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Does a low-fat diet help prevent breast cancer?
No. Studies show no evidence that reducing dietary fat decreases a woman’s risk of developing postmenopausal breast cancer within the subsequent 14 years (strength of recommendation [SOR]: B, based on large heterogeneous prospective cohort studies and appropriate meta-analyses of these studies). Overall, evidence is insufficient to recommend for or against reduction in dietary fat to reduce risk of breast cancer for women, although recommendations for prudent fat intake may be justified on other grounds.
Losing weight is still a good strategy
Kathryn Kolasa, PhD, RD, LDN
East Carolina University, Greenville, NC
Women at risk for breast cancer—and cancer survivors—want to know about lifestyle changes that can reduce their risks for cancer or recurrence. There is growing evidence that obesity plays a role in cancer development and promotion.
A low-fat diet has been demonstrated as a successful strategy for weight loss. However, for most women, making these changes can be difficult without extensive instruction, support, and motivation. Limiting sweetened beverages, increasing consumption of fruits and vegetables, and limiting fat intake are 3 strategies women can use to achieve a healthy weight. If this turns out to reduce their risk of breast cancer, so much the better!
Evidence summary
Our Medline search retrieved 1114 English-language studies published from 1960 through October 2006. We limited this set to randomized controlled trials and cohort studies, leaving 212 articles. We then excluded articles that had small sample sizes, did not follow subjects for at least 5 years, did not include original data, included men, did not give prevalence or incidence rate of breast cancer in the subjects, or did not discuss diet assessment tools. Of the remaining articles, we selected the 11 best studies to include in the review.
Early studies evaluating national average dietary fat intake and breast cancer incidence rates showed an almost linear relationship between increased dietary fat and increased breast cancer incidence.1 However, increased fat intake occurs primarily in industrialized nations, providing multiple possible confounders for increased rates of breast cancer, such as pollutants and increased consumption of preservatives, pesticides, and other chemicals.
Case-control studies have shown some minimally increased risk related to dietary fat consumption, but there is concern about recall bias in these studies.2 Since the late 1970s, 7 large, well-designed prospective cohort studies have examined the possible relationship between dietary fat and breast cancer.1 The findings have been somewhat contradictory, with some studies showing statistically significant associations toward increased risk with higher fat intake.3-5
Since the late 1990s, several meta-analyses, a systematic review of these cohort studies, and the Women’s Health Initiative Randomized Controlled Diet Initiative have largely concluded that there is no difference in breast cancer incidence between women with a low-fat diet (<20% of total calories from fat) and women with average or high-fat diets (>40% total calories from fat).1,3,6,7
The meta-analysis performed by Boyd et al did find a statistically significant difference, with relative risks ranging from 1.11 for overall to 1.19 for high-saturated-fat diets.8 The upper limit of all confidence intervals was no higher than 1.35, however, suggesting a lack of clinical significance. The best-designed studies also evaluated dietary composition with regard to key types of fat (saturated, mono- and poly-unsaturated; animal vs vegetable vs marine) and found no significant differences based on type of fat consumed.1
Preliminary evidence indicates that lowering dietary fat consumption may help with secondary prevention of breast cancer, but no large studies have been performed to date.9 Recently, a nested study within the Women’s Intervention Nutrition Study did show that women with breast cancer who decreased their fat intake to a median of 33 g/day had a hazard ratio of 0.76 for relapse over 60 months (compared with controls who ate a median of 51 g/day).10
Recommendations from others
There are no evidence-based or specific recommendations for the primary prevention of postmenopausal breast cancer for women through dietary fat reduction. In particular, neither the American Academy of Family Physicians, American College of Surgeons, National Institutes of Health, American College of Obstetricians and Gynecologists, American College of Physicians, US Preventive Services Task Force, or the Centers for Disease Control and Prevention provide any guidelines on dietary fat restriction for primary prevention of postmenopausal breast cancer.
The American Heart Association does have guidelines for coronary artery disease prevention for women, which include a low-fat diet.11 The USPSTF has no specific guidelines regarding dietary fat consumption for the general population.
1. Willett WC. Diet and breast cancer. J Intern Med 2001;249:395-411.
2. Bingham SA, Luben R, Welch A, Wareham N, Khaw KT, Day N. Are imprecise methods obscuring a relation between fat and breast cancer?. Lancet 2003;362:212-214.
3. Mattisson I, Wirfalt E, Wallstrom P, Gullberg B, Olsson H, Berglund G. High fat and alcohol intakes are risk factors of postmenopausal breast cancer: a prospective study from the Malmo diet and cancer cohort. Int J Cancer 2004;110:589-597.
