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How often should you follow up on a patient with newly diagnosed hypothyroidism?
Six to 8 weeks after the start of levothyroxine therapy you should reexamine patients and measure their serum thyroid-stimulating hormone (TSH) (strength of recommendation [SOR]: C, common practice and expert opinion). If thyroid function is normal at that time, examine the patient and measure serum TSH again in 4 to 6 months because clearance of levothyroxine increases in the euthyroid (normal) state (SOR: C, expert opinion).
Once the proper maintenance dose of levothyroxine is achieved, evaluate the patient and obtain a serum TSH at least annually, or as clinically indicated (SOR: C, expert opinion).
Evidence summary
There is very little patient-oriented research to help answer this question. Virtually all of the literature is based on bench research and expert opinion.
Wait at least 6 weeks to follow up after starting therapy
Serial serum TSH measurements are adequate to follow adults with newly diagnosed, uncomplicated primary hypothyroidism. However, serum thyroid hormone levels normalize before serum TSH. Serum thyroid hormone concentrations increase first, then the TSH secretion falls because of the negative feedback action of levothyroxine on the pituitary and hypothalamus. Levothyroxine has a 1-week plasma half-life; a steady state is achieved about 6 weeks (6 half-lives) after the start of treatment or a change in dose. The TSH level should, therefore, be evaluated no earlier than 6 weeks after initiating therapy or adjusting levothyroxine dosage.1,2 The full effects of thyroid hormone replacement on the TSH level may not become apparent until 8 weeks of therapy.3
Check TSH 4 to 6 months after initial follow-up
If the initial dose doesn’t require adjustment, reevaluate the patient and measure serum TSH again in 4 to 6 months because levothyroxine clearance can increase after the euthyroid state is established.4 If a dosage change is needed, make adjustments every 6 weeks, based on serum TSH values, until TSH values return to the reference range. Successful treatment reverses all the signs and symptoms of hypothyroidism, although some neuropsychologic and biochemical abnormalities, such as depressed mood and lipid abnormalities, may persist for several months.3
Monitor stable patients annually, especially the elderly
Examine the patient and measure serum TSH annually after identifying the proper maintenance dose, more often if an abnormal result or a change in the patient’s status occurs.2 Certain situations such as pregnancy, initiation of new medications, or liver or kidney disease may require more frequent monitoring.
Generally, once a stable maintenance dosage of levothyroxine is achieved, the dosage will remain adequate until the patient has a significant weight change or reaches his or her seventh or eighth decade.1 Although monitoring less often than once a year can be justified in younger adult patients whose weight is stable, patients older than 65 years must be monitored annually to avoid overreplacement. With age, thyroid binding may decrease, and the serum albumin level may decline. This can result in a 20% reduction in the dose of levothyroxine required.5,6
Recommendations
The American Association of Clinical Endocrinologists (AACE) recommends reassessment and repeat lab work at least 6 weeks after any change in levothyroxine brand or dose. The AACE practice guidelines suggest follow-up with appropriate interim history, physical exam, and pertinent lab studies at 6 months, and then annually after the TSH level has normalized.7
1. Hueston WJ. Treatment of hypothyroidism. Am Fam Physician. 2001;64:1717-1724.
2. Singer PA, Cooper DS, Levy EG, et al. For the Standards of Care Committee, American Thyroid Association. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. JAMA. 1995;273:808-812.
3. Felig P, Baxter JD, Frohman LA. Endocrinology and Metabolism. 3rd ed. New York: McGraw-Hill, Inc.; 1995:504-505.
4. Braverman LE, Utiger RD. Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text. 7th ed. Philadelphia: Lippincott-Raven; 1996:884-885.
5. Rosenbaum RL, Barzel US. Levothyroxine replacement dose for primary hypothyroidism decreases with age. Ann Intern Med. 1982;96:53-55.
6. Sawin CT, Geller A, Hershman JM, et al. The aging thyroid. The use of thyroid hormone in older persons. JAMA. 1989;261:2653-2655.
7. American Association of Clinical Endocrinologists Medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8:457469.
Six to 8 weeks after the start of levothyroxine therapy you should reexamine patients and measure their serum thyroid-stimulating hormone (TSH) (strength of recommendation [SOR]: C, common practice and expert opinion). If thyroid function is normal at that time, examine the patient and measure serum TSH again in 4 to 6 months because clearance of levothyroxine increases in the euthyroid (normal) state (SOR: C, expert opinion).
Once the proper maintenance dose of levothyroxine is achieved, evaluate the patient and obtain a serum TSH at least annually, or as clinically indicated (SOR: C, expert opinion).
Evidence summary
There is very little patient-oriented research to help answer this question. Virtually all of the literature is based on bench research and expert opinion.
Wait at least 6 weeks to follow up after starting therapy
Serial serum TSH measurements are adequate to follow adults with newly diagnosed, uncomplicated primary hypothyroidism. However, serum thyroid hormone levels normalize before serum TSH. Serum thyroid hormone concentrations increase first, then the TSH secretion falls because of the negative feedback action of levothyroxine on the pituitary and hypothalamus. Levothyroxine has a 1-week plasma half-life; a steady state is achieved about 6 weeks (6 half-lives) after the start of treatment or a change in dose. The TSH level should, therefore, be evaluated no earlier than 6 weeks after initiating therapy or adjusting levothyroxine dosage.1,2 The full effects of thyroid hormone replacement on the TSH level may not become apparent until 8 weeks of therapy.3
Check TSH 4 to 6 months after initial follow-up
If the initial dose doesn’t require adjustment, reevaluate the patient and measure serum TSH again in 4 to 6 months because levothyroxine clearance can increase after the euthyroid state is established.4 If a dosage change is needed, make adjustments every 6 weeks, based on serum TSH values, until TSH values return to the reference range. Successful treatment reverses all the signs and symptoms of hypothyroidism, although some neuropsychologic and biochemical abnormalities, such as depressed mood and lipid abnormalities, may persist for several months.3
Monitor stable patients annually, especially the elderly
Examine the patient and measure serum TSH annually after identifying the proper maintenance dose, more often if an abnormal result or a change in the patient’s status occurs.2 Certain situations such as pregnancy, initiation of new medications, or liver or kidney disease may require more frequent monitoring.
Generally, once a stable maintenance dosage of levothyroxine is achieved, the dosage will remain adequate until the patient has a significant weight change or reaches his or her seventh or eighth decade.1 Although monitoring less often than once a year can be justified in younger adult patients whose weight is stable, patients older than 65 years must be monitored annually to avoid overreplacement. With age, thyroid binding may decrease, and the serum albumin level may decline. This can result in a 20% reduction in the dose of levothyroxine required.5,6
Recommendations
The American Association of Clinical Endocrinologists (AACE) recommends reassessment and repeat lab work at least 6 weeks after any change in levothyroxine brand or dose. The AACE practice guidelines suggest follow-up with appropriate interim history, physical exam, and pertinent lab studies at 6 months, and then annually after the TSH level has normalized.7
Six to 8 weeks after the start of levothyroxine therapy you should reexamine patients and measure their serum thyroid-stimulating hormone (TSH) (strength of recommendation [SOR]: C, common practice and expert opinion). If thyroid function is normal at that time, examine the patient and measure serum TSH again in 4 to 6 months because clearance of levothyroxine increases in the euthyroid (normal) state (SOR: C, expert opinion).
Once the proper maintenance dose of levothyroxine is achieved, evaluate the patient and obtain a serum TSH at least annually, or as clinically indicated (SOR: C, expert opinion).
Evidence summary
There is very little patient-oriented research to help answer this question. Virtually all of the literature is based on bench research and expert opinion.
Wait at least 6 weeks to follow up after starting therapy
Serial serum TSH measurements are adequate to follow adults with newly diagnosed, uncomplicated primary hypothyroidism. However, serum thyroid hormone levels normalize before serum TSH. Serum thyroid hormone concentrations increase first, then the TSH secretion falls because of the negative feedback action of levothyroxine on the pituitary and hypothalamus. Levothyroxine has a 1-week plasma half-life; a steady state is achieved about 6 weeks (6 half-lives) after the start of treatment or a change in dose. The TSH level should, therefore, be evaluated no earlier than 6 weeks after initiating therapy or adjusting levothyroxine dosage.1,2 The full effects of thyroid hormone replacement on the TSH level may not become apparent until 8 weeks of therapy.3
Check TSH 4 to 6 months after initial follow-up
If the initial dose doesn’t require adjustment, reevaluate the patient and measure serum TSH again in 4 to 6 months because levothyroxine clearance can increase after the euthyroid state is established.4 If a dosage change is needed, make adjustments every 6 weeks, based on serum TSH values, until TSH values return to the reference range. Successful treatment reverses all the signs and symptoms of hypothyroidism, although some neuropsychologic and biochemical abnormalities, such as depressed mood and lipid abnormalities, may persist for several months.3
Monitor stable patients annually, especially the elderly
Examine the patient and measure serum TSH annually after identifying the proper maintenance dose, more often if an abnormal result or a change in the patient’s status occurs.2 Certain situations such as pregnancy, initiation of new medications, or liver or kidney disease may require more frequent monitoring.
