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Can coffee reduce weight?
Caffeine in the form of tea and coffee is the most widely consumed, socially acceptable stimulant around the globe. More than 150 million people in the United States drink coffee daily, with an average intake of 2 cups (which contains about 280 mg of caffeine).
Caffeine results in the release of excitatory neurotransmitters. Caffeine may increase energy expenditure and has been associated with reduced body mass. Studies have observed lower body mass index (BMI) in coffee consumers, compared with individuals who don’t consume coffee. Coffee may reduce appetite and dietary intake.
Greek researchers at Harokopio University, Athens, conducted a cross-over study to evaluate the effects of caffeinated coffee on appetite and dietary intake (Obesity 2013;21:1127-32). Sixteen normal-weight and 17 overweight/obese habitual coffee consumers (at least 1 cup of coffee/day) were enrolled. Each participant took part in three trials at least 1 week apart. Participants were required to abstain from caffeine for 24 hours and then reported to the lab to consume a breakfast and 200 mL of one of three experimental beverages: instant coffee with 3 mg caffeine/kg body weight (Coffee 3); instant coffee with 6 mg caffeine/kg (Coffee 6); or water. Participants had to consume the breakfast and the beverage within 5 minutes.
During a 3-hour period following beverage consumption, appetite feelings and participants’ dietary intake the day before the experiment were assessed. After this 3-hour period, participants were offered an ad libitum lunch buffet. The following day, participants reported by telephone their food and fluid intake for the rest of the experiment day.
Normal-weight participants consumed comparable energy in the ad libitum meal and in their total daily intake in the three interventions. However, among overweight/obese individuals, Coffee 6 resulted in significantly reduced energy intake during the ad libitum meal, compared with Coffee 3, and in significantly reduced total day energy intake, compared with both water and Coffee 3.
Doses used in this study for participants were somewhat staggering. The average caffeine content of the beverage in the Coffee 6 group was 526 mg. This is the caffeine content of roughly four 8-ounce cups of brewed coffee. The authors acknowledged that the Coffee 6 beverage was not easily consumed by "most of the volunteers."
We need to be cautious about the use of this dosing in the clinical setting. But as part of comprehensive weight-management strategy, caffeinated coffee may be helpful for reducing energy intake.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Caffeine in the form of tea and coffee is the most widely consumed, socially acceptable stimulant around the globe. More than 150 million people in the United States drink coffee daily, with an average intake of 2 cups (which contains about 280 mg of caffeine).
Caffeine results in the release of excitatory neurotransmitters. Caffeine may increase energy expenditure and has been associated with reduced body mass. Studies have observed lower body mass index (BMI) in coffee consumers, compared with individuals who don’t consume coffee. Coffee may reduce appetite and dietary intake.
Greek researchers at Harokopio University, Athens, conducted a cross-over study to evaluate the effects of caffeinated coffee on appetite and dietary intake (Obesity 2013;21:1127-32). Sixteen normal-weight and 17 overweight/obese habitual coffee consumers (at least 1 cup of coffee/day) were enrolled. Each participant took part in three trials at least 1 week apart. Participants were required to abstain from caffeine for 24 hours and then reported to the lab to consume a breakfast and 200 mL of one of three experimental beverages: instant coffee with 3 mg caffeine/kg body weight (Coffee 3); instant coffee with 6 mg caffeine/kg (Coffee 6); or water. Participants had to consume the breakfast and the beverage within 5 minutes.
During a 3-hour period following beverage consumption, appetite feelings and participants’ dietary intake the day before the experiment were assessed. After this 3-hour period, participants were offered an ad libitum lunch buffet. The following day, participants reported by telephone their food and fluid intake for the rest of the experiment day.
Normal-weight participants consumed comparable energy in the ad libitum meal and in their total daily intake in the three interventions. However, among overweight/obese individuals, Coffee 6 resulted in significantly reduced energy intake during the ad libitum meal, compared with Coffee 3, and in significantly reduced total day energy intake, compared with both water and Coffee 3.
Doses used in this study for participants were somewhat staggering. The average caffeine content of the beverage in the Coffee 6 group was 526 mg. This is the caffeine content of roughly four 8-ounce cups of brewed coffee. The authors acknowledged that the Coffee 6 beverage was not easily consumed by "most of the volunteers."
We need to be cautious about the use of this dosing in the clinical setting. But as part of comprehensive weight-management strategy, caffeinated coffee may be helpful for reducing energy intake.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Caffeine in the form of tea and coffee is the most widely consumed, socially acceptable stimulant around the globe. More than 150 million people in the United States drink coffee daily, with an average intake of 2 cups (which contains about 280 mg of caffeine).
Caffeine results in the release of excitatory neurotransmitters. Caffeine may increase energy expenditure and has been associated with reduced body mass. Studies have observed lower body mass index (BMI) in coffee consumers, compared with individuals who don’t consume coffee. Coffee may reduce appetite and dietary intake.
Greek researchers at Harokopio University, Athens, conducted a cross-over study to evaluate the effects of caffeinated coffee on appetite and dietary intake (Obesity 2013;21:1127-32). Sixteen normal-weight and 17 overweight/obese habitual coffee consumers (at least 1 cup of coffee/day) were enrolled. Each participant took part in three trials at least 1 week apart. Participants were required to abstain from caffeine for 24 hours and then reported to the lab to consume a breakfast and 200 mL of one of three experimental beverages: instant coffee with 3 mg caffeine/kg body weight (Coffee 3); instant coffee with 6 mg caffeine/kg (Coffee 6); or water. Participants had to consume the breakfast and the beverage within 5 minutes.
During a 3-hour period following beverage consumption, appetite feelings and participants’ dietary intake the day before the experiment were assessed. After this 3-hour period, participants were offered an ad libitum lunch buffet. The following day, participants reported by telephone their food and fluid intake for the rest of the experiment day.
Normal-weight participants consumed comparable energy in the ad libitum meal and in their total daily intake in the three interventions. However, among overweight/obese individuals, Coffee 6 resulted in significantly reduced energy intake during the ad libitum meal, compared with Coffee 3, and in significantly reduced total day energy intake, compared with both water and Coffee 3.
Doses used in this study for participants were somewhat staggering. The average caffeine content of the beverage in the Coffee 6 group was 526 mg. This is the caffeine content of roughly four 8-ounce cups of brewed coffee. The authors acknowledged that the Coffee 6 beverage was not easily consumed by "most of the volunteers."
We need to be cautious about the use of this dosing in the clinical setting. But as part of comprehensive weight-management strategy, caffeinated coffee may be helpful for reducing energy intake.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Gabapentin for alcohol use disorder
Two-thirds of U.S. adults currently consume alcohol, according to the National Health Interview Survey. While most are infrequent or light drinkers, 8% are problem drinkers (more than 14 drinks per week for men and more than 7 drinks per week for women).
Alcohol consumption is the second-leading cause of preventable death and disability in the United States. Annually, excessive alcohol consumption costs us almost a quarter of a trillion dollars in lost productivity, health care, law enforcement, and motor vehicle collisions.
Alcoholism is a relapsing and remitting disease characterized by psychosocial impairment and drug craving and withdrawal. Challenged by access inequalities to formal treatment services, few alcoholics, when interacting with the medical setting for other reasons, are offered or receive treatment. Some patients may be open to receiving treatment by primary care providers, but few drugs are available (naltrexone, acamprosate, and disulfiram). Clinicians may be unconvinced of their efficacy or uncomfortable with their use.
Gabapentin is an antiepileptic used commonly in primary care settings, mostly for neuropathic pain. Gabapentin is well tolerated, with a favorable pharmacokinetic profile and a broad therapeutic index. Preclinical data suggest that gabapentin normalizes stress-induced GABA (gamma-aminobutyric acid) activation associated with alcohol use disorder. Human data suggest that gabapentin reduces alcohol craving and alcohol-associated sleep and mood problems.
Mason and colleagues published the results from a randomized controlled clinical trial evaluating the efficacy and safety of different doses of gabapentin for increasing alcohol abstinence and reducing heavy drinking, insomnia, dysphoria, and craving. Potential participants were eligible for enrollment if they were aged 18 years or older, met criteria for alcohol dependence, and were recently abstinent from alcohol (at least 3 days). Participants were randomized to gabapentin 900 mg/day, gabapentin 1,800 mg/day, or placebo. Treatment was received for 12 weeks with titration and tapering (JAMA Intern. Med. 2014;174:70-7).
A total of 150 patients were randomized, and the groups were similar at baseline. Abstinence rates were 17%, 11.1%, and 4.1% in the 1,800-mg, 900-mg, and placebo groups (P = .04 for linear dose effect), respectively. The no-heavy-drinking rates were 44.7%, 29.6%, and 22.5% (P = .02 for linear dose effect). A dose effect was also observed for reductions in mood disturbance, sleep problems, and craving. No serious adverse events were reported.
We need to try to meet patients where they are. Patients should be directed to alcohol treatment services if they are willing to go. In my experience, many of them are not. In these cases, recommending an Alcoholics Anonymous group, trying gabapentin, and following them up in a clinic is a harm-reduction strategy worth trying.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Two-thirds of U.S. adults currently consume alcohol, according to the National Health Interview Survey. While most are infrequent or light drinkers, 8% are problem drinkers (more than 14 drinks per week for men and more than 7 drinks per week for women).
Alcohol consumption is the second-leading cause of preventable death and disability in the United States. Annually, excessive alcohol consumption costs us almost a quarter of a trillion dollars in lost productivity, health care, law enforcement, and motor vehicle collisions.
Alcoholism is a relapsing and remitting disease characterized by psychosocial impairment and drug craving and withdrawal. Challenged by access inequalities to formal treatment services, few alcoholics, when interacting with the medical setting for other reasons, are offered or receive treatment. Some patients may be open to receiving treatment by primary care providers, but few drugs are available (naltrexone, acamprosate, and disulfiram). Clinicians may be unconvinced of their efficacy or uncomfortable with their use.
Gabapentin is an antiepileptic used commonly in primary care settings, mostly for neuropathic pain. Gabapentin is well tolerated, with a favorable pharmacokinetic profile and a broad therapeutic index. Preclinical data suggest that gabapentin normalizes stress-induced GABA (gamma-aminobutyric acid) activation associated with alcohol use disorder. Human data suggest that gabapentin reduces alcohol craving and alcohol-associated sleep and mood problems.