4. Sieri S, Krogh V, Muti P, et al. Fat and Protein Intake and subsequent Breast Cancer risk in Postmenopausal Women. Nutr Cancer 2004;42:10-17.
5. Velie E, Kulldorff M, Schairer C, Block G, Albanes D, Schatzkin A. Dietary fat, fat subtypes, and breast cancer in postmenopausal women: a prospective cohort study. J Natl Cancer Inst 2000;92:833-839.
6. Holmes MD, Hunter DJ, Colditz GA, et al. Association of dietary intake of fat and fatty acids with risk of breast cancer. JAMA 1999;281:914-920.
7. Low-Fat Dietary Pattern and risk of Breast Cancer, Colorectal Cancer, and Cardiovascular Disease: The Women’s Health Initiative randomized Controlled Dietary Modification Trial. Available at: www.whi.org/findings/dm/dm.php. Accessed on June 14, 2007.
8. Boyd NF, Stone J, Vogt KN, Connelly BS, Martin LJ, Minkin S. Dietary fat and breast cancer risk revisited: a meta-analysis of the published literature. Br J Cancer 2003;89:1672-1685.
9. Rock CL. Diet and breast cancer: can dietary factors influence survival? J Mammary Gland Biol Neoplasia 2003;8:119-132.
10. Rowan T, Chlebowski GL, Blackburn CA, et al. Dietary Fat Reduction and Breast Cancer Outcome: Interim Efficacy Results From the Women’s Intervention Nutrition Study. J Natl Cancer Inst 2006;98:1767-1776.
11. Mosca L, Appel LJ, Benjamin EJ, et al. Evidence-based guidelines for cardiovascular disease prevention in women. Circulation 2004;109:672-693.
No. Studies show no evidence that reducing dietary fat decreases a woman’s risk of developing postmenopausal breast cancer within the subsequent 14 years (strength of recommendation [SOR]: B, based on large heterogeneous prospective cohort studies and appropriate meta-analyses of these studies). Overall, evidence is insufficient to recommend for or against reduction in dietary fat to reduce risk of breast cancer for women, although recommendations for prudent fat intake may be justified on other grounds.
Losing weight is still a good strategy
Kathryn Kolasa, PhD, RD, LDN
East Carolina University, Greenville, NC
Women at risk for breast cancer—and cancer survivors—want to know about lifestyle changes that can reduce their risks for cancer or recurrence. There is growing evidence that obesity plays a role in cancer development and promotion.
A low-fat diet has been demonstrated as a successful strategy for weight loss. However, for most women, making these changes can be difficult without extensive instruction, support, and motivation. Limiting sweetened beverages, increasing consumption of fruits and vegetables, and limiting fat intake are 3 strategies women can use to achieve a healthy weight. If this turns out to reduce their risk of breast cancer, so much the better!
Evidence summary
Our Medline search retrieved 1114 English-language studies published from 1960 through October 2006. We limited this set to randomized controlled trials and cohort studies, leaving 212 articles. We then excluded articles that had small sample sizes, did not follow subjects for at least 5 years, did not include original data, included men, did not give prevalence or incidence rate of breast cancer in the subjects, or did not discuss diet assessment tools. Of the remaining articles, we selected the 11 best studies to include in the review.
Early studies evaluating national average dietary fat intake and breast cancer incidence rates showed an almost linear relationship between increased dietary fat and increased breast cancer incidence.1 However, increased fat intake occurs primarily in industrialized nations, providing multiple possible confounders for increased rates of breast cancer, such as pollutants and increased consumption of preservatives, pesticides, and other chemicals.