Generally, once a stable maintenance dosage of levothyroxine is achieved, the dosage will remain adequate until the patient has a significant weight change or reaches his or her seventh or eighth decade.1 Although monitoring less often than once a year can be justified in younger adult patients whose weight is stable, patients older than 65 years must be monitored annually to avoid overreplacement. With age, thyroid binding may decrease, and the serum albumin level may decline. This can result in a 20% reduction in the dose of levothyroxine required.5,6
Recommendations
The American Association of Clinical Endocrinologists (AACE) recommends reassessment and repeat lab work at least 6 weeks after any change in levothyroxine brand or dose. The AACE practice guidelines suggest follow-up with appropriate interim history, physical exam, and pertinent lab studies at 6 months, and then annually after the TSH level has normalized.7
1. Hueston WJ. Treatment of hypothyroidism. Am Fam Physician. 2001;64:1717-1724.
2. Singer PA, Cooper DS, Levy EG, et al. For the Standards of Care Committee, American Thyroid Association. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. JAMA. 1995;273:808-812.
3. Felig P, Baxter JD, Frohman LA. Endocrinology and Metabolism. 3rd ed. New York: McGraw-Hill, Inc.; 1995:504-505.
4. Braverman LE, Utiger RD. Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text. 7th ed. Philadelphia: Lippincott-Raven; 1996:884-885.
5. Rosenbaum RL, Barzel US. Levothyroxine replacement dose for primary hypothyroidism decreases with age. Ann Intern Med. 1982;96:53-55.
6. Sawin CT, Geller A, Hershman JM, et al. The aging thyroid. The use of thyroid hormone in older persons. JAMA. 1989;261:2653-2655.
7. American Association of Clinical Endocrinologists Medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8:457469.
1. Hueston WJ. Treatment of hypothyroidism. Am Fam Physician. 2001;64:1717-1724.
2. Singer PA, Cooper DS, Levy EG, et al. For the Standards of Care Committee, American Thyroid Association. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. JAMA. 1995;273:808-812.
3. Felig P, Baxter JD, Frohman LA. Endocrinology and Metabolism. 3rd ed. New York: McGraw-Hill, Inc.; 1995:504-505.
4. Braverman LE, Utiger RD. Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text. 7th ed. Philadelphia: Lippincott-Raven; 1996:884-885.
5. Rosenbaum RL, Barzel US. Levothyroxine replacement dose for primary hypothyroidism decreases with age. Ann Intern Med. 1982;96:53-55.
6. Sawin CT, Geller A, Hershman JM, et al. The aging thyroid. The use of thyroid hormone in older persons. JAMA. 1989;261:2653-2655.
7. American Association of Clinical Endocrinologists Medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8:457469.
Evidence-based answers from the Family Physicians Inquiries Network
Which lifestyle interventions effectively lower LDL cholesterol?
Counseling, weight loss, exercise, and drinking alcohol all effectively lower low-density lipoprotein cholesterol (LDL-C). Specifically, one to 2 daily drinks of alcohol lowers LDL-C, if consumed regularly for more than 4 weeks (strength of recommendation [SOR]: A, based on consistent results of multiple randomized controlled trials [RCTs]).
Counseling by physicians, dieticians, or pharmacists is effective at increasing patient compliance with medications, thereby lowering LDL-C (SOR: C, good evidence that intervention lowers LDL-C, insufficient to prove that it reduces mortality/morbidity).
Weight loss has been associated with reductions in LDL-C. However, other factors—including degree of caloric restriction, drug intervention, and diet composition—may play a more significant role than weight loss alone (SOR: A, based on a meta-analysis and consistent results of RCTs).
Exercise significantly lowers LDL-C (SOR: A, based on meta-analyses and consistent results of RCTs). Smoking cessation may have a beneficial effect (SOR: B, based on inconsistent results from RCTs that it lowers LDL-C). Exercise-based alternative practices (yoga and tai chi) lower LDL, and meditation may have a beneficial effect (SOR: C, moderate evidence that intervention lowers LDL, insufficient evidence to prove that it reduces mortality/morbidity).
Consider patient preference when discussing lifestyle modification
Vincent Lo, MD
San Joaquin Family Medicine Residency, French Camp, Calif
Therapeutic lifestyle changes are the initial treatment of choice for reduction of cardiac risk factors, but both patients and physicians often see these modifications as confusing and difficult to achieve. A recent year-long study on different diets concluded that dietary adherence is more important than a specific type of diet for weight loss and reduction of cardiac risk factors.1 Another recent study reports no difference in weight loss among diets, based on different exercise duration and intensities over 1 year in a group of sedentary and overweight women.2 Therefore, family physicians should consider culture, patient preference, and practical issues such as cost and availability, when discussing therapeutic lifestyle modification with patients.
Evidence summary
Elevated LDL-C is an independent risk factor for coronary heart disease (CHD),3 the leading cause of death in the US.4 Lowering LDL-C by 60 mg/dL reduces CHD events by 50% after 2 years.5 Although medications successfully lower LDL-C and decrease CHD risk, therapeutic lifestyle changes remain the initial therapy for most adult patients.3,6
Our search located evidence about alcohol consumption, counseling, exercise, weight loss, alternative lifestyle measures, and smoking cessation. The TABLE summarizes the evidence for each.
TABLE
A- and B-level evidence points to effectiveness of lifestyle interventions
| LIFESTYLE INTERVENTION | MAGNITUDE OF EFFECT ON LDL-C | % REDUCTION DATA LDL-C | DATA SOURCES | SOR |
|---|---|---|---|---|
| Alcohol | 4–10 mg/dL | 4%–8% | 4 RCTs | A |
| Counseling | 0–58 mg/dL | 0%–33% | 15 RCTs, 8 CTs | A |
| Exercise | 3–16 mg/dL | 2.5%–4% | 5 meta-analysis | A |
| Meditation | 0–28 mg/dL | 0%–19% | 3 RCTs | B |
| Smoking | 0–5 mg/dL | 0%–4% | 2 RCTs | B |
| Weight loss: | ||||
| –diet, exercise, supplements | 0–42 mg/dL | 0%–22% | 28 RCTs, 14 CTs, 1 meta-analysis | A |
| –drug therapy | 10–31 mg/dL | 11%–32% | 4 RCTs, 2 CTs | |
| Yoga/tai chi | 20–26 mg/dL | 15%–20% | 2 RCTs, 1 CT | A |
| LDL-C, low-density lipoprotein cholesterol; SOR, strength of recommendation; RCT, randomized controlled trial; CT, clinical trials. | ||||
| SOR: A, good evidence that intervention lowers LDL. SOR: B, moderate evidence. | ||||
1 to 2 drinks daily reduced LDL-C
One 5-year-long cohort study (N=933) showed that alcohol was associated with LDL-C reduction in a dose-dependent manner.7 Two crossover trials (4–6 weeks in duration) conducted among heavy drinkers showed that LDL-C increased when alcohol intake decreased. Two randomized crossover trials (8–12 weeks in duration) found a statistically significant decrease in LDL-C with consumption of 1 to 2 drinks daily.
Counseling improves medication adherence
An RCT (N=167) with 8 years of follow-up found that patient education and counseling effectively improved medication adherence.8 Another RCT (N=1162) lasting 1 year, however, found that nutrition counseling by primary care physicians resulted in no significant change in LDL-C compared with usual care.9
Studies focused on enhancing dietary compliance did not find consistent post-intervention improvement. Greater medication adherence or improved dietary compliance did result in consistent significant improvements in LDL-C.
Exercise lowers LDL; weight loss a factor
Aerobic exercise effectively lowers LDL-C. This reduction is enhanced by weight loss and diet and mitigated by weight gain.10 An analysis of 4 RCTs showed that LDL-C also decreased with resistance training.
A higher body-mass index is associated with higher LDL-C. However, the effect of weight loss perse on LDL-C remains unclear. Multiple short-term studies have found that a modest amount of weight loss (5%–10%) is associated with a significant reduction in LDL-C.11 A meta-analysis found a 0.8 mg/dL LDL-C decrease for every kg of weight lost. Long-term follow-up, however, showed that LDL-C returned to baseline even when weight loss was maintained. Eight clinical trials failed to demonstrate a reduction in LDL-C postintervention with up to 10 kg of weight loss. Studies using weight-loss drugs (Sibutramine, Orlistat) found more significant weight loss during treatment, along with greater decrease in LDL-C, when compared with studies using only lifestyle modifications.
Other measures have mixed results
High-quality RCTs (N=267) with yoga or tai chi as the exercise intervention showed a statistically significant decrease in LDL-C over 12 to 14 weeks.12 Two RCTs investigated the effect of meditation on LDL-C with mixed results. One (N=16) showed a significant decrease in LDL-C over 8 weeks, while a second (N=60) showed no difference in LDL-C. A high-quality RCT (N=91) with a combined intervention (counseling, exercise, and meditation over 1 year) showed a significant decrease in LDL-C.
In cross-sectional surveys, LDL-C does not appear to differ between smokers and nonsmokers. One meta-analysis found a dose-dependent relationship between smoking and LDL-C, with overall LDL-C 1.7% higher for smokers compared with nonsmokers.13 Two RCTs investigated the effect of smoking cessation on LDL-C with mixed results. One (N=935) showed a decrease in nonfasting LDL-C while a second (N=140) showed no difference in LDL-C.