Mason and colleagues published the results from a randomized controlled clinical trial evaluating the efficacy and safety of different doses of gabapentin for increasing alcohol abstinence and reducing heavy drinking, insomnia, dysphoria, and craving. Potential participants were eligible for enrollment if they were aged 18 years or older, met criteria for alcohol dependence, and were recently abstinent from alcohol (at least 3 days). Participants were randomized to gabapentin 900 mg/day, gabapentin 1,800 mg/day, or placebo. Treatment was received for 12 weeks with titration and tapering (JAMA Intern. Med. 2014;174:70-7).
A total of 150 patients were randomized, and the groups were similar at baseline. Abstinence rates were 17%, 11.1%, and 4.1% in the 1,800-mg, 900-mg, and placebo groups (P = .04 for linear dose effect), respectively. The no-heavy-drinking rates were 44.7%, 29.6%, and 22.5% (P = .02 for linear dose effect). A dose effect was also observed for reductions in mood disturbance, sleep problems, and craving. No serious adverse events were reported.
We need to try to meet patients where they are. Patients should be directed to alcohol treatment services if they are willing to go. In my experience, many of them are not. In these cases, recommending an Alcoholics Anonymous group, trying gabapentin, and following them up in a clinic is a harm-reduction strategy worth trying.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Two-thirds of U.S. adults currently consume alcohol, according to the National Health Interview Survey. While most are infrequent or light drinkers, 8% are problem drinkers (more than 14 drinks per week for men and more than 7 drinks per week for women).
Alcohol consumption is the second-leading cause of preventable death and disability in the United States. Annually, excessive alcohol consumption costs us almost a quarter of a trillion dollars in lost productivity, health care, law enforcement, and motor vehicle collisions.
Alcoholism is a relapsing and remitting disease characterized by psychosocial impairment and drug craving and withdrawal. Challenged by access inequalities to formal treatment services, few alcoholics, when interacting with the medical setting for other reasons, are offered or receive treatment. Some patients may be open to receiving treatment by primary care providers, but few drugs are available (naltrexone, acamprosate, and disulfiram). Clinicians may be unconvinced of their efficacy or uncomfortable with their use.
Gabapentin is an antiepileptic used commonly in primary care settings, mostly for neuropathic pain. Gabapentin is well tolerated, with a favorable pharmacokinetic profile and a broad therapeutic index. Preclinical data suggest that gabapentin normalizes stress-induced GABA (gamma-aminobutyric acid) activation associated with alcohol use disorder. Human data suggest that gabapentin reduces alcohol craving and alcohol-associated sleep and mood problems.
Mason and colleagues published the results from a randomized controlled clinical trial evaluating the efficacy and safety of different doses of gabapentin for increasing alcohol abstinence and reducing heavy drinking, insomnia, dysphoria, and craving. Potential participants were eligible for enrollment if they were aged 18 years or older, met criteria for alcohol dependence, and were recently abstinent from alcohol (at least 3 days). Participants were randomized to gabapentin 900 mg/day, gabapentin 1,800 mg/day, or placebo. Treatment was received for 12 weeks with titration and tapering (JAMA Intern. Med. 2014;174:70-7).
A total of 150 patients were randomized, and the groups were similar at baseline. Abstinence rates were 17%, 11.1%, and 4.1% in the 1,800-mg, 900-mg, and placebo groups (P = .04 for linear dose effect), respectively. The no-heavy-drinking rates were 44.7%, 29.6%, and 22.5% (P = .02 for linear dose effect). A dose effect was also observed for reductions in mood disturbance, sleep problems, and craving. No serious adverse events were reported.
We need to try to meet patients where they are. Patients should be directed to alcohol treatment services if they are willing to go. In my experience, many of them are not. In these cases, recommending an Alcoholics Anonymous group, trying gabapentin, and following them up in a clinic is a harm-reduction strategy worth trying.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Treating female pattern hair loss
Female pattern hair loss, which affects over 21 million women in the United States, is a nonscarring hair loss primarily involving the frontal and vertex scalp. FPHS causes women significant emotional and psychological distress. We see, and will continue to see, a lot of these cases in primary care. If left untreated or unaddressed, FPHL results in a slow, progressive decline in the density of scalp hair.
FPHL is characterized by the production of shorter and finer hairs and shortening of the growth phase of hair follicles. One may find it important to rule out secondary causes of hair loss, such as hyperandrogenism. So after excluding secondary causes, what are the best treatment options for treatment?
Researchers conducted a systematic review (Cochrane Database Syst. Rev. 2012 May, CD007628 [doi:10.1002/14651858.CD007628.pub3]) assessing the effectiveness of interventions for female pattern hair loss. Studies were included if they compared any type of monotherapy or combination therapy to treat FPHL. Studies evaluating treatments in women with increased circulating androgens (such as polycystic ovarian syndrome) were included. Primary outcomes included self-reported hair regrowth, quality of life, and adverse effects.
The Cochrane review included 22 studies that enrolled a total of 2,349 subjects. Ten studies evaluated minoxidil, four evaluated finasteride, two cyproterone acetate, and two flutamide. A variety of other exotic interventions was evaluated, including topical melatonin-alcohol solution, adenosine lotion, and pulsed electrostatic field.
The best data continue to exist for minoxidil. "Pooled data from 4 studies indicated that a greater proportion of participants (121/488) treated with minoxidil reported a moderate increase in their hair regrowth when compared with placebo (64/476) (risk ratio, 1.86; 95% confidence interval [CI], 1.42 to 2.43). In 7 studies, there was an important increase of 13.28 in total hair count per cm² in the minoxidil group compared to the placebo group (95% CI, 10.89 to 15.68). There was no difference in the number of adverse events in the twice daily minoxidil and placebo intervention groups, with the exception of a reported increase of adverse events (additional hair growth on areas other than the scalp) with minoxidil (5%) twice daily," according to the Cochrane report.
Other promising agents might be octyl nicotinate (0.5%), myristyl nicotinate (5%), and flutamide. Fulvestrant, adenosine, pulsed electrostatic field, and estradiol valerate are ineffective.
Minoxidil it is. It may be important to remind patients that 2% twice daily may be as effective and safe as 5% once a day.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Female pattern hair loss, which affects over 21 million women in the United States, is a nonscarring hair loss primarily involving the frontal and vertex scalp. FPHS causes women significant emotional and psychological distress. We see, and will continue to see, a lot of these cases in primary care. If left untreated or unaddressed, FPHL results in a slow, progressive decline in the density of scalp hair.
FPHL is characterized by the production of shorter and finer hairs and shortening of the growth phase of hair follicles. One may find it important to rule out secondary causes of hair loss, such as hyperandrogenism. So after excluding secondary causes, what are the best treatment options for treatment?
Researchers conducted a systematic review (Cochrane Database Syst. Rev. 2012 May, CD007628 [doi:10.1002/14651858.CD007628.pub3]) assessing the effectiveness of interventions for female pattern hair loss. Studies were included if they compared any type of monotherapy or combination therapy to treat FPHL. Studies evaluating treatments in women with increased circulating androgens (such as polycystic ovarian syndrome) were included. Primary outcomes included self-reported hair regrowth, quality of life, and adverse effects.
The Cochrane review included 22 studies that enrolled a total of 2,349 subjects. Ten studies evaluated minoxidil, four evaluated finasteride, two cyproterone acetate, and two flutamide. A variety of other exotic interventions was evaluated, including topical melatonin-alcohol solution, adenosine lotion, and pulsed electrostatic field.
The best data continue to exist for minoxidil. "Pooled data from 4 studies indicated that a greater proportion of participants (121/488) treated with minoxidil reported a moderate increase in their hair regrowth when compared with placebo (64/476) (risk ratio, 1.86; 95% confidence interval [CI], 1.42 to 2.43). In 7 studies, there was an important increase of 13.28 in total hair count per cm² in the minoxidil group compared to the placebo group (95% CI, 10.89 to 15.68). There was no difference in the number of adverse events in the twice daily minoxidil and placebo intervention groups, with the exception of a reported increase of adverse events (additional hair growth on areas other than the scalp) with minoxidil (5%) twice daily," according to the Cochrane report.
Other promising agents might be octyl nicotinate (0.5%), myristyl nicotinate (5%), and flutamide. Fulvestrant, adenosine, pulsed electrostatic field, and estradiol valerate are ineffective.
Minoxidil it is. It may be important to remind patients that 2% twice daily may be as effective and safe as 5% once a day.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Female pattern hair loss, which affects over 21 million women in the United States, is a nonscarring hair loss primarily involving the frontal and vertex scalp. FPHS causes women significant emotional and psychological distress. We see, and will continue to see, a lot of these cases in primary care. If left untreated or unaddressed, FPHL results in a slow, progressive decline in the density of scalp hair.
FPHL is characterized by the production of shorter and finer hairs and shortening of the growth phase of hair follicles. One may find it important to rule out secondary causes of hair loss, such as hyperandrogenism. So after excluding secondary causes, what are the best treatment options for treatment?
Researchers conducted a systematic review (Cochrane Database Syst. Rev. 2012 May, CD007628 [doi:10.1002/14651858.CD007628.pub3]) assessing the effectiveness of interventions for female pattern hair loss. Studies were included if they compared any type of monotherapy or combination therapy to treat FPHL. Studies evaluating treatments in women with increased circulating androgens (such as polycystic ovarian syndrome) were included. Primary outcomes included self-reported hair regrowth, quality of life, and adverse effects.
The Cochrane review included 22 studies that enrolled a total of 2,349 subjects. Ten studies evaluated minoxidil, four evaluated finasteride, two cyproterone acetate, and two flutamide. A variety of other exotic interventions was evaluated, including topical melatonin-alcohol solution, adenosine lotion, and pulsed electrostatic field.
The best data continue to exist for minoxidil. "Pooled data from 4 studies indicated that a greater proportion of participants (121/488) treated with minoxidil reported a moderate increase in their hair regrowth when compared with placebo (64/476) (risk ratio, 1.86; 95% confidence interval [CI], 1.42 to 2.43). In 7 studies, there was an important increase of 13.28 in total hair count per cm² in the minoxidil group compared to the placebo group (95% CI, 10.89 to 15.68). There was no difference in the number of adverse events in the twice daily minoxidil and placebo intervention groups, with the exception of a reported increase of adverse events (additional hair growth on areas other than the scalp) with minoxidil (5%) twice daily," according to the Cochrane report.