Case-control studies have shown some minimally increased risk related to dietary fat consumption, but there is concern about recall bias in these studies.2 Since the late 1970s, 7 large, well-designed prospective cohort studies have examined the possible relationship between dietary fat and breast cancer.1 The findings have been somewhat contradictory, with some studies showing statistically significant associations toward increased risk with higher fat intake.3-5
Since the late 1990s, several meta-analyses, a systematic review of these cohort studies, and the Women’s Health Initiative Randomized Controlled Diet Initiative have largely concluded that there is no difference in breast cancer incidence between women with a low-fat diet (<20% of total calories from fat) and women with average or high-fat diets (>40% total calories from fat).1,3,6,7
The meta-analysis performed by Boyd et al did find a statistically significant difference, with relative risks ranging from 1.11 for overall to 1.19 for high-saturated-fat diets.8 The upper limit of all confidence intervals was no higher than 1.35, however, suggesting a lack of clinical significance. The best-designed studies also evaluated dietary composition with regard to key types of fat (saturated, mono- and poly-unsaturated; animal vs vegetable vs marine) and found no significant differences based on type of fat consumed.1
Preliminary evidence indicates that lowering dietary fat consumption may help with secondary prevention of breast cancer, but no large studies have been performed to date.9 Recently, a nested study within the Women’s Intervention Nutrition Study did show that women with breast cancer who decreased their fat intake to a median of 33 g/day had a hazard ratio of 0.76 for relapse over 60 months (compared with controls who ate a median of 51 g/day).10
Recommendations from others
There are no evidence-based or specific recommendations for the primary prevention of postmenopausal breast cancer for women through dietary fat reduction. In particular, neither the American Academy of Family Physicians, American College of Surgeons, National Institutes of Health, American College of Obstetricians and Gynecologists, American College of Physicians, US Preventive Services Task Force, or the Centers for Disease Control and Prevention provide any guidelines on dietary fat restriction for primary prevention of postmenopausal breast cancer.
The American Heart Association does have guidelines for coronary artery disease prevention for women, which include a low-fat diet.11 The USPSTF has no specific guidelines regarding dietary fat consumption for the general population.
No. Studies show no evidence that reducing dietary fat decreases a woman’s risk of developing postmenopausal breast cancer within the subsequent 14 years (strength of recommendation [SOR]: B, based on large heterogeneous prospective cohort studies and appropriate meta-analyses of these studies). Overall, evidence is insufficient to recommend for or against reduction in dietary fat to reduce risk of breast cancer for women, although recommendations for prudent fat intake may be justified on other grounds.
Losing weight is still a good strategy
Kathryn Kolasa, PhD, RD, LDN
East Carolina University, Greenville, NC
Women at risk for breast cancer—and cancer survivors—want to know about lifestyle changes that can reduce their risks for cancer or recurrence. There is growing evidence that obesity plays a role in cancer development and promotion.
A low-fat diet has been demonstrated as a successful strategy for weight loss. However, for most women, making these changes can be difficult without extensive instruction, support, and motivation. Limiting sweetened beverages, increasing consumption of fruits and vegetables, and limiting fat intake are 3 strategies women can use to achieve a healthy weight. If this turns out to reduce their risk of breast cancer, so much the better!
Evidence summary
Our Medline search retrieved 1114 English-language studies published from 1960 through October 2006. We limited this set to randomized controlled trials and cohort studies, leaving 212 articles. We then excluded articles that had small sample sizes, did not follow subjects for at least 5 years, did not include original data, included men, did not give prevalence or incidence rate of breast cancer in the subjects, or did not discuss diet assessment tools. Of the remaining articles, we selected the 11 best studies to include in the review.
Early studies evaluating national average dietary fat intake and breast cancer incidence rates showed an almost linear relationship between increased dietary fat and increased breast cancer incidence.1 However, increased fat intake occurs primarily in industrialized nations, providing multiple possible confounders for increased rates of breast cancer, such as pollutants and increased consumption of preservatives, pesticides, and other chemicals.
Case-control studies have shown some minimally increased risk related to dietary fat consumption, but there is concern about recall bias in these studies.2 Since the late 1970s, 7 large, well-designed prospective cohort studies have examined the possible relationship between dietary fat and breast cancer.1 The findings have been somewhat contradictory, with some studies showing statistically significant associations toward increased risk with higher fat intake.3-5
Since the late 1990s, several meta-analyses, a systematic review of these cohort studies, and the Women’s Health Initiative Randomized Controlled Diet Initiative have largely concluded that there is no difference in breast cancer incidence between women with a low-fat diet (<20% of total calories from fat) and women with average or high-fat diets (>40% total calories from fat).1,3,6,7
The meta-analysis performed by Boyd et al did find a statistically significant difference, with relative risks ranging from 1.11 for overall to 1.19 for high-saturated-fat diets.8 The upper limit of all confidence intervals was no higher than 1.35, however, suggesting a lack of clinical significance. The best-designed studies also evaluated dietary composition with regard to key types of fat (saturated, mono- and poly-unsaturated; animal vs vegetable vs marine) and found no significant differences based on type of fat consumed.1
Preliminary evidence indicates that lowering dietary fat consumption may help with secondary prevention of breast cancer, but no large studies have been performed to date.9 Recently, a nested study within the Women’s Intervention Nutrition Study did show that women with breast cancer who decreased their fat intake to a median of 33 g/day had a hazard ratio of 0.76 for relapse over 60 months (compared with controls who ate a median of 51 g/day).10
Recommendations from others
There are no evidence-based or specific recommendations for the primary prevention of postmenopausal breast cancer for women through dietary fat reduction. In particular, neither the American Academy of Family Physicians, American College of Surgeons, National Institutes of Health, American College of Obstetricians and Gynecologists, American College of Physicians, US Preventive Services Task Force, or the Centers for Disease Control and Prevention provide any guidelines on dietary fat restriction for primary prevention of postmenopausal breast cancer.