Recommendations from others
According to ATP III guidelines,3 all adults with LDL-C above goal should be treated with therapeutic lifestyle changes for primary and secondary prevention of CHD. These include a diet intervention, increased physical activity, and weight loss. Physicians are encouraged to refer patients to a nutritionist. If LDL-C is not at goal after 6 weeks, changes are intensified; physicians should consider pharmacologic therapy if a patient is still unable to attain his or her goal. ACP III guidelines recommend an office visit every 4 to 6 months to monitor adherence.
American Heart Association guidelines recommend that physicians counsel smokers at every office visit to stop smoking. The American College of Cardiology recommends abstinence from alcohol for patients with suspected alcoholic cardiomyopathy. For patients with heart failure from any other cause, alcohol consumption is usually limited to 1 drink per day.
Counseling, weight loss, exercise, and drinking alcohol all effectively lower low-density lipoprotein cholesterol (LDL-C). Specifically, one to 2 daily drinks of alcohol lowers LDL-C, if consumed regularly for more than 4 weeks (strength of recommendation [SOR]: A, based on consistent results of multiple randomized controlled trials [RCTs]).
Counseling by physicians, dieticians, or pharmacists is effective at increasing patient compliance with medications, thereby lowering LDL-C (SOR: C, good evidence that intervention lowers LDL-C, insufficient to prove that it reduces mortality/morbidity).
Weight loss has been associated with reductions in LDL-C. However, other factors—including degree of caloric restriction, drug intervention, and diet composition—may play a more significant role than weight loss alone (SOR: A, based on a meta-analysis and consistent results of RCTs).
Exercise significantly lowers LDL-C (SOR: A, based on meta-analyses and consistent results of RCTs). Smoking cessation may have a beneficial effect (SOR: B, based on inconsistent results from RCTs that it lowers LDL-C). Exercise-based alternative practices (yoga and tai chi) lower LDL, and meditation may have a beneficial effect (SOR: C, moderate evidence that intervention lowers LDL, insufficient evidence to prove that it reduces mortality/morbidity).
Consider patient preference when discussing lifestyle modification
Vincent Lo, MD
San Joaquin Family Medicine Residency, French Camp, Calif
Therapeutic lifestyle changes are the initial treatment of choice for reduction of cardiac risk factors, but both patients and physicians often see these modifications as confusing and difficult to achieve. A recent year-long study on different diets concluded that dietary adherence is more important than a specific type of diet for weight loss and reduction of cardiac risk factors.1 Another recent study reports no difference in weight loss among diets, based on different exercise duration and intensities over 1 year in a group of sedentary and overweight women.2 Therefore, family physicians should consider culture, patient preference, and practical issues such as cost and availability, when discussing therapeutic lifestyle modification with patients.
Evidence summary
Elevated LDL-C is an independent risk factor for coronary heart disease (CHD),3 the leading cause of death in the US.4 Lowering LDL-C by 60 mg/dL reduces CHD events by 50% after 2 years.5 Although medications successfully lower LDL-C and decrease CHD risk, therapeutic lifestyle changes remain the initial therapy for most adult patients.3,6
Our search located evidence about alcohol consumption, counseling, exercise, weight loss, alternative lifestyle measures, and smoking cessation. The TABLE summarizes the evidence for each.
TABLE
A- and B-level evidence points to effectiveness of lifestyle interventions
| LIFESTYLE INTERVENTION | MAGNITUDE OF EFFECT ON LDL-C | % REDUCTION DATA LDL-C | DATA SOURCES | SOR |
|---|---|---|---|---|
| Alcohol | 4–10 mg/dL | 4%–8% | 4 RCTs | A |
| Counseling | 0–58 mg/dL | 0%–33% | 15 RCTs, 8 CTs | A |
| Exercise | 3–16 mg/dL | 2.5%–4% | 5 meta-analysis | A |
| Meditation | 0–28 mg/dL | 0%–19% | 3 RCTs | B |
| Smoking | 0–5 mg/dL | 0%–4% | 2 RCTs | B |
| Weight loss: | ||||
| –diet, exercise, supplements | 0–42 mg/dL | 0%–22% | 28 RCTs, 14 CTs, 1 meta-analysis | A |
| –drug therapy | 10–31 mg/dL | 11%–32% | 4 RCTs, 2 CTs | |
| Yoga/tai chi | 20–26 mg/dL | 15%–20% | 2 RCTs, 1 CT | A |
| LDL-C, low-density lipoprotein cholesterol; SOR, strength of recommendation; RCT, randomized controlled trial; CT, clinical trials. | ||||
| SOR: A, good evidence that intervention lowers LDL. SOR: B, moderate evidence. | ||||
1 to 2 drinks daily reduced LDL-C
One 5-year-long cohort study (N=933) showed that alcohol was associated with LDL-C reduction in a dose-dependent manner.7 Two crossover trials (4–6 weeks in duration) conducted among heavy drinkers showed that LDL-C increased when alcohol intake decreased. Two randomized crossover trials (8–12 weeks in duration) found a statistically significant decrease in LDL-C with consumption of 1 to 2 drinks daily.
Counseling improves medication adherence
An RCT (N=167) with 8 years of follow-up found that patient education and counseling effectively improved medication adherence.8 Another RCT (N=1162) lasting 1 year, however, found that nutrition counseling by primary care physicians resulted in no significant change in LDL-C compared with usual care.9
Studies focused on enhancing dietary compliance did not find consistent post-intervention improvement. Greater medication adherence or improved dietary compliance did result in consistent significant improvements in LDL-C.
Exercise lowers LDL; weight loss a factor
Aerobic exercise effectively lowers LDL-C. This reduction is enhanced by weight loss and diet and mitigated by weight gain.10 An analysis of 4 RCTs showed that LDL-C also decreased with resistance training.
A higher body-mass index is associated with higher LDL-C. However, the effect of weight loss perse on LDL-C remains unclear. Multiple short-term studies have found that a modest amount of weight loss (5%–10%) is associated with a significant reduction in LDL-C.11 A meta-analysis found a 0.8 mg/dL LDL-C decrease for every kg of weight lost. Long-term follow-up, however, showed that LDL-C returned to baseline even when weight loss was maintained. Eight clinical trials failed to demonstrate a reduction in LDL-C postintervention with up to 10 kg of weight loss. Studies using weight-loss drugs (Sibutramine, Orlistat) found more significant weight loss during treatment, along with greater decrease in LDL-C, when compared with studies using only lifestyle modifications.
Other measures have mixed results
High-quality RCTs (N=267) with yoga or tai chi as the exercise intervention showed a statistically significant decrease in LDL-C over 12 to 14 weeks.12 Two RCTs investigated the effect of meditation on LDL-C with mixed results. One (N=16) showed a significant decrease in LDL-C over 8 weeks, while a second (N=60) showed no difference in LDL-C. A high-quality RCT (N=91) with a combined intervention (counseling, exercise, and meditation over 1 year) showed a significant decrease in LDL-C.
In cross-sectional surveys, LDL-C does not appear to differ between smokers and nonsmokers. One meta-analysis found a dose-dependent relationship between smoking and LDL-C, with overall LDL-C 1.7% higher for smokers compared with nonsmokers.13 Two RCTs investigated the effect of smoking cessation on LDL-C with mixed results. One (N=935) showed a decrease in nonfasting LDL-C while a second (N=140) showed no difference in LDL-C.
Recommendations from others
According to ATP III guidelines,3 all adults with LDL-C above goal should be treated with therapeutic lifestyle changes for primary and secondary prevention of CHD. These include a diet intervention, increased physical activity, and weight loss. Physicians are encouraged to refer patients to a nutritionist. If LDL-C is not at goal after 6 weeks, changes are intensified; physicians should consider pharmacologic therapy if a patient is still unable to attain his or her goal. ACP III guidelines recommend an office visit every 4 to 6 months to monitor adherence.
American Heart Association guidelines recommend that physicians counsel smokers at every office visit to stop smoking. The American College of Cardiology recommends abstinence from alcohol for patients with suspected alcoholic cardiomyopathy. For patients with heart failure from any other cause, alcohol consumption is usually limited to 1 drink per day.
Counseling, weight loss, exercise, and drinking alcohol all effectively lower low-density lipoprotein cholesterol (LDL-C). Specifically, one to 2 daily drinks of alcohol lowers LDL-C, if consumed regularly for more than 4 weeks (strength of recommendation [SOR]: A, based on consistent results of multiple randomized controlled trials [RCTs]).
Counseling by physicians, dieticians, or pharmacists is effective at increasing patient compliance with medications, thereby lowering LDL-C (SOR: C, good evidence that intervention lowers LDL-C, insufficient to prove that it reduces mortality/morbidity).
Weight loss has been associated with reductions in LDL-C. However, other factors—including degree of caloric restriction, drug intervention, and diet composition—may play a more significant role than weight loss alone (SOR: A, based on a meta-analysis and consistent results of RCTs).