Other promising agents might be octyl nicotinate (0.5%), myristyl nicotinate (5%), and flutamide. Fulvestrant, adenosine, pulsed electrostatic field, and estradiol valerate are ineffective.
Minoxidil it is. It may be important to remind patients that 2% twice daily may be as effective and safe as 5% once a day.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Actinic keratoses: The cold truth
Actinic keratosis, or solar keratosis, results from the proliferation of atypical epidermal keratinocytes. When we can take the time to do a skin examination, we all see a lot of them especially among our older and middle-aged sun worshippers and sunscreen agnostics. My traditional approach, for better or for worse, has been to acquire the liquid nitrogen bottle on the floor and go to work. But my recent review of guidelines prepared on behalf of the British Association of Dermatologists and published several years ago have prompted me to open my eyes a bit more to other possible approaches.
Reassuringly, the likelihood of progression of an AK to squamous cell carcinoma (SCC) is low. Estimates from a large U.S. cohort revealed a rate of transformation to invasive or in situ SCC of 0.6% after 1 year and 2.6 % after 4 years. But we have to remember that although the progression rate is low, 60% of SCC arise from AKs.
The AK guideline authors synthesized and graded published evidence. Topical therapies receiving an "A grade" (i.e., good evidence) included no therapy or emollients for mild AKs and 5-fluorouracil. Therapies with a "B grade" (i.e., fair evidence) include diclofenac gel and imiquimod.
Other treatments include cryosurgery (A grade) and photodynamic therapy (B grade). We do a lot of cryotherapy in our practice but patients need to be informed of the scarring and possible hyper- or hypopigmentation that can occur with treatment. Photodynamic therapy will, in most cases, be administered by dermatologists.
According to a recent paper in the Drugs and Therapeutic Bulletin, patients should be referred to a dermatologist if there is diagnostic uncertainty, concerns about malignancy, treatment failure or management concerns, or if the patient is at high risk (e.g., organ transplant recipients, multiple large lesions, or previous SCC).
The guideline authors suggest that most patients can be evaluated and treated in the primary care setting. They go on to say that there is inadequate evidence to justify treatment of all AKs in an attempt to prevent malignant transformation. While reassuring, this requires us to consider all possible treatment approaches. One liquid nitrogen bottle does not fit all.
Dr. Ebbert is professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Actinic keratosis, or solar keratosis, results from the proliferation of atypical epidermal keratinocytes. When we can take the time to do a skin examination, we all see a lot of them especially among our older and middle-aged sun worshippers and sunscreen agnostics. My traditional approach, for better or for worse, has been to acquire the liquid nitrogen bottle on the floor and go to work. But my recent review of guidelines prepared on behalf of the British Association of Dermatologists and published several years ago have prompted me to open my eyes a bit more to other possible approaches.
Reassuringly, the likelihood of progression of an AK to squamous cell carcinoma (SCC) is low. Estimates from a large U.S. cohort revealed a rate of transformation to invasive or in situ SCC of 0.6% after 1 year and 2.6 % after 4 years. But we have to remember that although the progression rate is low, 60% of SCC arise from AKs.
The AK guideline authors synthesized and graded published evidence. Topical therapies receiving an "A grade" (i.e., good evidence) included no therapy or emollients for mild AKs and 5-fluorouracil. Therapies with a "B grade" (i.e., fair evidence) include diclofenac gel and imiquimod.
Other treatments include cryosurgery (A grade) and photodynamic therapy (B grade). We do a lot of cryotherapy in our practice but patients need to be informed of the scarring and possible hyper- or hypopigmentation that can occur with treatment. Photodynamic therapy will, in most cases, be administered by dermatologists.
According to a recent paper in the Drugs and Therapeutic Bulletin, patients should be referred to a dermatologist if there is diagnostic uncertainty, concerns about malignancy, treatment failure or management concerns, or if the patient is at high risk (e.g., organ transplant recipients, multiple large lesions, or previous SCC).
The guideline authors suggest that most patients can be evaluated and treated in the primary care setting. They go on to say that there is inadequate evidence to justify treatment of all AKs in an attempt to prevent malignant transformation. While reassuring, this requires us to consider all possible treatment approaches. One liquid nitrogen bottle does not fit all.
Dr. Ebbert is professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Actinic keratosis, or solar keratosis, results from the proliferation of atypical epidermal keratinocytes. When we can take the time to do a skin examination, we all see a lot of them especially among our older and middle-aged sun worshippers and sunscreen agnostics. My traditional approach, for better or for worse, has been to acquire the liquid nitrogen bottle on the floor and go to work. But my recent review of guidelines prepared on behalf of the British Association of Dermatologists and published several years ago have prompted me to open my eyes a bit more to other possible approaches.
Reassuringly, the likelihood of progression of an AK to squamous cell carcinoma (SCC) is low. Estimates from a large U.S. cohort revealed a rate of transformation to invasive or in situ SCC of 0.6% after 1 year and 2.6 % after 4 years. But we have to remember that although the progression rate is low, 60% of SCC arise from AKs.
The AK guideline authors synthesized and graded published evidence. Topical therapies receiving an "A grade" (i.e., good evidence) included no therapy or emollients for mild AKs and 5-fluorouracil. Therapies with a "B grade" (i.e., fair evidence) include diclofenac gel and imiquimod.
Other treatments include cryosurgery (A grade) and photodynamic therapy (B grade). We do a lot of cryotherapy in our practice but patients need to be informed of the scarring and possible hyper- or hypopigmentation that can occur with treatment. Photodynamic therapy will, in most cases, be administered by dermatologists.
According to a recent paper in the Drugs and Therapeutic Bulletin, patients should be referred to a dermatologist if there is diagnostic uncertainty, concerns about malignancy, treatment failure or management concerns, or if the patient is at high risk (e.g., organ transplant recipients, multiple large lesions, or previous SCC).
The guideline authors suggest that most patients can be evaluated and treated in the primary care setting. They go on to say that there is inadequate evidence to justify treatment of all AKs in an attempt to prevent malignant transformation. While reassuring, this requires us to consider all possible treatment approaches. One liquid nitrogen bottle does not fit all.
Dr. Ebbert is professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Zinc for colds
Zinc was recognized as an element in 1509 and as an essential mineral much later. In 1961, zinc deficiency was linked with hypogonadism. Zinc is included in almost all over-the-counter daily vitamins and mineral supplements, typically in the form of zinc oxide, zinc acetate, and zinc gluconate. Zinc is absorbed through the small bowel with an efficiency of 20%-40%. It is the second most important metal in the body after iron and is present in virtually 100% of proteins.
Zinc inhibits viral replication. Because of this, it has been investigated as a way to decrease the duration of symptoms from the common cold. With some evidence suggesting that it works, we know little about the right dose for zinc to exert its magical effects.
In a recently published systematic review, Singh and Das updated a previous Cochrane systematic review and, once again, evaluated the efficacy of zinc in reducing the incidence, severity, and duration of common cold symptoms (Cochrane Database Syst. Rev. 2013;6:CD001364). Studies were included if they were randomized, double-blind, placebo-controlled trials using zinc for at least 5 days for treatment or 5 months for prevention of the common cold.
Sixteen therapeutic trails involving a total of 1,387 people, and two preventive trials with 394 participants were included in the meta-analysis. Zinc came in the form of syrup, lozenges, or tablets. Zinc was associated with statistically significant reductions in the duration but not the severity of symptoms. The mean difference in reduction duration was 1 day (95% confidence interval, –1.72 to –0.34). After 7 days of treatment, significantly fewer subjects had symptoms. Zinc was associated with a reduced incidence of colds, absences from school, and receipt of antibiotics. Bad taste and nausea were significantly higher in patients treated with zinc. The authors suggested that there is a significant reduction in the duration of cold symptoms at a dose of at least 75 mg/day in the lozenge form.
Inhaled zinc can cause permanent anosmia, and so this delivery route was not investigated. Lozenges may be the best bet, since we know the daily dose should be at least 75 mg for treatment. For patients interested in using zinc for prevention, no clear dosage recommendations can be made. Megadose supplementation or high zinc intake has been associated with abdominal pain, diarrhea, nausea, and vomiting. Zinc may interfere with copper absorption, and high zinc intake (greater than 150 mg/day) can lead to copper deficiency and should be avoided.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Zinc was recognized as an element in 1509 and as an essential mineral much later. In 1961, zinc deficiency was linked with hypogonadism. Zinc is included in almost all over-the-counter daily vitamins and mineral supplements, typically in the form of zinc oxide, zinc acetate, and zinc gluconate. Zinc is absorbed through the small bowel with an efficiency of 20%-40%. It is the second most important metal in the body after iron and is present in virtually 100% of proteins.
Zinc inhibits viral replication. Because of this, it has been investigated as a way to decrease the duration of symptoms from the common cold. With some evidence suggesting that it works, we know little about the right dose for zinc to exert its magical effects.
In a recently published systematic review, Singh and Das updated a previous Cochrane systematic review and, once again, evaluated the efficacy of zinc in reducing the incidence, severity, and duration of common cold symptoms (Cochrane Database Syst. Rev. 2013;6:CD001364). Studies were included if they were randomized, double-blind, placebo-controlled trials using zinc for at least 5 days for treatment or 5 months for prevention of the common cold.
Sixteen therapeutic trails involving a total of 1,387 people, and two preventive trials with 394 participants were included in the meta-analysis. Zinc came in the form of syrup, lozenges, or tablets. Zinc was associated with statistically significant reductions in the duration but not the severity of symptoms. The mean difference in reduction duration was 1 day (95% confidence interval, –1.72 to –0.34). After 7 days of treatment, significantly fewer subjects had symptoms. Zinc was associated with a reduced incidence of colds, absences from school, and receipt of antibiotics. Bad taste and nausea were significantly higher in patients treated with zinc. The authors suggested that there is a significant reduction in the duration of cold symptoms at a dose of at least 75 mg/day in the lozenge form.