The American Heart Association does have guidelines for coronary artery disease prevention for women, which include a low-fat diet.11 The USPSTF has no specific guidelines regarding dietary fat consumption for the general population.
1. Willett WC. Diet and breast cancer. J Intern Med 2001;249:395-411.
2. Bingham SA, Luben R, Welch A, Wareham N, Khaw KT, Day N. Are imprecise methods obscuring a relation between fat and breast cancer?. Lancet 2003;362:212-214.
3. Mattisson I, Wirfalt E, Wallstrom P, Gullberg B, Olsson H, Berglund G. High fat and alcohol intakes are risk factors of postmenopausal breast cancer: a prospective study from the Malmo diet and cancer cohort. Int J Cancer 2004;110:589-597.
4. Sieri S, Krogh V, Muti P, et al. Fat and Protein Intake and subsequent Breast Cancer risk in Postmenopausal Women. Nutr Cancer 2004;42:10-17.
5. Velie E, Kulldorff M, Schairer C, Block G, Albanes D, Schatzkin A. Dietary fat, fat subtypes, and breast cancer in postmenopausal women: a prospective cohort study. J Natl Cancer Inst 2000;92:833-839.
6. Holmes MD, Hunter DJ, Colditz GA, et al. Association of dietary intake of fat and fatty acids with risk of breast cancer. JAMA 1999;281:914-920.
7. Low-Fat Dietary Pattern and risk of Breast Cancer, Colorectal Cancer, and Cardiovascular Disease: The Women’s Health Initiative randomized Controlled Dietary Modification Trial. Available at: www.whi.org/findings/dm/dm.php. Accessed on June 14, 2007.
8. Boyd NF, Stone J, Vogt KN, Connelly BS, Martin LJ, Minkin S. Dietary fat and breast cancer risk revisited: a meta-analysis of the published literature. Br J Cancer 2003;89:1672-1685.
9. Rock CL. Diet and breast cancer: can dietary factors influence survival? J Mammary Gland Biol Neoplasia 2003;8:119-132.
10. Rowan T, Chlebowski GL, Blackburn CA, et al. Dietary Fat Reduction and Breast Cancer Outcome: Interim Efficacy Results From the Women’s Intervention Nutrition Study. J Natl Cancer Inst 2006;98:1767-1776.
11. Mosca L, Appel LJ, Benjamin EJ, et al. Evidence-based guidelines for cardiovascular disease prevention in women. Circulation 2004;109:672-693.
1. Willett WC. Diet and breast cancer. J Intern Med 2001;249:395-411.
2. Bingham SA, Luben R, Welch A, Wareham N, Khaw KT, Day N. Are imprecise methods obscuring a relation between fat and breast cancer?. Lancet 2003;362:212-214.
3. Mattisson I, Wirfalt E, Wallstrom P, Gullberg B, Olsson H, Berglund G. High fat and alcohol intakes are risk factors of postmenopausal breast cancer: a prospective study from the Malmo diet and cancer cohort. Int J Cancer 2004;110:589-597.
4. Sieri S, Krogh V, Muti P, et al. Fat and Protein Intake and subsequent Breast Cancer risk in Postmenopausal Women. Nutr Cancer 2004;42:10-17.
5. Velie E, Kulldorff M, Schairer C, Block G, Albanes D, Schatzkin A. Dietary fat, fat subtypes, and breast cancer in postmenopausal women: a prospective cohort study. J Natl Cancer Inst 2000;92:833-839.
6. Holmes MD, Hunter DJ, Colditz GA, et al. Association of dietary intake of fat and fatty acids with risk of breast cancer. JAMA 1999;281:914-920.
7. Low-Fat Dietary Pattern and risk of Breast Cancer, Colorectal Cancer, and Cardiovascular Disease: The Women’s Health Initiative randomized Controlled Dietary Modification Trial. Available at: www.whi.org/findings/dm/dm.php. Accessed on June 14, 2007.
8. Boyd NF, Stone J, Vogt KN, Connelly BS, Martin LJ, Minkin S. Dietary fat and breast cancer risk revisited: a meta-analysis of the published literature. Br J Cancer 2003;89:1672-1685.