Exercise significantly lowers LDL-C (SOR: A, based on meta-analyses and consistent results of RCTs). Smoking cessation may have a beneficial effect (SOR: B, based on inconsistent results from RCTs that it lowers LDL-C). Exercise-based alternative practices (yoga and tai chi) lower LDL, and meditation may have a beneficial effect (SOR: C, moderate evidence that intervention lowers LDL, insufficient evidence to prove that it reduces mortality/morbidity).
Consider patient preference when discussing lifestyle modification
Vincent Lo, MD
San Joaquin Family Medicine Residency, French Camp, Calif
Therapeutic lifestyle changes are the initial treatment of choice for reduction of cardiac risk factors, but both patients and physicians often see these modifications as confusing and difficult to achieve. A recent year-long study on different diets concluded that dietary adherence is more important than a specific type of diet for weight loss and reduction of cardiac risk factors.1 Another recent study reports no difference in weight loss among diets, based on different exercise duration and intensities over 1 year in a group of sedentary and overweight women.2 Therefore, family physicians should consider culture, patient preference, and practical issues such as cost and availability, when discussing therapeutic lifestyle modification with patients.
Evidence summary
Elevated LDL-C is an independent risk factor for coronary heart disease (CHD),3 the leading cause of death in the US.4 Lowering LDL-C by 60 mg/dL reduces CHD events by 50% after 2 years.5 Although medications successfully lower LDL-C and decrease CHD risk, therapeutic lifestyle changes remain the initial therapy for most adult patients.3,6
Our search located evidence about alcohol consumption, counseling, exercise, weight loss, alternative lifestyle measures, and smoking cessation. The TABLE summarizes the evidence for each.
TABLE
A- and B-level evidence points to effectiveness of lifestyle interventions
| LIFESTYLE INTERVENTION | MAGNITUDE OF EFFECT ON LDL-C | % REDUCTION DATA LDL-C | DATA SOURCES | SOR |
|---|---|---|---|---|
| Alcohol | 4–10 mg/dL | 4%–8% | 4 RCTs | A |
| Counseling | 0–58 mg/dL | 0%–33% | 15 RCTs, 8 CTs | A |
| Exercise | 3–16 mg/dL | 2.5%–4% | 5 meta-analysis | A |
| Meditation | 0–28 mg/dL | 0%–19% | 3 RCTs | B |
| Smoking | 0–5 mg/dL | 0%–4% | 2 RCTs | B |
| Weight loss: | ||||
| –diet, exercise, supplements | 0–42 mg/dL | 0%–22% | 28 RCTs, 14 CTs, 1 meta-analysis | A |
| –drug therapy | 10–31 mg/dL | 11%–32% | 4 RCTs, 2 CTs | |
| Yoga/tai chi | 20–26 mg/dL | 15%–20% | 2 RCTs, 1 CT | A |
| LDL-C, low-density lipoprotein cholesterol; SOR, strength of recommendation; RCT, randomized controlled trial; CT, clinical trials. | ||||
| SOR: A, good evidence that intervention lowers LDL. SOR: B, moderate evidence. | ||||
1 to 2 drinks daily reduced LDL-C
One 5-year-long cohort study (N=933) showed that alcohol was associated with LDL-C reduction in a dose-dependent manner.7 Two crossover trials (4–6 weeks in duration) conducted among heavy drinkers showed that LDL-C increased when alcohol intake decreased. Two randomized crossover trials (8–12 weeks in duration) found a statistically significant decrease in LDL-C with consumption of 1 to 2 drinks daily.
Counseling improves medication adherence
An RCT (N=167) with 8 years of follow-up found that patient education and counseling effectively improved medication adherence.8 Another RCT (N=1162) lasting 1 year, however, found that nutrition counseling by primary care physicians resulted in no significant change in LDL-C compared with usual care.9
Studies focused on enhancing dietary compliance did not find consistent post-intervention improvement. Greater medication adherence or improved dietary compliance did result in consistent significant improvements in LDL-C.
Exercise lowers LDL; weight loss a factor
Aerobic exercise effectively lowers LDL-C. This reduction is enhanced by weight loss and diet and mitigated by weight gain.10 An analysis of 4 RCTs showed that LDL-C also decreased with resistance training.
A higher body-mass index is associated with higher LDL-C. However, the effect of weight loss perse on LDL-C remains unclear. Multiple short-term studies have found that a modest amount of weight loss (5%–10%) is associated with a significant reduction in LDL-C.11 A meta-analysis found a 0.8 mg/dL LDL-C decrease for every kg of weight lost. Long-term follow-up, however, showed that LDL-C returned to baseline even when weight loss was maintained. Eight clinical trials failed to demonstrate a reduction in LDL-C postintervention with up to 10 kg of weight loss. Studies using weight-loss drugs (Sibutramine, Orlistat) found more significant weight loss during treatment, along with greater decrease in LDL-C, when compared with studies using only lifestyle modifications.
Other measures have mixed results
High-quality RCTs (N=267) with yoga or tai chi as the exercise intervention showed a statistically significant decrease in LDL-C over 12 to 14 weeks.12 Two RCTs investigated the effect of meditation on LDL-C with mixed results. One (N=16) showed a significant decrease in LDL-C over 8 weeks, while a second (N=60) showed no difference in LDL-C. A high-quality RCT (N=91) with a combined intervention (counseling, exercise, and meditation over 1 year) showed a significant decrease in LDL-C.
In cross-sectional surveys, LDL-C does not appear to differ between smokers and nonsmokers. One meta-analysis found a dose-dependent relationship between smoking and LDL-C, with overall LDL-C 1.7% higher for smokers compared with nonsmokers.13 Two RCTs investigated the effect of smoking cessation on LDL-C with mixed results. One (N=935) showed a decrease in nonfasting LDL-C while a second (N=140) showed no difference in LDL-C.
Recommendations from others
According to ATP III guidelines,3 all adults with LDL-C above goal should be treated with therapeutic lifestyle changes for primary and secondary prevention of CHD. These include a diet intervention, increased physical activity, and weight loss. Physicians are encouraged to refer patients to a nutritionist. If LDL-C is not at goal after 6 weeks, changes are intensified; physicians should consider pharmacologic therapy if a patient is still unable to attain his or her goal. ACP III guidelines recommend an office visit every 4 to 6 months to monitor adherence.
American Heart Association guidelines recommend that physicians counsel smokers at every office visit to stop smoking. The American College of Cardiology recommends abstinence from alcohol for patients with suspected alcoholic cardiomyopathy. For patients with heart failure from any other cause, alcohol consumption is usually limited to 1 drink per day.
Evidence-based answers from the Family Physicians Inquiries Network
Should you restrict your cardiac patient from driving?
That depends, of course, on your patient’s particular condition, but your decision can be guided by various cardiovascular society consensus conferences, such as the one from the Canadian Cardiovascular society (TABLE), since no evidence-based guidelines exist. It seems sensible to say, though, that impairment of consciousness associated with any heart disease needs further evaluation, with a complete restriction of driving for at least 6 months (strength of recommendation [SOR]: C, based on expert opinion and extrapolation from observational studies).
Helpful guide stratifies risk
Drew Malloy, MD
University of California Santa Cruz Student Health Service
This review points out the lack of evidence for a common clinical problem. Evidence is scant, but the TABLE helps the busy clinician stratify risks for different types of heart disease and provides some rational basis for the duration of restrictions. The existing expert consensus guidelines are sensible and useful when discussing this important issue with patients and their families after diagnosis of heart disease. However, to be quite frank, when I am driving I am more worried about the teenager on a cell phone behind the wheel of an SUV than my grandmother with an ICD.
Evidence summary
Our search identified no randomized controlled trials, no systematic reviews, 6 observational studies, and 3 consensus panel guidelines on risks from driving and cardiovascular disease. No studies deal specifically with coronary artery disease, congestive heart failure, or valvular heart disease and the risk of motor vehicle crashes for patients with these conditions. A population-based case control study of 5204 male drivers ages 45 to 70 in Quebec found no increased risk of crash for drivers with unspecified cardiovascular disease.1
Car accidents among ICD patients are low
The most studied patients are those with life-threatening ventricular arrhythmias—particularly those with implantable cardioverter-defibrillators (ICDs). Based on observational studies of patients and their physicians, patients with ventricular arrhythmias treated with ICDs do not have an increased risk of motor vehicle crashes.2-4 The largest of the studies2 prospectively and anonymously surveyed 627 patients from the Antiarrhythmics vs Implantable Defibrillators Trial. During follow-up, 2% of patients had a syncopal episode while driving, and 11% had dizziness or palpitations that required stopping the vehicle.
Of the 55 car crashes that occurred during 1619 patient-years after resumption of driving, 11% were preceded by a possible symptom of arrhythmia (0.4% per patient per year). The annual incidence of car accidents for patients with an ICD was 3.4% per patient-year. This is substantially lower than the 7.1% rate among the general driving population in the US.
Recommendations from others
Expert panel guidelines regarding fitness to drive for patients with heart disease are available from the Canadian Cardiovascular Society (CCS),5 the European Society of Cardiology, the American Heart Association, the North American Society of Pacing and Physiology,6 and the Cardiac Society of Australia and New Zealand.7 The 2004 CCS guidelines are the most recent and include a “Risk of Harm” formula that attempts to assign a quantitative level of risk to drivers with heart disease. These guidelines appear sensible but are not evidence-based (TABLE).