Inhaled zinc can cause permanent anosmia, and so this delivery route was not investigated. Lozenges may be the best bet, since we know the daily dose should be at least 75 mg for treatment. For patients interested in using zinc for prevention, no clear dosage recommendations can be made. Megadose supplementation or high zinc intake has been associated with abdominal pain, diarrhea, nausea, and vomiting. Zinc may interfere with copper absorption, and high zinc intake (greater than 150 mg/day) can lead to copper deficiency and should be avoided.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Zinc was recognized as an element in 1509 and as an essential mineral much later. In 1961, zinc deficiency was linked with hypogonadism. Zinc is included in almost all over-the-counter daily vitamins and mineral supplements, typically in the form of zinc oxide, zinc acetate, and zinc gluconate. Zinc is absorbed through the small bowel with an efficiency of 20%-40%. It is the second most important metal in the body after iron and is present in virtually 100% of proteins.
Zinc inhibits viral replication. Because of this, it has been investigated as a way to decrease the duration of symptoms from the common cold. With some evidence suggesting that it works, we know little about the right dose for zinc to exert its magical effects.
In a recently published systematic review, Singh and Das updated a previous Cochrane systematic review and, once again, evaluated the efficacy of zinc in reducing the incidence, severity, and duration of common cold symptoms (Cochrane Database Syst. Rev. 2013;6:CD001364). Studies were included if they were randomized, double-blind, placebo-controlled trials using zinc for at least 5 days for treatment or 5 months for prevention of the common cold.
Sixteen therapeutic trails involving a total of 1,387 people, and two preventive trials with 394 participants were included in the meta-analysis. Zinc came in the form of syrup, lozenges, or tablets. Zinc was associated with statistically significant reductions in the duration but not the severity of symptoms. The mean difference in reduction duration was 1 day (95% confidence interval, –1.72 to –0.34). After 7 days of treatment, significantly fewer subjects had symptoms. Zinc was associated with a reduced incidence of colds, absences from school, and receipt of antibiotics. Bad taste and nausea were significantly higher in patients treated with zinc. The authors suggested that there is a significant reduction in the duration of cold symptoms at a dose of at least 75 mg/day in the lozenge form.
Inhaled zinc can cause permanent anosmia, and so this delivery route was not investigated. Lozenges may be the best bet, since we know the daily dose should be at least 75 mg for treatment. For patients interested in using zinc for prevention, no clear dosage recommendations can be made. Megadose supplementation or high zinc intake has been associated with abdominal pain, diarrhea, nausea, and vomiting. Zinc may interfere with copper absorption, and high zinc intake (greater than 150 mg/day) can lead to copper deficiency and should be avoided.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
What Matters: Bacterial vaginosis
The most common cause of vaginal discharge in women of childbearing age is bacterial vaginosis, which is characterized by a complex change in the vaginal flora with a reduction of lactobacilli and an increase in anaerobic bacteria such as Gardnerella vaginalis.
Among women with bacterial vaginosis (BV), 50%-75% are asymptomatic. Symptomatic women usually present with vaginal odor and/or discharge that is off-white, thin, and homogeneous in most cases. BV can create complications in pregnancy, but up to half of cases resolve spontaneously. Treatment is usually with antibiotics, but BV will recur in 69% of women within 1 year. Other than treatment with antibiotics, are there alternative ways to manage this disease?
Both oral and vaginal delivery of lactobacilli are known to renew vaginal microbiota. But is oral lactobacillus alone effective for treating BV?
Vujic et al. conducted a double-blind, randomized, placebo-controlled clinical trial evaluating the efficacy of a probiotic containing lactobacilli for the treatment of women with BV (Eur. J. Obstet. Gynecol. Reprod. Biol. 2013;168:75-9). Women were eligible for inclusion if they were older than 18 years of age and diagnosed with vaginal infection including BV, candidiasis, trichomoniasis, or a combination of these conditions. Women were excluded if they were pregnant, lactating, or menstruating. Subjects received either two capsules containing greater than 1 x 109 CFU lactobacillus daily or matching placebo for 6 weeks. At 6 and 12 weeks after randomization, subjects underwent gynecologic examinations for a wet mount evaluation and recovery of vaginal flora on agar plates. The primary outcome of the study was the rate of restitution of normal vaginal microbiota at 6 weeks.
In all, 544 subjects were randomized (395 to probiotic and 149 to placebo). Adherence to medication was greater than 90% in both groups. Restitution of balanced vaginal microbiota was evident in 243 subjects (61.5%) in the probiotic group and 40 subjects (26.9%) in the placebo group (P less than .001). At 12 weeks, normal vaginal microbiota was present in 51% of subjects in the probiotic group but only 21% of subjects taking placebo (P less than .001). The number-needed-to-treat was 2.9 with a relative risk reduction of 47.4% at 6 weeks.
For nonpregnant women with mild symptoms, the use of oral probiotics may be a reasonable option. For women who have recurrent episodes of BV, data suggest that probiotics could prevent future episodes, but more data is needed to evaluate this hypothesis.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.
The most common cause of vaginal discharge in women of childbearing age is bacterial vaginosis, which is characterized by a complex change in the vaginal flora with a reduction of lactobacilli and an increase in anaerobic bacteria such as Gardnerella vaginalis.
Among women with bacterial vaginosis (BV), 50%-75% are asymptomatic. Symptomatic women usually present with vaginal odor and/or discharge that is off-white, thin, and homogeneous in most cases. BV can create complications in pregnancy, but up to half of cases resolve spontaneously. Treatment is usually with antibiotics, but BV will recur in 69% of women within 1 year. Other than treatment with antibiotics, are there alternative ways to manage this disease?
Both oral and vaginal delivery of lactobacilli are known to renew vaginal microbiota. But is oral lactobacillus alone effective for treating BV?
Vujic et al. conducted a double-blind, randomized, placebo-controlled clinical trial evaluating the efficacy of a probiotic containing lactobacilli for the treatment of women with BV (Eur. J. Obstet. Gynecol. Reprod. Biol. 2013;168:75-9). Women were eligible for inclusion if they were older than 18 years of age and diagnosed with vaginal infection including BV, candidiasis, trichomoniasis, or a combination of these conditions. Women were excluded if they were pregnant, lactating, or menstruating. Subjects received either two capsules containing greater than 1 x 109 CFU lactobacillus daily or matching placebo for 6 weeks. At 6 and 12 weeks after randomization, subjects underwent gynecologic examinations for a wet mount evaluation and recovery of vaginal flora on agar plates. The primary outcome of the study was the rate of restitution of normal vaginal microbiota at 6 weeks.
In all, 544 subjects were randomized (395 to probiotic and 149 to placebo). Adherence to medication was greater than 90% in both groups. Restitution of balanced vaginal microbiota was evident in 243 subjects (61.5%) in the probiotic group and 40 subjects (26.9%) in the placebo group (P less than .001). At 12 weeks, normal vaginal microbiota was present in 51% of subjects in the probiotic group but only 21% of subjects taking placebo (P less than .001). The number-needed-to-treat was 2.9 with a relative risk reduction of 47.4% at 6 weeks.
For nonpregnant women with mild symptoms, the use of oral probiotics may be a reasonable option. For women who have recurrent episodes of BV, data suggest that probiotics could prevent future episodes, but more data is needed to evaluate this hypothesis.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.
The most common cause of vaginal discharge in women of childbearing age is bacterial vaginosis, which is characterized by a complex change in the vaginal flora with a reduction of lactobacilli and an increase in anaerobic bacteria such as Gardnerella vaginalis.
Among women with bacterial vaginosis (BV), 50%-75% are asymptomatic. Symptomatic women usually present with vaginal odor and/or discharge that is off-white, thin, and homogeneous in most cases. BV can create complications in pregnancy, but up to half of cases resolve spontaneously. Treatment is usually with antibiotics, but BV will recur in 69% of women within 1 year. Other than treatment with antibiotics, are there alternative ways to manage this disease?
Both oral and vaginal delivery of lactobacilli are known to renew vaginal microbiota. But is oral lactobacillus alone effective for treating BV?
Vujic et al. conducted a double-blind, randomized, placebo-controlled clinical trial evaluating the efficacy of a probiotic containing lactobacilli for the treatment of women with BV (Eur. J. Obstet. Gynecol. Reprod. Biol. 2013;168:75-9). Women were eligible for inclusion if they were older than 18 years of age and diagnosed with vaginal infection including BV, candidiasis, trichomoniasis, or a combination of these conditions. Women were excluded if they were pregnant, lactating, or menstruating. Subjects received either two capsules containing greater than 1 x 109 CFU lactobacillus daily or matching placebo for 6 weeks. At 6 and 12 weeks after randomization, subjects underwent gynecologic examinations for a wet mount evaluation and recovery of vaginal flora on agar plates. The primary outcome of the study was the rate of restitution of normal vaginal microbiota at 6 weeks.
In all, 544 subjects were randomized (395 to probiotic and 149 to placebo). Adherence to medication was greater than 90% in both groups. Restitution of balanced vaginal microbiota was evident in 243 subjects (61.5%) in the probiotic group and 40 subjects (26.9%) in the placebo group (P less than .001). At 12 weeks, normal vaginal microbiota was present in 51% of subjects in the probiotic group but only 21% of subjects taking placebo (P less than .001). The number-needed-to-treat was 2.9 with a relative risk reduction of 47.4% at 6 weeks.
For nonpregnant women with mild symptoms, the use of oral probiotics may be a reasonable option. For women who have recurrent episodes of BV, data suggest that probiotics could prevent future episodes, but more data is needed to evaluate this hypothesis.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.
When ADHD doesn’t improve, check medication adherence first
NEW YORK – Assessing nonresponsiveness to attention-deficit/hyperactivity disorder treatment requires a bit of detective work, according to Dr. Laurence L. Greenhill.
The reason can be as simple as a little kid not being able to swallow a big pill, or as complex as a dysfunctional family dynamic that interferes with medication adherence. But once the problem is rooted out and addressed, most refractory patients can experience a good response, Dr. Greenhill said at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Since primary care physicians usually continue to manage children who respond to ADHD medications, psychiatrists are usually the ones who see nonresponders, said Dr. Greenhill, a child and adolescent psychiatrist at the New York Psychiatric Institute.
Medication nonadherence, the most common cause of a failure to improve, can arise from numerous situations.
On the simple side, it might be a matter of finding the right form of medication; a liquid or sprinkle capsule might be much easier for a child to take than a pill. And not all pills are created equally easy to take.