9. Rock CL. Diet and breast cancer: can dietary factors influence survival? J Mammary Gland Biol Neoplasia 2003;8:119-132.
10. Rowan T, Chlebowski GL, Blackburn CA, et al. Dietary Fat Reduction and Breast Cancer Outcome: Interim Efficacy Results From the Women’s Intervention Nutrition Study. J Natl Cancer Inst 2006;98:1767-1776.
11. Mosca L, Appel LJ, Benjamin EJ, et al. Evidence-based guidelines for cardiovascular disease prevention in women. Circulation 2004;109:672-693.
Evidence-based answers from the Family Physicians Inquiries Network
What is the appropriate evaluation and treatment of children who are “toe walkers”?
The evaluation of toe-walking focuses on differentiating normal children from those with mild cerebral palsy. Gait analysis may be a useful diagnostic tool, but further investigation is needed to confirm its reliability (strength of recommendation [SOR]: C, based on case series).
Observation alone is generally as successful as serial casting and surgery in decreasing the frequency of toe-walking at follow-up (SOR: C, based on case series).
Avoid overmedicalizing a problem that appears to run a benign course
Vince Winkler-Prins, MD
Michigan State University, East Lansing
The challenge with idiopathic toe-walking appears to be how to discriminate it from the more serious entities of cerebral palsy and muscular dystrophy. Idiopathic toe-walking should be evident in an otherwise healthy child as he or she begins to walk. It should be bilateral, there should be no spasticity and reflexes should not be overly brisk. A few follow-up visits at 3- or 6-month intervals should reassure all that this problem is nonprogressive. I have seen many toe-walking children over the years but no toe-walking adults without cerebral palsy or muscular dystrophy. This seems to confirm this review’s findings that observation appears to be as useful as casting or surgery. Until there is a natural history study of toe-walking, we need to be watchful to not overmedicalize a problem that appears to run a benign course.
Evidence summary
Idiopathic toe-walking is a childhood condition of unknown cause characterized by persistence of a tiptoe gait pattern without evidence of neurologic, orthopedic, or psychiatric disease.1 The incidence in the general population is not known. Children with idiopathic toe-walking usually have limited ankle dorsiflexion and are able to walk with a heel-strike for short periods when asked to do so. Longitudinal data is lacking to determine whether ankle equinus is the primary cause of idiopathic toe-walking or is a consequence of chronically walking on tiptoes. A family history of toe-walking ranges from 30% to 71% in the literature and is considered a characteristic of idiopathic toe walking.2-4
Evaluation. An important element of the evaluation of idiopathic toe-walking is to distinguish it from neuromuscular disorders associated with toe-walking, such as mild cerebral palsy. Case series with small numbers of subjects (range=27–41) have used gait electromyography (EMG) to distinguish cerebral palsy from idiopathic toe-walking.4-6 The overlap in gait EMG values in cerebral palsy and idiopathic toe-walking precludes its use as a differentiating diagnostic test.
The only aspect of EMG testing that has been useful in differentiating cerebral palsy from idiopathic toe-walking is gastrocnemius coactivation during resisted knee extension—a finding indicative of neurologic pathology.5,6 Kinematic analysis and observation of gait and measurement of ankle range of motion have been studied as diagnostic tools to differentiate idiopathic toe-walking from cerebral palsy.5-8 In the largest of these 4 studies (23 children with mild cerebral palsy and 22 with idiopathic toe-walking), maximal knee extension occurred at ground contact in the idiopathic toe-walking group whereas in the mild cerebral palsy group, the knee was flexed at ground contact.7 Measurement of ankle range of motion is not reliable in distinguishing between idiopathic toe-walking and cerebral palsy groups.5-7
Treatment. Simple observation, physical therapy, serial casting, and Achilles tendon lengthening surgery have been studied in the treatment of idiopathic toe-walking.2,3,9-11 In the largest case series (n=136),10 the frequency of toe-walking decreased in 51% of those in both the observation and casted groups. In this same study, the surgical group had lower rates of toe-walking, but no direct comparisons could be made to the nonsurgical groups because the patients in the surgical group were older and had longer follow-up than the other groups.
In a retrospective comparison3 of observation (which included physical therapy and special shoes), casting, and surgery among 80 children with idiopathic toe-walking, surgery resulted in significantly higher parental satisfaction (satisfied was defined as “child rarely walks on tiptoe”), 67% vs 25% and 24% for observation and casting groups respectively (P<.05). Three smaller studies (from 13 to 18 subjects) also showed decreased toe-walking at follow-up, regardless of treatment.2,9,11
There is no convincing evidence that treatment is necessary for this condition. We found no randomized trials of treatment for idiopathic toe-walking and no follow-up studies of sufficient size and duration that evaluate long-term effects of toe walking on the patient later in life.