TABLE
Should your heart patient get behind the wheel? A helpful guide
| CONDITIONS | TIME TO RESUME DRIVING |
|---|---|
| Coronary artery disease | |
| Coronary bypass graft | 1 month after discharge |
| ST elevation myocardial infarction | 1 month after discharge |
| Unstable angina | |
| – PCI during hospital stay | 48 hours after PCI |
| – PCI not done during hospital stay | 7 days after discharge |
| Ventricular arrhythmias | |
| Non-sustained VT with no loss of consciousness | No restriction |
| VF or unstable VT | 6 months after event |
| Implantable cardioverter defibrillator | |
| For VF or VT with decreased level of consciousness | 6 months after event |
| Rhythm disturbances | |
| Atrial flutter (without impaired level of consciousness) | No restriction |
| Supraventricular tachycardia | No restriction |
| Atrial fibrillation | No restriction |
| Heart block | |
| First- and second-degree atrioventricular block, Mobitz Type 1 (without impairment of consciousness) | No restriction |
| Second-degree atrioventricular block, Mobitz Type II | No driving |
| Permanent pacemaker | |
| All patients | 1 week after implant; normal pacer function; no impaired level of consciousness |
| Congestive heart failure | |
| NYHA Classes I–III | No restriction |
| NYHA Classes IV | No driving |
| Adapted from Canadian Cardiovascular Society Consensus Conference 2003.5 | |
| PCI, percutaneous coronary intervention; VF, ventricular fibrillation; | |
| VT, ventricular tachycardia; NYHA, New York Heart Association | |
1. Guibert R, Potvin L, Ciampi A, Loiselle J, Philibert L, Franco ED. Are drivers with CVD more at risk for motor vehicle crashes? Study of men aged 45 to 70. Can Fam Physician 1998;44:770-776.
2. Akiyama T, Powell JL, Mitchell LB, Ehlert FA, Baessler C. Resumption of driving after life-threatening ventricular tachyarrhythmia. N Engl J Med 2001;345:391-397.
3. Trappe HJ, Wenzlaff P, Grellman G. Should patients with implantable cardioverter defibrillators be allowed to drive? Observations in 291 patients from a single center over an 11-year period. J Interv Card Electrophysiol 1998;2:193-201.
4. Curtis AB, Conti JB, Tucker KJ, Kubilis PS, Reilly RE, Woodard DA. Motor vehicle accidents in patients with an implantable cardioverter-defibrillator. J Am Coll Cardiol 1995;26:180-184.
5. CCS Consensus Conference 2003: Assessment of the cardiac patient fitness to drive and fly—executive summary. Can J Cardiol 2004;20:1313-1323.
6. Epstein AE, Miles WM, Benditt DG, et al. Personal and public safety issues related to arrhythmias that may affect consciousness: Implications for regulation and physician recommendations. A medical/scientific statement from the American Heart Association and the North American Society of Pacing and Electrophysiology. Circulation 1996;94:1147-1166.
7. Cardiac Society of Australia and New Zealand. Cardiovascular Disease and Driving 2002. Available at: www.csanz.edu.au/guidelines/practice/Drivegl2002.pdf. Accessed on April 3, 2007.
That depends, of course, on your patient’s particular condition, but your decision can be guided by various cardiovascular society consensus conferences, such as the one from the Canadian Cardiovascular society (TABLE), since no evidence-based guidelines exist. It seems sensible to say, though, that impairment of consciousness associated with any heart disease needs further evaluation, with a complete restriction of driving for at least 6 months (strength of recommendation [SOR]: C, based on expert opinion and extrapolation from observational studies).
Helpful guide stratifies risk
Drew Malloy, MD
University of California Santa Cruz Student Health Service
This review points out the lack of evidence for a common clinical problem. Evidence is scant, but the TABLE helps the busy clinician stratify risks for different types of heart disease and provides some rational basis for the duration of restrictions. The existing expert consensus guidelines are sensible and useful when discussing this important issue with patients and their families after diagnosis of heart disease. However, to be quite frank, when I am driving I am more worried about the teenager on a cell phone behind the wheel of an SUV than my grandmother with an ICD.
Evidence summary
Our search identified no randomized controlled trials, no systematic reviews, 6 observational studies, and 3 consensus panel guidelines on risks from driving and cardiovascular disease. No studies deal specifically with coronary artery disease, congestive heart failure, or valvular heart disease and the risk of motor vehicle crashes for patients with these conditions. A population-based case control study of 5204 male drivers ages 45 to 70 in Quebec found no increased risk of crash for drivers with unspecified cardiovascular disease.1
Car accidents among ICD patients are low
The most studied patients are those with life-threatening ventricular arrhythmias—particularly those with implantable cardioverter-defibrillators (ICDs). Based on observational studies of patients and their physicians, patients with ventricular arrhythmias treated with ICDs do not have an increased risk of motor vehicle crashes.2-4 The largest of the studies2 prospectively and anonymously surveyed 627 patients from the Antiarrhythmics vs Implantable Defibrillators Trial. During follow-up, 2% of patients had a syncopal episode while driving, and 11% had dizziness or palpitations that required stopping the vehicle.
Of the 55 car crashes that occurred during 1619 patient-years after resumption of driving, 11% were preceded by a possible symptom of arrhythmia (0.4% per patient per year). The annual incidence of car accidents for patients with an ICD was 3.4% per patient-year. This is substantially lower than the 7.1% rate among the general driving population in the US.
Recommendations from others
Expert panel guidelines regarding fitness to drive for patients with heart disease are available from the Canadian Cardiovascular Society (CCS),5 the European Society of Cardiology, the American Heart Association, the North American Society of Pacing and Physiology,6 and the Cardiac Society of Australia and New Zealand.7 The 2004 CCS guidelines are the most recent and include a “Risk of Harm” formula that attempts to assign a quantitative level of risk to drivers with heart disease. These guidelines appear sensible but are not evidence-based (TABLE).
TABLE
Should your heart patient get behind the wheel? A helpful guide
| CONDITIONS | TIME TO RESUME DRIVING |
|---|---|
| Coronary artery disease | |
| Coronary bypass graft | 1 month after discharge |
| ST elevation myocardial infarction | 1 month after discharge |
| Unstable angina | |
| – PCI during hospital stay | 48 hours after PCI |
| – PCI not done during hospital stay | 7 days after discharge |
| Ventricular arrhythmias | |
| Non-sustained VT with no loss of consciousness | No restriction |
| VF or unstable VT | 6 months after event |
| Implantable cardioverter defibrillator | |
| For VF or VT with decreased level of consciousness | 6 months after event |
| Rhythm disturbances | |
| Atrial flutter (without impaired level of consciousness) | No restriction |
| Supraventricular tachycardia | No restriction |
| Atrial fibrillation | No restriction |
| Heart block | |
| First- and second-degree atrioventricular block, Mobitz Type 1 (without impairment of consciousness) | No restriction |
| Second-degree atrioventricular block, Mobitz Type II | No driving |
| Permanent pacemaker | |
| All patients | 1 week after implant; normal pacer function; no impaired level of consciousness |
| Congestive heart failure | |
| NYHA Classes I–III | No restriction |
| NYHA Classes IV | No driving |
| Adapted from Canadian Cardiovascular Society Consensus Conference 2003.5 | |
| PCI, percutaneous coronary intervention; VF, ventricular fibrillation; | |
| VT, ventricular tachycardia; NYHA, New York Heart Association | |
That depends, of course, on your patient’s particular condition, but your decision can be guided by various cardiovascular society consensus conferences, such as the one from the Canadian Cardiovascular society (TABLE), since no evidence-based guidelines exist. It seems sensible to say, though, that impairment of consciousness associated with any heart disease needs further evaluation, with a complete restriction of driving for at least 6 months (strength of recommendation [SOR]: C, based on expert opinion and extrapolation from observational studies).
Helpful guide stratifies risk
Drew Malloy, MD
University of California Santa Cruz Student Health Service
This review points out the lack of evidence for a common clinical problem. Evidence is scant, but the TABLE helps the busy clinician stratify risks for different types of heart disease and provides some rational basis for the duration of restrictions. The existing expert consensus guidelines are sensible and useful when discussing this important issue with patients and their families after diagnosis of heart disease. However, to be quite frank, when I am driving I am more worried about the teenager on a cell phone behind the wheel of an SUV than my grandmother with an ICD.
Evidence summary
Our search identified no randomized controlled trials, no systematic reviews, 6 observational studies, and 3 consensus panel guidelines on risks from driving and cardiovascular disease. No studies deal specifically with coronary artery disease, congestive heart failure, or valvular heart disease and the risk of motor vehicle crashes for patients with these conditions. A population-based case control study of 5204 male drivers ages 45 to 70 in Quebec found no increased risk of crash for drivers with unspecified cardiovascular disease.1
Car accidents among ICD patients are low
The most studied patients are those with life-threatening ventricular arrhythmias—particularly those with implantable cardioverter-defibrillators (ICDs). Based on observational studies of patients and their physicians, patients with ventricular arrhythmias treated with ICDs do not have an increased risk of motor vehicle crashes.2-4 The largest of the studies2 prospectively and anonymously surveyed 627 patients from the Antiarrhythmics vs Implantable Defibrillators Trial. During follow-up, 2% of patients had a syncopal episode while driving, and 11% had dizziness or palpitations that required stopping the vehicle.