"For example, [the osmotic controlled release oral delivery system methylphenidate] just went off patent, and generics are now available. But some of these generics are much bigger. In fact, one of the 18-mg pills is twice as large as the patent medicine, and lots of kids can’t swallow it," he said.
The ADHD medication guide published by Long Island Jewish Hospital can be a helpful tool when working with parents on this issue. It lists all the Food and Drug Administration–approved medications for ADHD, with full-size photographs of each capsule, tablet, or pill.
Some generics are not pharmacokinetically or pharmacodynamically identical to the original formulation, Dr. Greenhill noted. Although the drug has to be molecularly identical and dose identical, "the ascending dose curve and duration of action need not be matched." Some generic formulations do fall into this problematic category. "For this reason, I try to encourage parents to get the brand," said Dr. Greenhill, adding that he has no financial interest in any of the drugs.
Medication nonadherence also can be attributable to uncomfortable or even intolerable side effects. These can include gastrointestinal issues, trouble sleeping, lack of appetite, restlessness, irritability, and "feeling fidgety."
Dosage adjustments or a medication change might be in order. For appetite issues, recommend giving the medication after meals, and reassure parents it’s OK to let a child eat later in the evening, when hunger may return.
It’s important to get the child’s growth records from the pediatrician, and plot height and weight curves every 6 months. If there’s a consistent fall-off, consider lowering the dose or changing to another drug.
Contrary to widely held belief, stimulants don’t pose significant cardiac risks to most children. A baseline electrocardiogram is really only necessary for a child who has a family history of sudden cardiac death or a personal history of syncope or cardiac abnormalities. Blood pressure and pulse should be monitored at every visit.
Melatonin is worth a try for youngsters whose ADHD meds interfere with good sleep, Dr. Greenhill said.
"I would start at 1 mg/night and work up," he said. "Starting at a high dose can actually shut off the naturally occurring melatonin. Plasma levels peak about an hour after taking it, so timing is important. I usually start with it about 3 hours before the scheduled sleeping time and then adjust."
Family dynamics also can play a big role in medication nonadherence. "ADHD families are often poor at scheduling activities, sometimes to the extent that parents are the ones who forget to give the medication. They also might not have a clear idea of how to give it, and just leave it on the kitchen table, making it the child’s responsibility to take it every day.
"If this is a child who can’t remember to bring homework back from school, then how is he going to remember to stay on schedule with medication?"
If it’s clear that parents are having difficulty in this area, the simplest thing to do is send the medicine to school and ask the nurse to administer it. Switching to a long-acting form might help, too, since it’s just easier to remember to take one pill than to take two.
The ADHD Parents Medication Guide is a great resource that can be used to get parents actively involved with the child’s drug therapy, Dr. Greenhill said. Developed by the American Psychiatric Association and the American Academy of Child and Adolescent Psychiatry, the online guide is designed to help families and physicians work together to make the best decisions about a child’s care.
Dr. Greenhill is on the advisory board of Quotient, which manufactures an ADHD testing system, and is a consultant for the Health Information Technology Lab.
NEW YORK – Assessing nonresponsiveness to attention-deficit/hyperactivity disorder treatment requires a bit of detective work, according to Dr. Laurence L. Greenhill.
The reason can be as simple as a little kid not being able to swallow a big pill, or as complex as a dysfunctional family dynamic that interferes with medication adherence. But once the problem is rooted out and addressed, most refractory patients can experience a good response, Dr. Greenhill said at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Since primary care physicians usually continue to manage children who respond to ADHD medications, psychiatrists are usually the ones who see nonresponders, said Dr. Greenhill, a child and adolescent psychiatrist at the New York Psychiatric Institute.
Medication nonadherence, the most common cause of a failure to improve, can arise from numerous situations.
On the simple side, it might be a matter of finding the right form of medication; a liquid or sprinkle capsule might be much easier for a child to take than a pill. And not all pills are created equally easy to take.
"For example, [the osmotic controlled release oral delivery system methylphenidate] just went off patent, and generics are now available. But some of these generics are much bigger. In fact, one of the 18-mg pills is twice as large as the patent medicine, and lots of kids can’t swallow it," he said.
The ADHD medication guide published by Long Island Jewish Hospital can be a helpful tool when working with parents on this issue. It lists all the Food and Drug Administration–approved medications for ADHD, with full-size photographs of each capsule, tablet, or pill.
Some generics are not pharmacokinetically or pharmacodynamically identical to the original formulation, Dr. Greenhill noted. Although the drug has to be molecularly identical and dose identical, "the ascending dose curve and duration of action need not be matched." Some generic formulations do fall into this problematic category. "For this reason, I try to encourage parents to get the brand," said Dr. Greenhill, adding that he has no financial interest in any of the drugs.
Medication nonadherence also can be attributable to uncomfortable or even intolerable side effects. These can include gastrointestinal issues, trouble sleeping, lack of appetite, restlessness, irritability, and "feeling fidgety."
Dosage adjustments or a medication change might be in order. For appetite issues, recommend giving the medication after meals, and reassure parents it’s OK to let a child eat later in the evening, when hunger may return.
It’s important to get the child’s growth records from the pediatrician, and plot height and weight curves every 6 months. If there’s a consistent fall-off, consider lowering the dose or changing to another drug.
Contrary to widely held belief, stimulants don’t pose significant cardiac risks to most children. A baseline electrocardiogram is really only necessary for a child who has a family history of sudden cardiac death or a personal history of syncope or cardiac abnormalities. Blood pressure and pulse should be monitored at every visit.
Melatonin is worth a try for youngsters whose ADHD meds interfere with good sleep, Dr. Greenhill said.
"I would start at 1 mg/night and work up," he said. "Starting at a high dose can actually shut off the naturally occurring melatonin. Plasma levels peak about an hour after taking it, so timing is important. I usually start with it about 3 hours before the scheduled sleeping time and then adjust."
Family dynamics also can play a big role in medication nonadherence. "ADHD families are often poor at scheduling activities, sometimes to the extent that parents are the ones who forget to give the medication. They also might not have a clear idea of how to give it, and just leave it on the kitchen table, making it the child’s responsibility to take it every day.
"If this is a child who can’t remember to bring homework back from school, then how is he going to remember to stay on schedule with medication?"
If it’s clear that parents are having difficulty in this area, the simplest thing to do is send the medicine to school and ask the nurse to administer it. Switching to a long-acting form might help, too, since it’s just easier to remember to take one pill than to take two.
The ADHD Parents Medication Guide is a great resource that can be used to get parents actively involved with the child’s drug therapy, Dr. Greenhill said. Developed by the American Psychiatric Association and the American Academy of Child and Adolescent Psychiatry, the online guide is designed to help families and physicians work together to make the best decisions about a child’s care.
Dr. Greenhill is on the advisory board of Quotient, which manufactures an ADHD testing system, and is a consultant for the Health Information Technology Lab.
NEW YORK – Assessing nonresponsiveness to attention-deficit/hyperactivity disorder treatment requires a bit of detective work, according to Dr. Laurence L. Greenhill.
The reason can be as simple as a little kid not being able to swallow a big pill, or as complex as a dysfunctional family dynamic that interferes with medication adherence. But once the problem is rooted out and addressed, most refractory patients can experience a good response, Dr. Greenhill said at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Since primary care physicians usually continue to manage children who respond to ADHD medications, psychiatrists are usually the ones who see nonresponders, said Dr. Greenhill, a child and adolescent psychiatrist at the New York Psychiatric Institute.
Medication nonadherence, the most common cause of a failure to improve, can arise from numerous situations.
On the simple side, it might be a matter of finding the right form of medication; a liquid or sprinkle capsule might be much easier for a child to take than a pill. And not all pills are created equally easy to take.
"For example, [the osmotic controlled release oral delivery system methylphenidate] just went off patent, and generics are now available. But some of these generics are much bigger. In fact, one of the 18-mg pills is twice as large as the patent medicine, and lots of kids can’t swallow it," he said.
The ADHD medication guide published by Long Island Jewish Hospital can be a helpful tool when working with parents on this issue. It lists all the Food and Drug Administration–approved medications for ADHD, with full-size photographs of each capsule, tablet, or pill.
Some generics are not pharmacokinetically or pharmacodynamically identical to the original formulation, Dr. Greenhill noted. Although the drug has to be molecularly identical and dose identical, "the ascending dose curve and duration of action need not be matched." Some generic formulations do fall into this problematic category. "For this reason, I try to encourage parents to get the brand," said Dr. Greenhill, adding that he has no financial interest in any of the drugs.
Medication nonadherence also can be attributable to uncomfortable or even intolerable side effects. These can include gastrointestinal issues, trouble sleeping, lack of appetite, restlessness, irritability, and "feeling fidgety."
Dosage adjustments or a medication change might be in order. For appetite issues, recommend giving the medication after meals, and reassure parents it’s OK to let a child eat later in the evening, when hunger may return.
It’s important to get the child’s growth records from the pediatrician, and plot height and weight curves every 6 months. If there’s a consistent fall-off, consider lowering the dose or changing to another drug.
Contrary to widely held belief, stimulants don’t pose significant cardiac risks to most children. A baseline electrocardiogram is really only necessary for a child who has a family history of sudden cardiac death or a personal history of syncope or cardiac abnormalities. Blood pressure and pulse should be monitored at every visit.
Melatonin is worth a try for youngsters whose ADHD meds interfere with good sleep, Dr. Greenhill said.
"I would start at 1 mg/night and work up," he said. "Starting at a high dose can actually shut off the naturally occurring melatonin. Plasma levels peak about an hour after taking it, so timing is important. I usually start with it about 3 hours before the scheduled sleeping time and then adjust."
Family dynamics also can play a big role in medication nonadherence. "ADHD families are often poor at scheduling activities, sometimes to the extent that parents are the ones who forget to give the medication. They also might not have a clear idea of how to give it, and just leave it on the kitchen table, making it the child’s responsibility to take it every day.
"If this is a child who can’t remember to bring homework back from school, then how is he going to remember to stay on schedule with medication?"
If it’s clear that parents are having difficulty in this area, the simplest thing to do is send the medicine to school and ask the nurse to administer it. Switching to a long-acting form might help, too, since it’s just easier to remember to take one pill than to take two.
The ADHD Parents Medication Guide is a great resource that can be used to get parents actively involved with the child’s drug therapy, Dr. Greenhill said. Developed by the American Psychiatric Association and the American Academy of Child and Adolescent Psychiatry, the online guide is designed to help families and physicians work together to make the best decisions about a child’s care.