Recommendations from others
No recommendations or guidelines were found.
1. Hall JE, Salter RB, Bhalla SK. Congenital short tendo calcaneus. J Bone Joint Surg Br 1967;49B:695-697.
2. Hirsch G, Wagner B. The natural history of idiopathic toe-walking: a long-term follow-up of fourteen conservatively treated children. Acta Paediatr 2004;93:196-199.
3. Stricker SJ, Angulo JC. Idiopathic toe walking: a comparison of treatment methods. J Pediatr Orthop 1998;18:289-293.
4. Kalen V, Adler N, Bleck EE. Electromyography of idiopathic toe walking. J Pediatr Orthop 1986;6:31-33.
5. Policy JF, Torburn L, Rinsky LA, Rose J. Electromyographic test to differentiate mild diplegic cerebral palsy and idiopathic toe-walking. J Pediatr Orthop 2001;21:784-789.
6. Rose J, Martin JG, Torburn L, Rinsky LA, Gamble JG. Electromyographic differentiation of diplegic cerebral palsy from idiopathic toe walking: involuntary coactivation of the quadriceps and gastrocnemius. J Pediatr Orthop 1999;19:677-682.
7. Kelly IP, Jenkinson A, Stephens M, O’Brien T. The kinematic patterns of toe-walkers. J Pediatr Orthop 1997;17:478-480.
8. Hicks R, Durinick N, Gage JR. Differentiation of idiopathic toe-walking and cerebral palsy. J Pediatr Orthop 1988;8:160-163.
9. Stott NS, Walt SE, Lobb GA, Reynolds N, Nicol RO. Treatment for idiopathic toe-walking: results at skeletal maturity. J Pediatr Orthop 2004;24:63-69.
10. Eastwood DM, Menelaus MB, Dickens DR, Broughton NS, Cole WG. Idiopathic toe-walking: does treatment alter the natural history. J Pediatr Orthop B 2000;9:47-49.
11. Brouwer B, Davidson LK, Olney SJ. Serial casting in idiopathic toe-walkers and children with spastic cerebral palsy. J Pediatr Orthop 2000;20:221-225.
The evaluation of toe-walking focuses on differentiating normal children from those with mild cerebral palsy. Gait analysis may be a useful diagnostic tool, but further investigation is needed to confirm its reliability (strength of recommendation [SOR]: C, based on case series).
Observation alone is generally as successful as serial casting and surgery in decreasing the frequency of toe-walking at follow-up (SOR: C, based on case series).
Avoid overmedicalizing a problem that appears to run a benign course
Vince Winkler-Prins, MD
Michigan State University, East Lansing
The challenge with idiopathic toe-walking appears to be how to discriminate it from the more serious entities of cerebral palsy and muscular dystrophy. Idiopathic toe-walking should be evident in an otherwise healthy child as he or she begins to walk. It should be bilateral, there should be no spasticity and reflexes should not be overly brisk. A few follow-up visits at 3- or 6-month intervals should reassure all that this problem is nonprogressive. I have seen many toe-walking children over the years but no toe-walking adults without cerebral palsy or muscular dystrophy. This seems to confirm this review’s findings that observation appears to be as useful as casting or surgery. Until there is a natural history study of toe-walking, we need to be watchful to not overmedicalize a problem that appears to run a benign course.
Evidence summary
Idiopathic toe-walking is a childhood condition of unknown cause characterized by persistence of a tiptoe gait pattern without evidence of neurologic, orthopedic, or psychiatric disease.1 The incidence in the general population is not known. Children with idiopathic toe-walking usually have limited ankle dorsiflexion and are able to walk with a heel-strike for short periods when asked to do so. Longitudinal data is lacking to determine whether ankle equinus is the primary cause of idiopathic toe-walking or is a consequence of chronically walking on tiptoes. A family history of toe-walking ranges from 30% to 71% in the literature and is considered a characteristic of idiopathic toe walking.2-4
Evaluation. An important element of the evaluation of idiopathic toe-walking is to distinguish it from neuromuscular disorders associated with toe-walking, such as mild cerebral palsy. Case series with small numbers of subjects (range=27–41) have used gait electromyography (EMG) to distinguish cerebral palsy from idiopathic toe-walking.4-6 The overlap in gait EMG values in cerebral palsy and idiopathic toe-walking precludes its use as a differentiating diagnostic test.