Of the 55 car crashes that occurred during 1619 patient-years after resumption of driving, 11% were preceded by a possible symptom of arrhythmia (0.4% per patient per year). The annual incidence of car accidents for patients with an ICD was 3.4% per patient-year. This is substantially lower than the 7.1% rate among the general driving population in the US.
Recommendations from others
Expert panel guidelines regarding fitness to drive for patients with heart disease are available from the Canadian Cardiovascular Society (CCS),5 the European Society of Cardiology, the American Heart Association, the North American Society of Pacing and Physiology,6 and the Cardiac Society of Australia and New Zealand.7 The 2004 CCS guidelines are the most recent and include a “Risk of Harm” formula that attempts to assign a quantitative level of risk to drivers with heart disease. These guidelines appear sensible but are not evidence-based (TABLE).
TABLE
Should your heart patient get behind the wheel? A helpful guide
| CONDITIONS | TIME TO RESUME DRIVING |
|---|---|
| Coronary artery disease | |
| Coronary bypass graft | 1 month after discharge |
| ST elevation myocardial infarction | 1 month after discharge |
| Unstable angina | |
| – PCI during hospital stay | 48 hours after PCI |
| – PCI not done during hospital stay | 7 days after discharge |
| Ventricular arrhythmias | |
| Non-sustained VT with no loss of consciousness | No restriction |
| VF or unstable VT | 6 months after event |
| Implantable cardioverter defibrillator | |
| For VF or VT with decreased level of consciousness | 6 months after event |
| Rhythm disturbances | |
| Atrial flutter (without impaired level of consciousness) | No restriction |
| Supraventricular tachycardia | No restriction |
| Atrial fibrillation | No restriction |
| Heart block | |
| First- and second-degree atrioventricular block, Mobitz Type 1 (without impairment of consciousness) | No restriction |
| Second-degree atrioventricular block, Mobitz Type II | No driving |
| Permanent pacemaker | |
| All patients | 1 week after implant; normal pacer function; no impaired level of consciousness |
| Congestive heart failure | |
| NYHA Classes I–III | No restriction |
| NYHA Classes IV | No driving |
| Adapted from Canadian Cardiovascular Society Consensus Conference 2003.5 | |
| PCI, percutaneous coronary intervention; VF, ventricular fibrillation; | |
| VT, ventricular tachycardia; NYHA, New York Heart Association | |
1. Guibert R, Potvin L, Ciampi A, Loiselle J, Philibert L, Franco ED. Are drivers with CVD more at risk for motor vehicle crashes? Study of men aged 45 to 70. Can Fam Physician 1998;44:770-776.
2. Akiyama T, Powell JL, Mitchell LB, Ehlert FA, Baessler C. Resumption of driving after life-threatening ventricular tachyarrhythmia. N Engl J Med 2001;345:391-397.
3. Trappe HJ, Wenzlaff P, Grellman G. Should patients with implantable cardioverter defibrillators be allowed to drive? Observations in 291 patients from a single center over an 11-year period. J Interv Card Electrophysiol 1998;2:193-201.
4. Curtis AB, Conti JB, Tucker KJ, Kubilis PS, Reilly RE, Woodard DA. Motor vehicle accidents in patients with an implantable cardioverter-defibrillator. J Am Coll Cardiol 1995;26:180-184.
5. CCS Consensus Conference 2003: Assessment of the cardiac patient fitness to drive and fly—executive summary. Can J Cardiol 2004;20:1313-1323.
6. Epstein AE, Miles WM, Benditt DG, et al. Personal and public safety issues related to arrhythmias that may affect consciousness: Implications for regulation and physician recommendations. A medical/scientific statement from the American Heart Association and the North American Society of Pacing and Electrophysiology. Circulation 1996;94:1147-1166.
7. Cardiac Society of Australia and New Zealand. Cardiovascular Disease and Driving 2002. Available at: www.csanz.edu.au/guidelines/practice/Drivegl2002.pdf. Accessed on April 3, 2007.
1. Guibert R, Potvin L, Ciampi A, Loiselle J, Philibert L, Franco ED. Are drivers with CVD more at risk for motor vehicle crashes? Study of men aged 45 to 70. Can Fam Physician 1998;44:770-776.
2. Akiyama T, Powell JL, Mitchell LB, Ehlert FA, Baessler C. Resumption of driving after life-threatening ventricular tachyarrhythmia. N Engl J Med 2001;345:391-397.
3. Trappe HJ, Wenzlaff P, Grellman G. Should patients with implantable cardioverter defibrillators be allowed to drive? Observations in 291 patients from a single center over an 11-year period. J Interv Card Electrophysiol 1998;2:193-201.
4. Curtis AB, Conti JB, Tucker KJ, Kubilis PS, Reilly RE, Woodard DA. Motor vehicle accidents in patients with an implantable cardioverter-defibrillator. J Am Coll Cardiol 1995;26:180-184.
5. CCS Consensus Conference 2003: Assessment of the cardiac patient fitness to drive and fly—executive summary. Can J Cardiol 2004;20:1313-1323.
6. Epstein AE, Miles WM, Benditt DG, et al. Personal and public safety issues related to arrhythmias that may affect consciousness: Implications for regulation and physician recommendations. A medical/scientific statement from the American Heart Association and the North American Society of Pacing and Electrophysiology. Circulation 1996;94:1147-1166.
7. Cardiac Society of Australia and New Zealand. Cardiovascular Disease and Driving 2002. Available at: www.csanz.edu.au/guidelines/practice/Drivegl2002.pdf. Accessed on April 3, 2007.
Evidence-based answers from the Family Physicians Inquiries Network
How effective are dietary interventions in lowering lipids in adults with dyslipidemia?
Diets lower in fat, higher in soy protein, or higher in fiber reduce serum total cholesterol, low-density lipoprotein (LDL), and triglycerides. More restrictive low-fat diets also lower high-density lipoprotein (HDL), while soy protein increases HDL. Average decreases in LDL range from 6.96 to 25.14 mg/dL, depending on the particular intervention and participants’ baseline characteristics (strength of recommendation [SOR]: C, based on meta-analyses of randomized controlled trials [RCTs] measuring intermediate endpoints). A “portfolio diet” that includes cholesterol-lowering “functional foods” can reduce total cholesterol and LDL; a Mediterranean-type diet can lower LDL (SOR: C, based on fair-quality RCTs, measuring intermediate endpoints). We do not yet know whether the these diets will also help patients live longer and more healthy lives or just improve their lipid profiles.
Simple interventions, like reducing fast food and increasing fruit and vegetable intake, are a good starting place
Rade N. Pejic, MD
Department of Family Medicine, Tulane University School of Medicine, New Orleans, La
Dietary modifications are necessary for the successful long-term treatment of lipid disorders, as well as many other chronic medical conditions. Patients are often encouraged when they learn they can reverse a disease process without taking a medication. We should take every opportunity to educate our patients and promote healthy lifestyles. Simple interventions, such as eating less fast food and more fresh fruits and vegetables, are often a good starting place. Other simple interventions to reduce cholesterol levels are taking fiber supplements and substituting commercially available margarines with plant sterols for butter.
Dietary counseling or referral to a medical nutritionist should be part of our overall treatment plan for patients with lipid disorders. regularly scheduled follow-up visits help promote adherence to therapeutic lifestyle changes and encourage a therapeutic alliance.
Evidence summary
Dietary changes are recommended as first-line treatment for mild to moderate dyslipidemia. We examined evidence on 5 common dietary interventions for adults with dyslipidemia. The average effects on lipid levels are reported in the TABLE.
TABLE
Average effect of dietary interventions on serum lipid levels
| DIETARY INTERVENTION | AVERAGE CHANGE IN MG/DL OF LIPID LEVELS (% CHANGE) | ||||
|---|---|---|---|---|---|
| TOTAL CHOLESTEROL | LDL | HDL | TRIGLYCERIDES | ||
| Low fat | NCEP Step I | –24.36* (–10%) | –18.95* (–12%) | –1.55 (–1.5%) | –15.10* (–8%) |
| NCEP Step II | –31.32* (–7%) | –25.14* (–13%) | –3.48* (–16%) | –16.83* (–8%) | |
| Soy | All | –8.51* (–3.77%) | –8.12* (–5.25%) | –1.55* + (+ 3.03%) | –8.86* (–7.27%) |
| Hypercholesterolemia | –9.67* | –6.96* | + 3.87* | –7.97* | |
| Fiber (per g/d) | –1.74* | –2.20* | –0.12 | + 0.27 | |
| “Portfolio” | –58.39* (–22.34%) | –51.82* (–29.71%) | 3.09 (–6.50%) | 18.60 (9.33%) | |
| Mediterranean | –15.47 (–6.06%) | –19.34* (–11.37%) | 0 (–12.50%) | –17.71 (0%) | |
| * Statistically significant at P≤.05 | |||||
Low-fat
A meta-analysis of 37 mostly good-quality controlled trials evaluated the former National Cholesterol Education Program (NCEP) Step I and Step II diets in 11,586 participants.1 The Step I diet restricted in-take of total fat (≤30% of total calories), saturated fat (≤10% of total calories), and cholesterol (≤300 mg/d). Step II goals were lower for saturated fat (<7%) and cholesterol (<200 mg/d). Mean baseline lipid values (mg/dL) were total cholesterol, 233.57; LDL, 155.10; HDL, 47.95; and triglycerides, 147.91. Both of these low-fat diets significantly reduced total cholesterol, LDL, and triglycerides. The Step II diet also reduced HDL.