Dr. Greenhill is on the advisory board of Quotient, which manufactures an ADHD testing system, and is a consultant for the Health Information Technology Lab.
EXPERT ANALYSIS FROM THE PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Combo therapy for tobacco dependence
The Jan. 8 issue of JAMA marked the 50th anniversary of the first surgeon general’s report on smoking and health. We are all witness to the human catastrophe we call tobacco use. What will future generations think when they look back on us and see that we accepted something that killed so many? Or why we don’t have more medications to treat it – only two new drugs in the last two decades.
I have spent the last 15 years researching how to help people quit tobacco use. One may think that I would have a panel free of patients who continue to smoke – or who may know better than to show up for visits with me.
Far from true. I can think of one patient in particular whom I am watching slowly die from this addiction. Three years ago, his forced expiratory volume in 1 second was 1.04 L, and he continues to smoke a pack of cigarettes per day and is now on supplemental oxygen (although, he tells me, not at the same time).
Tobacco addiction engages a dizzying network of neurotransmitters. Given this complexity, one may wonder if we would gain traction by administering therapies attacking the problem from different angles. Previous research, for example, has shown that combining the nicotine patch with bupropion is better than the nicotine patch alone.
Varenicline is one of the most effective therapies for smoking cessation and acts on the acetylcholine nicotinic receptor. Bupropion, the other first-line nonnicotine drug for smoking cessation, inhibits the reuptake of norepinephrine and dopamine. Some researchers have hypothesized that these medications may act together synergistically.
In that 50th anniversary issue, we published data from our multicenter, randomized clinical trial with our colleagues at the University of Minnesota (JAMA 2014;311:155-63). In this study, we randomized 506 smokers to either combination therapy with bupropion sustained release (SR) and varenicline or varenicline alone given for 3 months.
We were particularly intrigued by the subgroup analysis, which showed that among heavier (20 or more cigarettes per day) and more dependent smokers, combination therapy was superior to monotherapy out to 12 months. Importantly, 12 months is 9 months after stopping the medications.
As a treating clinician who sees smokers in both my primary care and addiction practices, I find these data helpful and motivating.
Helpful because they lead me to conclude that varenicline will work for my lighter smokers, and varenicline combined with bupropion SR may increase the chances of success in heavier ones. As in all good clinical practice, patients should be alerted to the possibility of mood changes and symptoms.
Motivating because I now have data supporting me to step up my game in helping my patients quit before they become another statistic.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reported ties to Pfizer, GlaxoSmithKline, Orexigen, and JHP Pharmaceuticals.
The Jan. 8 issue of JAMA marked the 50th anniversary of the first surgeon general’s report on smoking and health. We are all witness to the human catastrophe we call tobacco use. What will future generations think when they look back on us and see that we accepted something that killed so many? Or why we don’t have more medications to treat it – only two new drugs in the last two decades.
I have spent the last 15 years researching how to help people quit tobacco use. One may think that I would have a panel free of patients who continue to smoke – or who may know better than to show up for visits with me.
Far from true. I can think of one patient in particular whom I am watching slowly die from this addiction. Three years ago, his forced expiratory volume in 1 second was 1.04 L, and he continues to smoke a pack of cigarettes per day and is now on supplemental oxygen (although, he tells me, not at the same time).
Tobacco addiction engages a dizzying network of neurotransmitters. Given this complexity, one may wonder if we would gain traction by administering therapies attacking the problem from different angles. Previous research, for example, has shown that combining the nicotine patch with bupropion is better than the nicotine patch alone.
Varenicline is one of the most effective therapies for smoking cessation and acts on the acetylcholine nicotinic receptor. Bupropion, the other first-line nonnicotine drug for smoking cessation, inhibits the reuptake of norepinephrine and dopamine. Some researchers have hypothesized that these medications may act together synergistically.
In that 50th anniversary issue, we published data from our multicenter, randomized clinical trial with our colleagues at the University of Minnesota (JAMA 2014;311:155-63). In this study, we randomized 506 smokers to either combination therapy with bupropion sustained release (SR) and varenicline or varenicline alone given for 3 months.
We were particularly intrigued by the subgroup analysis, which showed that among heavier (20 or more cigarettes per day) and more dependent smokers, combination therapy was superior to monotherapy out to 12 months. Importantly, 12 months is 9 months after stopping the medications.
As a treating clinician who sees smokers in both my primary care and addiction practices, I find these data helpful and motivating.
Helpful because they lead me to conclude that varenicline will work for my lighter smokers, and varenicline combined with bupropion SR may increase the chances of success in heavier ones. As in all good clinical practice, patients should be alerted to the possibility of mood changes and symptoms.
Motivating because I now have data supporting me to step up my game in helping my patients quit before they become another statistic.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reported ties to Pfizer, GlaxoSmithKline, Orexigen, and JHP Pharmaceuticals.
The Jan. 8 issue of JAMA marked the 50th anniversary of the first surgeon general’s report on smoking and health. We are all witness to the human catastrophe we call tobacco use. What will future generations think when they look back on us and see that we accepted something that killed so many? Or why we don’t have more medications to treat it – only two new drugs in the last two decades.
I have spent the last 15 years researching how to help people quit tobacco use. One may think that I would have a panel free of patients who continue to smoke – or who may know better than to show up for visits with me.
Far from true. I can think of one patient in particular whom I am watching slowly die from this addiction. Three years ago, his forced expiratory volume in 1 second was 1.04 L, and he continues to smoke a pack of cigarettes per day and is now on supplemental oxygen (although, he tells me, not at the same time).
Tobacco addiction engages a dizzying network of neurotransmitters. Given this complexity, one may wonder if we would gain traction by administering therapies attacking the problem from different angles. Previous research, for example, has shown that combining the nicotine patch with bupropion is better than the nicotine patch alone.
Varenicline is one of the most effective therapies for smoking cessation and acts on the acetylcholine nicotinic receptor. Bupropion, the other first-line nonnicotine drug for smoking cessation, inhibits the reuptake of norepinephrine and dopamine. Some researchers have hypothesized that these medications may act together synergistically.
In that 50th anniversary issue, we published data from our multicenter, randomized clinical trial with our colleagues at the University of Minnesota (JAMA 2014;311:155-63). In this study, we randomized 506 smokers to either combination therapy with bupropion sustained release (SR) and varenicline or varenicline alone given for 3 months.
We were particularly intrigued by the subgroup analysis, which showed that among heavier (20 or more cigarettes per day) and more dependent smokers, combination therapy was superior to monotherapy out to 12 months. Importantly, 12 months is 9 months after stopping the medications.
As a treating clinician who sees smokers in both my primary care and addiction practices, I find these data helpful and motivating.
Helpful because they lead me to conclude that varenicline will work for my lighter smokers, and varenicline combined with bupropion SR may increase the chances of success in heavier ones. As in all good clinical practice, patients should be alerted to the possibility of mood changes and symptoms.
Motivating because I now have data supporting me to step up my game in helping my patients quit before they become another statistic.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reported ties to Pfizer, GlaxoSmithKline, Orexigen, and JHP Pharmaceuticals.
Psychoanalytic theory and the young child
I recently ran into a colleague who asked me whether I was still writing my column. I said yes and that I was currently writing an article on Selma H. Fraiberg. His response, "You don’t hear that name very much anymore," disappointed me. I responded by saying whenever a colleague, friend, or family member is having a baby, I send them a copy of "The Magic Years" with a clear statement that both parents must read it. It is clearly the best book on child rearing ever written in my opinion.
Ms. Fraiberg, creator of "The Magic Years," was a master’s in social work–trained psychoanalyst affiliated with the department of psychiatry at the University of California, San Francisco, who translated numerous concepts about babies, parents, and the first few years of life with wonderful examples of the type of incidents that every parent faces. She was highly regarded 50 years ago and received a great deal of praise for her book. But, at that time, there was a lot of prejudice against nonmedical degree psychoanalysts, and her book was not regarded as highly as I believe it should have been.
When I was a resident, I was required to read "The Magic Years," understand it, and be able to discuss it. Our teachers were concerned that we were busy being residents but also having children, and we really had to understand child rearing so that we could serve as resources for our residents and our analytic trainees.
Ms. Fraiberg translated psychoanalytic theory into child-rearing guidance in the book by looking at three age ranges: the first 18 months, 18 months to 3 years, and 3-6 years. Some of the examples are still fresh today, even though the book was published originally in 1959.
Dr. T. Berry Brazelton, the renowned pediatrician, wrote an introduction to the 50th anniversary of the book (New York: Scribner, 2008) saying that Ms. Fraiberg "makes each stage of emotional and mental development come alive!" I agree wholeheartedly. Furthermore, I would say that the concepts in the book can inform psychiatrists in our efforts to help our patients. After all, raising children (and growing up) is fraught with pitfalls. As Freud said early in his career, there are three impossible professions: governing nations, raising children, and psychoanalysis.
How the magic unfolds
Parents are often confused by things that children do or say, imaginary friends and animals – frustrating the child by pointing out reality when the child needs that imaginary friend or animal to survive. To the child, these imaginary friends and animals are not silly at all. A good example is what a niece of Ms. Fraiberg’s called the "Laughing Tiger."
Her niece, who was 2 years, 8 months old at the time, created the Laughing Tiger and many other imaginary companions at a time when she was afraid of ferocious animals. The niece’s "imaginary tiger gives her a kind of control over a danger which earlier had left her helpless and anxious," Ms. Fraiberg wrote. Instead of viewing this companion as problematic, it makes more sense to see this use of imagination as a healthy sign. Indeed, the child "can maintain his human ties and his good contact with reality while he maintains his imaginary world," she writes. "Moreover, it can be demonstrated that the child’s contact with the real world is strengthened by his periodic excursions into fantasy."
Virtually every chapter of the book is filled with insights that explain how young children interpret their world, which makes it invaluable for new parents. As we all know too well, the pitfalls in raising a child and growing up are many. I have not referred back to it for personal reasons in recent years. After all, my children are 54, 52, and 50 years old. But my wife and I did make very liberal use of the book throughout the years – while all of our friends were using Dr. Spock to help them navigate the waters of child rearing.