The only aspect of EMG testing that has been useful in differentiating cerebral palsy from idiopathic toe-walking is gastrocnemius coactivation during resisted knee extension—a finding indicative of neurologic pathology.5,6 Kinematic analysis and observation of gait and measurement of ankle range of motion have been studied as diagnostic tools to differentiate idiopathic toe-walking from cerebral palsy.5-8 In the largest of these 4 studies (23 children with mild cerebral palsy and 22 with idiopathic toe-walking), maximal knee extension occurred at ground contact in the idiopathic toe-walking group whereas in the mild cerebral palsy group, the knee was flexed at ground contact.7 Measurement of ankle range of motion is not reliable in distinguishing between idiopathic toe-walking and cerebral palsy groups.5-7
Treatment. Simple observation, physical therapy, serial casting, and Achilles tendon lengthening surgery have been studied in the treatment of idiopathic toe-walking.2,3,9-11 In the largest case series (n=136),10 the frequency of toe-walking decreased in 51% of those in both the observation and casted groups. In this same study, the surgical group had lower rates of toe-walking, but no direct comparisons could be made to the nonsurgical groups because the patients in the surgical group were older and had longer follow-up than the other groups.
In a retrospective comparison3 of observation (which included physical therapy and special shoes), casting, and surgery among 80 children with idiopathic toe-walking, surgery resulted in significantly higher parental satisfaction (satisfied was defined as “child rarely walks on tiptoe”), 67% vs 25% and 24% for observation and casting groups respectively (P<.05). Three smaller studies (from 13 to 18 subjects) also showed decreased toe-walking at follow-up, regardless of treatment.2,9,11
There is no convincing evidence that treatment is necessary for this condition. We found no randomized trials of treatment for idiopathic toe-walking and no follow-up studies of sufficient size and duration that evaluate long-term effects of toe walking on the patient later in life.
Recommendations from others
No recommendations or guidelines were found.
The evaluation of toe-walking focuses on differentiating normal children from those with mild cerebral palsy. Gait analysis may be a useful diagnostic tool, but further investigation is needed to confirm its reliability (strength of recommendation [SOR]: C, based on case series).
Observation alone is generally as successful as serial casting and surgery in decreasing the frequency of toe-walking at follow-up (SOR: C, based on case series).
Avoid overmedicalizing a problem that appears to run a benign course
Vince Winkler-Prins, MD
Michigan State University, East Lansing
The challenge with idiopathic toe-walking appears to be how to discriminate it from the more serious entities of cerebral palsy and muscular dystrophy. Idiopathic toe-walking should be evident in an otherwise healthy child as he or she begins to walk. It should be bilateral, there should be no spasticity and reflexes should not be overly brisk. A few follow-up visits at 3- or 6-month intervals should reassure all that this problem is nonprogressive. I have seen many toe-walking children over the years but no toe-walking adults without cerebral palsy or muscular dystrophy. This seems to confirm this review’s findings that observation appears to be as useful as casting or surgery. Until there is a natural history study of toe-walking, we need to be watchful to not overmedicalize a problem that appears to run a benign course.
Evidence summary
Idiopathic toe-walking is a childhood condition of unknown cause characterized by persistence of a tiptoe gait pattern without evidence of neurologic, orthopedic, or psychiatric disease.1 The incidence in the general population is not known. Children with idiopathic toe-walking usually have limited ankle dorsiflexion and are able to walk with a heel-strike for short periods when asked to do so. Longitudinal data is lacking to determine whether ankle equinus is the primary cause of idiopathic toe-walking or is a consequence of chronically walking on tiptoes. A family history of toe-walking ranges from 30% to 71% in the literature and is considered a characteristic of idiopathic toe walking.2-4
Evaluation. An important element of the evaluation of idiopathic toe-walking is to distinguish it from neuromuscular disorders associated with toe-walking, such as mild cerebral palsy. Case series with small numbers of subjects (range=27–41) have used gait electromyography (EMG) to distinguish cerebral palsy from idiopathic toe-walking.4-6 The overlap in gait EMG values in cerebral palsy and idiopathic toe-walking precludes its use as a differentiating diagnostic test.