Soy
A meta-analysis of 23 good-quality controlled trials with 1381 participants reported that soy protein with naturally occurring isoflavones significantly reduced total cholesterol, LDL, and triglycerides while significantly increasing HDL.2 The amount of soy isoflavone consumed varied across studies. One subgroup analysis showed that consumption of >80 mg/d was associated with a better effect on lipids. In subjects with baseline hypercholesterolemia (total cholesterol >240 mg/dL), greater reductions in total cholesterol, and greater increases in HDL were reported, with comparable changes in LDL and triglycerides.
Soluble fiber
A meta-analysis of 67 good-quality RCTs evaluated the effects of soluble dietary fiber in 2990 subjects (mean baseline lipid values [mg/dL]: total cholesterol, 240.9; LDL, 164.4).3 Diets high in soluble fiber (average dose of 9.5 g/d) were associated with a statistically significant decrease in total cholesterol and LDL and no significant change in HDL or triglycerides. Type of fiber (oat, psyllium, or pectin) was not influential after controlling for initial lipid level.
“Portfolio” diet
A fair-quality randomized crossover study with 34 participants found that a “portfolio diet,” which combines the fat intake of the NCEP Step II diet with cholesterol-lowering “functional foods” (including plant sterols, nuts, soluble fibers, and soy protein), markedly reduced total cholesterol and LDL.4 Mean baseline lipid values (mg/dL) were: total cholesterol, 261.41; LDL, 174.40; HDL, 47.56; triglycerides, 199.28.
Mediterranean diet
A fair-quality RCT with 88 participants reported reduced LDL among subjects assigned to a Mediterranean-type diet.5 Mean baseline lipid values (mg/dL) were total cholesterol, 255.22; LDL, 170.15; HDL, 58.01; triglycerides, 141.71.
Recommendations from others
The NCEP Adult Treatment Panel III and the American Heart Association recommend the Therapeutic Lifestyle Changes diet.6,7 The first stage of this diet emphasizes reduction in dietary saturated fat and cholesterol at the levels of the former NCEP Step II diet (≤7% of energy as saturated fat and ≤200 mg dietary cholesterol). If the LDL goal is not achieved, the second stage emphasizes the addition of functional foods and soluble fiber.
1. Yu-Poth S, Zhao G, Etherton T, et al. Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. Am J Clin Nutr 1999;69:632-646.
2. Zhan S, HO SC. Meta-analysis of the effects of soy protein containing isoflavones on the lipid profile. Am J Clin Nutr 2005;81:397-408.
3. Brown L, Rosner B, Willett WW, Sacks FM. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr 1999;69:30-42.
4. Jenkins DJA, Kendall CWC, Marchie A, et al. Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin in hypercholesterolemic participants. Am J Clin Nutr 2005;81:380-387.
5. Vincent-Baudry S, Defoort C, Gerber M, et al. The Medi-RIVAGE study: reduction of cardiovascular risk factors after a 3-mo intervention with a Mediterranean-type diet or a low-fat diet. Am J Clin Nutr 2005;82:964-971.
6. Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285:2486-2497.
7. Krauss RM, Eckel RH, Howard B, et al. AHA dietary guidelines revision 2000: a statement for health-care professionals from the Nutrition Committee of the American Heart Association. Circulation 2000;102:2284-2299.
Diets lower in fat, higher in soy protein, or higher in fiber reduce serum total cholesterol, low-density lipoprotein (LDL), and triglycerides. More restrictive low-fat diets also lower high-density lipoprotein (HDL), while soy protein increases HDL. Average decreases in LDL range from 6.96 to 25.14 mg/dL, depending on the particular intervention and participants’ baseline characteristics (strength of recommendation [SOR]: C, based on meta-analyses of randomized controlled trials [RCTs] measuring intermediate endpoints). A “portfolio diet” that includes cholesterol-lowering “functional foods” can reduce total cholesterol and LDL; a Mediterranean-type diet can lower LDL (SOR: C, based on fair-quality RCTs, measuring intermediate endpoints). We do not yet know whether the these diets will also help patients live longer and more healthy lives or just improve their lipid profiles.
Simple interventions, like reducing fast food and increasing fruit and vegetable intake, are a good starting place
Rade N. Pejic, MD
Department of Family Medicine, Tulane University School of Medicine, New Orleans, La
Dietary modifications are necessary for the successful long-term treatment of lipid disorders, as well as many other chronic medical conditions. Patients are often encouraged when they learn they can reverse a disease process without taking a medication. We should take every opportunity to educate our patients and promote healthy lifestyles. Simple interventions, such as eating less fast food and more fresh fruits and vegetables, are often a good starting place. Other simple interventions to reduce cholesterol levels are taking fiber supplements and substituting commercially available margarines with plant sterols for butter.
Dietary counseling or referral to a medical nutritionist should be part of our overall treatment plan for patients with lipid disorders. regularly scheduled follow-up visits help promote adherence to therapeutic lifestyle changes and encourage a therapeutic alliance.
Evidence summary
Dietary changes are recommended as first-line treatment for mild to moderate dyslipidemia. We examined evidence on 5 common dietary interventions for adults with dyslipidemia. The average effects on lipid levels are reported in the TABLE.
TABLE
Average effect of dietary interventions on serum lipid levels
| DIETARY INTERVENTION | AVERAGE CHANGE IN MG/DL OF LIPID LEVELS (% CHANGE) | ||||
|---|---|---|---|---|---|
| TOTAL CHOLESTEROL | LDL | HDL | TRIGLYCERIDES | ||
| Low fat | NCEP Step I | –24.36* (–10%) | –18.95* (–12%) | –1.55 (–1.5%) | –15.10* (–8%) |
| NCEP Step II | –31.32* (–7%) | –25.14* (–13%) | –3.48* (–16%) | –16.83* (–8%) | |
| Soy | All | –8.51* (–3.77%) | –8.12* (–5.25%) | –1.55* + (+ 3.03%) | –8.86* (–7.27%) |
| Hypercholesterolemia | –9.67* | –6.96* | + 3.87* | –7.97* | |
| Fiber (per g/d) | –1.74* | –2.20* | –0.12 | + 0.27 | |
| “Portfolio” | –58.39* (–22.34%) | –51.82* (–29.71%) | 3.09 (–6.50%) | 18.60 (9.33%) | |
| Mediterranean | –15.47 (–6.06%) | –19.34* (–11.37%) | 0 (–12.50%) | –17.71 (0%) | |
| * Statistically significant at P≤.05 | |||||
Low-fat
A meta-analysis of 37 mostly good-quality controlled trials evaluated the former National Cholesterol Education Program (NCEP) Step I and Step II diets in 11,586 participants.1 The Step I diet restricted in-take of total fat (≤30% of total calories), saturated fat (≤10% of total calories), and cholesterol (≤300 mg/d). Step II goals were lower for saturated fat (<7%) and cholesterol (<200 mg/d). Mean baseline lipid values (mg/dL) were total cholesterol, 233.57; LDL, 155.10; HDL, 47.95; and triglycerides, 147.91. Both of these low-fat diets significantly reduced total cholesterol, LDL, and triglycerides. The Step II diet also reduced HDL.
Soy
A meta-analysis of 23 good-quality controlled trials with 1381 participants reported that soy protein with naturally occurring isoflavones significantly reduced total cholesterol, LDL, and triglycerides while significantly increasing HDL.2 The amount of soy isoflavone consumed varied across studies. One subgroup analysis showed that consumption of >80 mg/d was associated with a better effect on lipids. In subjects with baseline hypercholesterolemia (total cholesterol >240 mg/dL), greater reductions in total cholesterol, and greater increases in HDL were reported, with comparable changes in LDL and triglycerides.
Soluble fiber
A meta-analysis of 67 good-quality RCTs evaluated the effects of soluble dietary fiber in 2990 subjects (mean baseline lipid values [mg/dL]: total cholesterol, 240.9; LDL, 164.4).3 Diets high in soluble fiber (average dose of 9.5 g/d) were associated with a statistically significant decrease in total cholesterol and LDL and no significant change in HDL or triglycerides. Type of fiber (oat, psyllium, or pectin) was not influential after controlling for initial lipid level.
“Portfolio” diet
A fair-quality randomized crossover study with 34 participants found that a “portfolio diet,” which combines the fat intake of the NCEP Step II diet with cholesterol-lowering “functional foods” (including plant sterols, nuts, soluble fibers, and soy protein), markedly reduced total cholesterol and LDL.4 Mean baseline lipid values (mg/dL) were: total cholesterol, 261.41; LDL, 174.40; HDL, 47.56; triglycerides, 199.28.
Mediterranean diet
A fair-quality RCT with 88 participants reported reduced LDL among subjects assigned to a Mediterranean-type diet.5 Mean baseline lipid values (mg/dL) were total cholesterol, 255.22; LDL, 170.15; HDL, 58.01; triglycerides, 141.71.
Recommendations from others
The NCEP Adult Treatment Panel III and the American Heart Association recommend the Therapeutic Lifestyle Changes diet.6,7 The first stage of this diet emphasizes reduction in dietary saturated fat and cholesterol at the levels of the former NCEP Step II diet (≤7% of energy as saturated fat and ≤200 mg dietary cholesterol). If the LDL goal is not achieved, the second stage emphasizes the addition of functional foods and soluble fiber.
Diets lower in fat, higher in soy protein, or higher in fiber reduce serum total cholesterol, low-density lipoprotein (LDL), and triglycerides. More restrictive low-fat diets also lower high-density lipoprotein (HDL), while soy protein increases HDL. Average decreases in LDL range from 6.96 to 25.14 mg/dL, depending on the particular intervention and participants’ baseline characteristics (strength of recommendation [SOR]: C, based on meta-analyses of randomized controlled trials [RCTs] measuring intermediate endpoints). A “portfolio diet” that includes cholesterol-lowering “functional foods” can reduce total cholesterol and LDL; a Mediterranean-type diet can lower LDL (SOR: C, based on fair-quality RCTs, measuring intermediate endpoints). We do not yet know whether the these diets will also help patients live longer and more healthy lives or just improve their lipid profiles.
Simple interventions, like reducing fast food and increasing fruit and vegetable intake, are a good starting place
Rade N. Pejic, MD
Department of Family Medicine, Tulane University School of Medicine, New Orleans, La
Dietary modifications are necessary for the successful long-term treatment of lipid disorders, as well as many other chronic medical conditions. Patients are often encouraged when they learn they can reverse a disease process without taking a medication. We should take every opportunity to educate our patients and promote healthy lifestyles. Simple interventions, such as eating less fast food and more fresh fruits and vegetables, are often a good starting place. Other simple interventions to reduce cholesterol levels are taking fiber supplements and substituting commercially available margarines with plant sterols for butter.
Dietary counseling or referral to a medical nutritionist should be part of our overall treatment plan for patients with lipid disorders. regularly scheduled follow-up visits help promote adherence to therapeutic lifestyle changes and encourage a therapeutic alliance.
Evidence summary
Dietary changes are recommended as first-line treatment for mild to moderate dyslipidemia. We examined evidence on 5 common dietary interventions for adults with dyslipidemia. The average effects on lipid levels are reported in the TABLE.
TABLE
Average effect of dietary interventions on serum lipid levels
| DIETARY INTERVENTION | AVERAGE CHANGE IN MG/DL OF LIPID LEVELS (% CHANGE) | ||||
|---|---|---|---|---|---|
| TOTAL CHOLESTEROL | LDL | HDL | TRIGLYCERIDES | ||
| Low fat | NCEP Step I | –24.36* (–10%) | –18.95* (–12%) | –1.55 (–1.5%) | –15.10* (–8%) |
| NCEP Step II | –31.32* (–7%) | –25.14* (–13%) | –3.48* (–16%) | –16.83* (–8%) | |
| Soy | All | –8.51* (–3.77%) | –8.12* (–5.25%) | –1.55* + (+ 3.03%) | –8.86* (–7.27%) |
| Hypercholesterolemia | –9.67* | –6.96* | + 3.87* | –7.97* | |
| Fiber (per g/d) | –1.74* | –2.20* | –0.12 | + 0.27 | |
| “Portfolio” | –58.39* (–22.34%) | –51.82* (–29.71%) | 3.09 (–6.50%) | 18.60 (9.33%) | |
| Mediterranean | –15.47 (–6.06%) | –19.34* (–11.37%) | 0 (–12.50%) | –17.71 (0%) | |
| * Statistically significant at P≤.05 | |||||
Low-fat
A meta-analysis of 37 mostly good-quality controlled trials evaluated the former National Cholesterol Education Program (NCEP) Step I and Step II diets in 11,586 participants.1 The Step I diet restricted in-take of total fat (≤30% of total calories), saturated fat (≤10% of total calories), and cholesterol (≤300 mg/d). Step II goals were lower for saturated fat (<7%) and cholesterol (<200 mg/d). Mean baseline lipid values (mg/dL) were total cholesterol, 233.57; LDL, 155.10; HDL, 47.95; and triglycerides, 147.91. Both of these low-fat diets significantly reduced total cholesterol, LDL, and triglycerides. The Step II diet also reduced HDL.
Soy
A meta-analysis of 23 good-quality controlled trials with 1381 participants reported that soy protein with naturally occurring isoflavones significantly reduced total cholesterol, LDL, and triglycerides while significantly increasing HDL.2 The amount of soy isoflavone consumed varied across studies. One subgroup analysis showed that consumption of >80 mg/d was associated with a better effect on lipids. In subjects with baseline hypercholesterolemia (total cholesterol >240 mg/dL), greater reductions in total cholesterol, and greater increases in HDL were reported, with comparable changes in LDL and triglycerides.
Soluble fiber
A meta-analysis of 67 good-quality RCTs evaluated the effects of soluble dietary fiber in 2990 subjects (mean baseline lipid values [mg/dL]: total cholesterol, 240.9; LDL, 164.4).3 Diets high in soluble fiber (average dose of 9.5 g/d) were associated with a statistically significant decrease in total cholesterol and LDL and no significant change in HDL or triglycerides. Type of fiber (oat, psyllium, or pectin) was not influential after controlling for initial lipid level.
“Portfolio” diet
A fair-quality randomized crossover study with 34 participants found that a “portfolio diet,” which combines the fat intake of the NCEP Step II diet with cholesterol-lowering “functional foods” (including plant sterols, nuts, soluble fibers, and soy protein), markedly reduced total cholesterol and LDL.4 Mean baseline lipid values (mg/dL) were: total cholesterol, 261.41; LDL, 174.40; HDL, 47.56; triglycerides, 199.28.
Mediterranean diet
A fair-quality RCT with 88 participants reported reduced LDL among subjects assigned to a Mediterranean-type diet.5 Mean baseline lipid values (mg/dL) were total cholesterol, 255.22; LDL, 170.15; HDL, 58.01; triglycerides, 141.71.
Recommendations from others
The NCEP Adult Treatment Panel III and the American Heart Association recommend the Therapeutic Lifestyle Changes diet.6,7 The first stage of this diet emphasizes reduction in dietary saturated fat and cholesterol at the levels of the former NCEP Step II diet (≤7% of energy as saturated fat and ≤200 mg dietary cholesterol). If the LDL goal is not achieved, the second stage emphasizes the addition of functional foods and soluble fiber.
1. Yu-Poth S, Zhao G, Etherton T, et al. Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. Am J Clin Nutr 1999;69:632-646.
2. Zhan S, HO SC. Meta-analysis of the effects of soy protein containing isoflavones on the lipid profile. Am J Clin Nutr 2005;81:397-408.
3. Brown L, Rosner B, Willett WW, Sacks FM. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr 1999;69:30-42.
4. Jenkins DJA, Kendall CWC, Marchie A, et al. Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin in hypercholesterolemic participants. Am J Clin Nutr 2005;81:380-387.
5. Vincent-Baudry S, Defoort C, Gerber M, et al. The Medi-RIVAGE study: reduction of cardiovascular risk factors after a 3-mo intervention with a Mediterranean-type diet or a low-fat diet. Am J Clin Nutr 2005;82:964-971.
6. Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285:2486-2497.
7. Krauss RM, Eckel RH, Howard B, et al. AHA dietary guidelines revision 2000: a statement for health-care professionals from the Nutrition Committee of the American Heart Association. Circulation 2000;102:2284-2299.
1. Yu-Poth S, Zhao G, Etherton T, et al. Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. Am J Clin Nutr 1999;69:632-646.
2. Zhan S, HO SC. Meta-analysis of the effects of soy protein containing isoflavones on the lipid profile. Am J Clin Nutr 2005;81:397-408.
3. Brown L, Rosner B, Willett WW, Sacks FM. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr 1999;69:30-42.
4. Jenkins DJA, Kendall CWC, Marchie A, et al. Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin in hypercholesterolemic participants. Am J Clin Nutr 2005;81:380-387.
5. Vincent-Baudry S, Defoort C, Gerber M, et al. The Medi-RIVAGE study: reduction of cardiovascular risk factors after a 3-mo intervention with a Mediterranean-type diet or a low-fat diet. Am J Clin Nutr 2005;82:964-971.
6. Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285:2486-2497.
7. Krauss RM, Eckel RH, Howard B, et al. AHA dietary guidelines revision 2000: a statement for health-care professionals from the Nutrition Committee of the American Heart Association. Circulation 2000;102:2284-2299.
Evidence-based answers from the Family Physicians Inquiries Network