Mastering fear
Ms. Fraiberg gently guides the reader in an understanding of the child’s developing mind, why they cry, why they have tantrums, why they use imagination and how to help mom deal with the child’s anxiety. Take the example of a 2-year-old who was afraid of the family vacuum cleaner. Some young children control their fear of what must seem like loud monsters to them by learning to control the switch. But this toddler, who was known for his tendency to carry around a pocket-size screwdriver, was not satisfied with that solution. He had another idea: "Tiny screws and wheels were removed and lost in this frantic search," Ms. Fraiberg wrote. "...Finally, this limping monster issued its dying croak and succumbed without giving up its secret."
After a couple of years, the youngster’s "drive to investigate" was motivated by factors other than anxiety. Instead, he found investigation, discovery, and reconstruction to be pleasures in themselves. Interestingly, this child grew up to be a physicist.
There are many lessons here for psychoanalysts and our patients. One is that children experience things in which adults have no conscious memory. This means that we can help patients become better parents if we can get them to empathize with the child’s fears and frustrations.
Attachment, active handling
Ms. Fraiberg tells the story of an infant who developed an extremely severe sleep disturbance when she was 8 months old. Around 11 p.m. nightly, the infant woke up screaming, despite her parents’ efforts to calm her down. When her parents checked on her, the baby clung to her mother.
The episodes started after the baby woke up one night when the parents were out and had left her in the care of a babysitter. These meltdowns came in contrast to the child’s earlier reactions to her parents’ absence: "She never seemed to mind before if she wakened and saw a babysitter instead of us," Ms. Fraiberg quotes the parents as saying. "We just didn’t expect anything like this." What might explain this sudden new reaction?
"We know that the attachment to the mother is especially strong at this stage of development and a strange face may disturb the child at this age, even when encountered in the daytime," she writes. "The reaction to the strange face, as we have seen, is an indication of the discrimination of the mother as a person and the recognition of her as the person who gives satisfactions and protection. The stranger’s face that appears when mother’s face is expected produces anxiety because it symbolizes the absence or loss of the mother."
As you can see from that scenario, Ms. Fraiberg lets the mother know how essential she is and how early the child is distressed by the mother’s disappearance. In general, some people argue that they have to go on with their lives and that the baby will have to learn to be away from their mothers. We have to help our patients understand that the learning process is a burden for the infant. Some kids take a long time to learn how to separate from mom. Ms. Fraiberg helped the baby under discussion overcome her anxiety through nursery games in which her mother would hide her face one minute and return the next. She said the game allowed the baby to "work out the problem in her waking hours so that gradually the sleep disturbance disappeared."
Ms. Fraiberg also applies psychoanalytic theory to explain why a 9-month-old with a healthy appetite stopped eating and went on what she calls a "food strike" that lasted for 3 days. The child’s mother – who wanted the meals to be neat and orderly events – had been feeding the baby. So what brought the strike to an end?
One day the child’s father took over the feeding, and to the parents’ surprise, the baby started eating again. The mother immediately blamed herself, but the child’s behavior had nothing to do with her, per se. When the baby’s father tried to feed him, he grabbed the spoon and "plastered his face with strained carrots. Papa seemed quite unconcerned." When the baby turned his cup upside down, allowing his milk to spill all over the floor, the father took the messiness in stride.
This scenario was in stark contrast to those that emerged when the baby’s mother was in charge. When the baby tried to snatch the spoon from his mother, she got an extra spoon. When he tried to play with his milk cup, she moved it out of reach. As soon as the baby’s father allowed him to have freedom in feeding himself, the strike ended.
The explanation for the baby’s behavior changes is rooted in child development theory, Ms. Fraiberg writes. "...A certain amount of active handling of objects is absolutely necessary for the child in discovering and learning about the world around him," she says.
The period of 18 months to 3 years is dominated by words. If the child wishes something, he will use whatever words he has learned up until then, not knowing that they might not have any relationship to what he’s wishing for. If he wants something, he demands it or screams. He does not have language that is precise in any way. He uses words that he hopes will satisfy his wishes.
When the child acquires the word "bye-bye," he "begins to take the departures of his parents with more grace." The acquisition of language also makes it possible for the child to show more self-control and plays a role in the formation of his conscience.
I consider myself a developmental psychiatrist, an area in which child development is essential to all therapeutic engagement. Much can be learned about the patient if we know about his childhood and parents. I often see the patient doing to his child what his parents did to him. Patients are always shocked when I point this out to them, and the process of understanding how they got to where they are occurs. I call it therapeutic living. The book is so important because it tries to help parents learn how to handle tough developmental moments and periods. The section on toilet training is classic.
Please read "The Magic Years," and get your colleagues and students to read it as well. Ms. Fraiberg was a true master of the analytic method.
Dr. Fink is a psychiatrist and consultant, and professor of psychiatry at Temple University, Philadelphia.
I recently ran into a colleague who asked me whether I was still writing my column. I said yes and that I was currently writing an article on Selma H. Fraiberg. His response, "You don’t hear that name very much anymore," disappointed me. I responded by saying whenever a colleague, friend, or family member is having a baby, I send them a copy of "The Magic Years" with a clear statement that both parents must read it. It is clearly the best book on child rearing ever written in my opinion.
Ms. Fraiberg, creator of "The Magic Years," was a master’s in social work–trained psychoanalyst affiliated with the department of psychiatry at the University of California, San Francisco, who translated numerous concepts about babies, parents, and the first few years of life with wonderful examples of the type of incidents that every parent faces. She was highly regarded 50 years ago and received a great deal of praise for her book. But, at that time, there was a lot of prejudice against nonmedical degree psychoanalysts, and her book was not regarded as highly as I believe it should have been.
When I was a resident, I was required to read "The Magic Years," understand it, and be able to discuss it. Our teachers were concerned that we were busy being residents but also having children, and we really had to understand child rearing so that we could serve as resources for our residents and our analytic trainees.
Ms. Fraiberg translated psychoanalytic theory into child-rearing guidance in the book by looking at three age ranges: the first 18 months, 18 months to 3 years, and 3-6 years. Some of the examples are still fresh today, even though the book was published originally in 1959.
Dr. T. Berry Brazelton, the renowned pediatrician, wrote an introduction to the 50th anniversary of the book (New York: Scribner, 2008) saying that Ms. Fraiberg "makes each stage of emotional and mental development come alive!" I agree wholeheartedly. Furthermore, I would say that the concepts in the book can inform psychiatrists in our efforts to help our patients. After all, raising children (and growing up) is fraught with pitfalls. As Freud said early in his career, there are three impossible professions: governing nations, raising children, and psychoanalysis.
How the magic unfolds
Parents are often confused by things that children do or say, imaginary friends and animals – frustrating the child by pointing out reality when the child needs that imaginary friend or animal to survive. To the child, these imaginary friends and animals are not silly at all. A good example is what a niece of Ms. Fraiberg’s called the "Laughing Tiger."
Her niece, who was 2 years, 8 months old at the time, created the Laughing Tiger and many other imaginary companions at a time when she was afraid of ferocious animals. The niece’s "imaginary tiger gives her a kind of control over a danger which earlier had left her helpless and anxious," Ms. Fraiberg wrote. Instead of viewing this companion as problematic, it makes more sense to see this use of imagination as a healthy sign. Indeed, the child "can maintain his human ties and his good contact with reality while he maintains his imaginary world," she writes. "Moreover, it can be demonstrated that the child’s contact with the real world is strengthened by his periodic excursions into fantasy."
Virtually every chapter of the book is filled with insights that explain how young children interpret their world, which makes it invaluable for new parents. As we all know too well, the pitfalls in raising a child and growing up are many. I have not referred back to it for personal reasons in recent years. After all, my children are 54, 52, and 50 years old. But my wife and I did make very liberal use of the book throughout the years – while all of our friends were using Dr. Spock to help them navigate the waters of child rearing.
Mastering fear
Ms. Fraiberg gently guides the reader in an understanding of the child’s developing mind, why they cry, why they have tantrums, why they use imagination and how to help mom deal with the child’s anxiety. Take the example of a 2-year-old who was afraid of the family vacuum cleaner. Some young children control their fear of what must seem like loud monsters to them by learning to control the switch. But this toddler, who was known for his tendency to carry around a pocket-size screwdriver, was not satisfied with that solution. He had another idea: "Tiny screws and wheels were removed and lost in this frantic search," Ms. Fraiberg wrote. "...Finally, this limping monster issued its dying croak and succumbed without giving up its secret."
After a couple of years, the youngster’s "drive to investigate" was motivated by factors other than anxiety. Instead, he found investigation, discovery, and reconstruction to be pleasures in themselves. Interestingly, this child grew up to be a physicist.
There are many lessons here for psychoanalysts and our patients. One is that children experience things in which adults have no conscious memory. This means that we can help patients become better parents if we can get them to empathize with the child’s fears and frustrations.
Attachment, active handling
Ms. Fraiberg tells the story of an infant who developed an extremely severe sleep disturbance when she was 8 months old. Around 11 p.m. nightly, the infant woke up screaming, despite her parents’ efforts to calm her down. When her parents checked on her, the baby clung to her mother.
The episodes started after the baby woke up one night when the parents were out and had left her in the care of a babysitter. These meltdowns came in contrast to the child’s earlier reactions to her parents’ absence: "She never seemed to mind before if she wakened and saw a babysitter instead of us," Ms. Fraiberg quotes the parents as saying. "We just didn’t expect anything like this." What might explain this sudden new reaction?
"We know that the attachment to the mother is especially strong at this stage of development and a strange face may disturb the child at this age, even when encountered in the daytime," she writes. "The reaction to the strange face, as we have seen, is an indication of the discrimination of the mother as a person and the recognition of her as the person who gives satisfactions and protection. The stranger’s face that appears when mother’s face is expected produces anxiety because it symbolizes the absence or loss of the mother."
As you can see from that scenario, Ms. Fraiberg lets the mother know how essential she is and how early the child is distressed by the mother’s disappearance. In general, some people argue that they have to go on with their lives and that the baby will have to learn to be away from their mothers. We have to help our patients understand that the learning process is a burden for the infant. Some kids take a long time to learn how to separate from mom. Ms. Fraiberg helped the baby under discussion overcome her anxiety through nursery games in which her mother would hide her face one minute and return the next. She said the game allowed the baby to "work out the problem in her waking hours so that gradually the sleep disturbance disappeared."