The only aspect of EMG testing that has been useful in differentiating cerebral palsy from idiopathic toe-walking is gastrocnemius coactivation during resisted knee extension—a finding indicative of neurologic pathology.5,6 Kinematic analysis and observation of gait and measurement of ankle range of motion have been studied as diagnostic tools to differentiate idiopathic toe-walking from cerebral palsy.5-8 In the largest of these 4 studies (23 children with mild cerebral palsy and 22 with idiopathic toe-walking), maximal knee extension occurred at ground contact in the idiopathic toe-walking group whereas in the mild cerebral palsy group, the knee was flexed at ground contact.7 Measurement of ankle range of motion is not reliable in distinguishing between idiopathic toe-walking and cerebral palsy groups.5-7
Treatment. Simple observation, physical therapy, serial casting, and Achilles tendon lengthening surgery have been studied in the treatment of idiopathic toe-walking.2,3,9-11 In the largest case series (n=136),10 the frequency of toe-walking decreased in 51% of those in both the observation and casted groups. In this same study, the surgical group had lower rates of toe-walking, but no direct comparisons could be made to the nonsurgical groups because the patients in the surgical group were older and had longer follow-up than the other groups.
In a retrospective comparison3 of observation (which included physical therapy and special shoes), casting, and surgery among 80 children with idiopathic toe-walking, surgery resulted in significantly higher parental satisfaction (satisfied was defined as “child rarely walks on tiptoe”), 67% vs 25% and 24% for observation and casting groups respectively (P<.05). Three smaller studies (from 13 to 18 subjects) also showed decreased toe-walking at follow-up, regardless of treatment.2,9,11
There is no convincing evidence that treatment is necessary for this condition. We found no randomized trials of treatment for idiopathic toe-walking and no follow-up studies of sufficient size and duration that evaluate long-term effects of toe walking on the patient later in life.
Recommendations from others
No recommendations or guidelines were found.
1. Hall JE, Salter RB, Bhalla SK. Congenital short tendo calcaneus. J Bone Joint Surg Br 1967;49B:695-697.
2. Hirsch G, Wagner B. The natural history of idiopathic toe-walking: a long-term follow-up of fourteen conservatively treated children. Acta Paediatr 2004;93:196-199.
3. Stricker SJ, Angulo JC. Idiopathic toe walking: a comparison of treatment methods. J Pediatr Orthop 1998;18:289-293.
4. Kalen V, Adler N, Bleck EE. Electromyography of idiopathic toe walking. J Pediatr Orthop 1986;6:31-33.
5. Policy JF, Torburn L, Rinsky LA, Rose J. Electromyographic test to differentiate mild diplegic cerebral palsy and idiopathic toe-walking. J Pediatr Orthop 2001;21:784-789.
6. Rose J, Martin JG, Torburn L, Rinsky LA, Gamble JG. Electromyographic differentiation of diplegic cerebral palsy from idiopathic toe walking: involuntary coactivation of the quadriceps and gastrocnemius. J Pediatr Orthop 1999;19:677-682.
7. Kelly IP, Jenkinson A, Stephens M, O’Brien T. The kinematic patterns of toe-walkers. J Pediatr Orthop 1997;17:478-480.
8. Hicks R, Durinick N, Gage JR. Differentiation of idiopathic toe-walking and cerebral palsy. J Pediatr Orthop 1988;8:160-163.
9. Stott NS, Walt SE, Lobb GA, Reynolds N, Nicol RO. Treatment for idiopathic toe-walking: results at skeletal maturity. J Pediatr Orthop 2004;24:63-69.
10. Eastwood DM, Menelaus MB, Dickens DR, Broughton NS, Cole WG. Idiopathic toe-walking: does treatment alter the natural history. J Pediatr Orthop B 2000;9:47-49.
11. Brouwer B, Davidson LK, Olney SJ. Serial casting in idiopathic toe-walkers and children with spastic cerebral palsy. J Pediatr Orthop 2000;20:221-225.
1. Hall JE, Salter RB, Bhalla SK. Congenital short tendo calcaneus. J Bone Joint Surg Br 1967;49B:695-697.
2. Hirsch G, Wagner B. The natural history of idiopathic toe-walking: a long-term follow-up of fourteen conservatively treated children. Acta Paediatr 2004;93:196-199.
3. Stricker SJ, Angulo JC. Idiopathic toe walking: a comparison of treatment methods. J Pediatr Orthop 1998;18:289-293.
4. Kalen V, Adler N, Bleck EE. Electromyography of idiopathic toe walking. J Pediatr Orthop 1986;6:31-33.
5. Policy JF, Torburn L, Rinsky LA, Rose J. Electromyographic test to differentiate mild diplegic cerebral palsy and idiopathic toe-walking. J Pediatr Orthop 2001;21:784-789.
6. Rose J, Martin JG, Torburn L, Rinsky LA, