of it as a “cognitive itch,” as researchers from the Netherlands put it. An earworm can be triggered by associating a song with a specific situation or emotion. Trying to suppress it just reminds you it’s there, “scratching” the itch and making it worse. “The more one tries to suppress the songs, the more their impetus increases, a mental process known as ironic process theory,” they wrote. 

“It’s also worth pointing out that earworms don’t always occur right after a song ends,” said Michael K. Scullin, PhD, an associate professor of psychology and neuroscience at Baylor University in Waco, Tex. “Sometimes they only occur many hours later, and sometimes the earworm isn’t the song you were most recently listening to.”

These processes aren’t fully understood, he said, “but they likely represent memory consolidation mechanisms; that is, the brain trying to reactivate and stabilize musical memories.” Kind of like switching “radio stations” in your head. 

When to worry

Earworms are most often harmless. “They’re part of a healthy brain,” said Dr. Silbersweig. But in rare cases, they indicate certain medical conditions. People with OCD, for example, have been shown to have earworms during times of stress. If this is the case, cognitive-behavioral therapy as well as some antidepressants may help.

Take an earworm seriously if it’s linked to other symptoms, said Elaine Jones, MD, a neurologist in Hilton Head, S.C., and a fellow of the American Academy of Neurology. Those symptoms could include “loss of consciousness or confusion, visual loss or changes, speech arrest, tremors of arms or legs,” she said.

“Most worrisome would be a seizure, but other causes could include a migraine aura. In a younger person, less than 20 years old, this kind of earworm could indicate a psychiatric condition like schizophrenia.” Drug toxicity or brain damage can also present with earworms.

Her bottom line: “If an earworm is persistent for more than 24 hours, or if it is associated with the other symptoms mentioned above, it would be important to reach out to your primary care doctor to ensure that nothing more serious is going on,” said Dr. Jones. With no other symptoms, “it is more likely to be just an earworm.”

Japanese research also indicates that an earworm that lasts for several hours in a day can be linked to depression. If a person has symptoms such as low mood, insomnia, and loss of appetite, along with earworms that last several hours a day, treatment may help. 

There’s another category called “musical hallucinations” – where the person thinks they are actually hearing music, which could be a symptom of depression, although scientists don’t know for sure. The drug vortioxetine, which may help boost serotonin in the brain, has shown some promise in reducing earworms. 

Some research has shown that diseases that damage the auditory pathway in the brain have a link to musical hallucinations. 

How to stop a simple earworm

Here are six easy ways to make it stop:

• Mix up your playlist. “Listening to songs repeatedly does increase the likelihood that they’ll get stuck,” said Dr. Margulis. 
• Take breaks from your tunes throughout the day. “Longer listening durations are more likely to lead to earworms,” Dr. Scullin said.
• Use your feet. than the beat of your earworm. This will interrupt your memory of the tempo and can help chase away the earworm.
• Stick with that song. “Listen to a song all the way through,” said Dr. Silbersweig. If you only listen to snippets of a song, the  can take hold. That’s the brain’s tendency to remember things that are interrupted more easily than completed things.
• Distract yourself. Lose yourself in a book, a movie, your work, or a hobby that requires concentration. “Redirecting attention to an absorbing task can be an effective way to dislodge an earworm,” said Dr. Margulis. 
• Chew gum.  shows that the action of doing so interferes with repetitive memories and stops your mind from “scanning” a song. Then enjoy the sound of silence!

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