Ms. Fraiberg also applies psychoanalytic theory to explain why a 9-month-old with a healthy appetite stopped eating and went on what she calls a "food strike" that lasted for 3 days. The child’s mother – who wanted the meals to be neat and orderly events – had been feeding the baby. So what brought the strike to an end?
One day the child’s father took over the feeding, and to the parents’ surprise, the baby started eating again. The mother immediately blamed herself, but the child’s behavior had nothing to do with her, per se. When the baby’s father tried to feed him, he grabbed the spoon and "plastered his face with strained carrots. Papa seemed quite unconcerned." When the baby turned his cup upside down, allowing his milk to spill all over the floor, the father took the messiness in stride.
This scenario was in stark contrast to those that emerged when the baby’s mother was in charge. When the baby tried to snatch the spoon from his mother, she got an extra spoon. When he tried to play with his milk cup, she moved it out of reach. As soon as the baby’s father allowed him to have freedom in feeding himself, the strike ended.
The explanation for the baby’s behavior changes is rooted in child development theory, Ms. Fraiberg writes. "...A certain amount of active handling of objects is absolutely necessary for the child in discovering and learning about the world around him," she says.
The period of 18 months to 3 years is dominated by words. If the child wishes something, he will use whatever words he has learned up until then, not knowing that they might not have any relationship to what he’s wishing for. If he wants something, he demands it or screams. He does not have language that is precise in any way. He uses words that he hopes will satisfy his wishes.
When the child acquires the word "bye-bye," he "begins to take the departures of his parents with more grace." The acquisition of language also makes it possible for the child to show more self-control and plays a role in the formation of his conscience.
I consider myself a developmental psychiatrist, an area in which child development is essential to all therapeutic engagement. Much can be learned about the patient if we know about his childhood and parents. I often see the patient doing to his child what his parents did to him. Patients are always shocked when I point this out to them, and the process of understanding how they got to where they are occurs. I call it therapeutic living. The book is so important because it tries to help parents learn how to handle tough developmental moments and periods. The section on toilet training is classic.
Please read "The Magic Years," and get your colleagues and students to read it as well. Ms. Fraiberg was a true master of the analytic method.
Dr. Fink is a psychiatrist and consultant, and professor of psychiatry at Temple University, Philadelphia.
I recently ran into a colleague who asked me whether I was still writing my column. I said yes and that I was currently writing an article on Selma H. Fraiberg. His response, "You don’t hear that name very much anymore," disappointed me. I responded by saying whenever a colleague, friend, or family member is having a baby, I send them a copy of "The Magic Years" with a clear statement that both parents must read it. It is clearly the best book on child rearing ever written in my opinion.
Ms. Fraiberg, creator of "The Magic Years," was a master’s in social work–trained psychoanalyst affiliated with the department of psychiatry at the University of California, San Francisco, who translated numerous concepts about babies, parents, and the first few years of life with wonderful examples of the type of incidents that every parent faces. She was highly regarded 50 years ago and received a great deal of praise for her book. But, at that time, there was a lot of prejudice against nonmedical degree psychoanalysts, and her book was not regarded as highly as I believe it should have been.
When I was a resident, I was required to read "The Magic Years," understand it, and be able to discuss it. Our teachers were concerned that we were busy being residents but also having children, and we really had to understand child rearing so that we could serve as resources for our residents and our analytic trainees.
Ms. Fraiberg translated psychoanalytic theory into child-rearing guidance in the book by looking at three age ranges: the first 18 months, 18 months to 3 years, and 3-6 years. Some of the examples are still fresh today, even though the book was published originally in 1959.
Dr. T. Berry Brazelton, the renowned pediatrician, wrote an introduction to the 50th anniversary of the book (New York: Scribner, 2008) saying that Ms. Fraiberg "makes each stage of emotional and mental development come alive!" I agree wholeheartedly. Furthermore, I would say that the concepts in the book can inform psychiatrists in our efforts to help our patients. After all, raising children (and growing up) is fraught with pitfalls. As Freud said early in his career, there are three impossible professions: governing nations, raising children, and psychoanalysis.
How the magic unfolds
Parents are often confused by things that children do or say, imaginary friends and animals – frustrating the child by pointing out reality when the child needs that imaginary friend or animal to survive. To the child, these imaginary friends and animals are not silly at all. A good example is what a niece of Ms. Fraiberg’s called the "Laughing Tiger."
Her niece, who was 2 years, 8 months old at the time, created the Laughing Tiger and many other imaginary companions at a time when she was afraid of ferocious animals. The niece’s "imaginary tiger gives her a kind of control over a danger which earlier had left her helpless and anxious," Ms. Fraiberg wrote. Instead of viewing this companion as problematic, it makes more sense to see this use of imagination as a healthy sign. Indeed, the child "can maintain his human ties and his good contact with reality while he maintains his imaginary world," she writes. "Moreover, it can be demonstrated that the child’s contact with the real world is strengthened by his periodic excursions into fantasy."
Virtually every chapter of the book is filled with insights that explain how young children interpret their world, which makes it invaluable for new parents. As we all know too well, the pitfalls in raising a child and growing up are many. I have not referred back to it for personal reasons in recent years. After all, my children are 54, 52, and 50 years old. But my wife and I did make very liberal use of the book throughout the years – while all of our friends were using Dr. Spock to help them navigate the waters of child rearing.
Mastering fear
Ms. Fraiberg gently guides the reader in an understanding of the child’s developing mind, why they cry, why they have tantrums, why they use imagination and how to help mom deal with the child’s anxiety. Take the example of a 2-year-old who was afraid of the family vacuum cleaner. Some young children control their fear of what must seem like loud monsters to them by learning to control the switch. But this toddler, who was known for his tendency to carry around a pocket-size screwdriver, was not satisfied with that solution. He had another idea: "Tiny screws and wheels were removed and lost in this frantic search," Ms. Fraiberg wrote. "...Finally, this limping monster issued its dying croak and succumbed without giving up its secret."
After a couple of years, the youngster’s "drive to investigate" was motivated by factors other than anxiety. Instead, he found investigation, discovery, and reconstruction to be pleasures in themselves. Interestingly, this child grew up to be a physicist.
There are many lessons here for psychoanalysts and our patients. One is that children experience things in which adults have no conscious memory. This means that we can help patients become better parents if we can get them to empathize with the child’s fears and frustrations.
Attachment, active handling
Ms. Fraiberg tells the story of an infant who developed an extremely severe sleep disturbance when she was 8 months old. Around 11 p.m. nightly, the infant woke up screaming, despite her parents’ efforts to calm her down. When her parents checked on her, the baby clung to her mother.
The episodes started after the baby woke up one night when the parents were out and had left her in the care of a babysitter. These meltdowns came in contrast to the child’s earlier reactions to her parents’ absence: "She never seemed to mind before if she wakened and saw a babysitter instead of us," Ms. Fraiberg quotes the parents as saying. "We just didn’t expect anything like this." What might explain this sudden new reaction?
"We know that the attachment to the mother is especially strong at this stage of development and a strange face may disturb the child at this age, even when encountered in the daytime," she writes. "The reaction to the strange face, as we have seen, is an indication of the discrimination of the mother as a person and the recognition of her as the person who gives satisfactions and protection. The stranger’s face that appears when mother’s face is expected produces anxiety because it symbolizes the absence or loss of the mother."
As you can see from that scenario, Ms. Fraiberg lets the mother know how essential she is and how early the child is distressed by the mother’s disappearance. In general, some people argue that they have to go on with their lives and that the baby will have to learn to be away from their mothers. We have to help our patients understand that the learning process is a burden for the infant. Some kids take a long time to learn how to separate from mom. Ms. Fraiberg helped the baby under discussion overcome her anxiety through nursery games in which her mother would hide her face one minute and return the next. She said the game allowed the baby to "work out the problem in her waking hours so that gradually the sleep disturbance disappeared."
Ms. Fraiberg also applies psychoanalytic theory to explain why a 9-month-old with a healthy appetite stopped eating and went on what she calls a "food strike" that lasted for 3 days. The child’s mother – who wanted the meals to be neat and orderly events – had been feeding the baby. So what brought the strike to an end?
One day the child’s father took over the feeding, and to the parents’ surprise, the baby started eating again. The mother immediately blamed herself, but the child’s behavior had nothing to do with her, per se. When the baby’s father tried to feed him, he grabbed the spoon and "plastered his face with strained carrots. Papa seemed quite unconcerned." When the baby turned his cup upside down, allowing his milk to spill all over the floor, the father took the messiness in stride.
This scenario was in stark contrast to those that emerged when the baby’s mother was in charge. When the baby tried to snatch the spoon from his mother, she got an extra spoon. When he tried to play with his milk cup, she moved it out of reach. As soon as the baby’s father allowed him to have freedom in feeding himself, the strike ended.
The explanation for the baby’s behavior changes is rooted in child development theory, Ms. Fraiberg writes. "...A certain amount of active handling of objects is absolutely necessary for the child in discovering and learning about the world around him," she says.
The period of 18 months to 3 years is dominated by words. If the child wishes something, he will use whatever words he has learned up until then, not knowing that they might not have any relationship to what he’s wishing for. If he wants something, he demands it or screams. He does not have language that is precise in any way. He uses words that he hopes will satisfy his wishes.
When the child acquires the word "bye-bye," he "begins to take the departures of his parents with more grace." The acquisition of language also makes it possible for the child to show more self-control and plays a role in the formation of his conscience.
I consider myself a developmental psychiatrist, an area in which child development is essential to all therapeutic engagement. Much can be learned about the patient if we know about his childhood and parents. I often see the patient doing to his child what his parents did to him. Patients are always shocked when I point this out to them, and the process of understanding how they got to where they are occurs. I call it therapeutic living. The book is so important because it tries to help parents learn how to handle tough developmental moments and periods. The section on toilet training is classic.
Please read "The Magic Years," and get your colleagues and students to read it as well. Ms. Fraiberg was a true master of the analytic method.
Dr. Fink is a psychiatrist and consultant, and professor of psychiatry at Temple University, Philadelphia.
Fiber in the new year
The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.
Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.
Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).
But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?
In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).
The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.
The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.
Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.
The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.
Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.
Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).
But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?
In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).
The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.
The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.
Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.
The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.
Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.
Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).
But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?
In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).
The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.
The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.
Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.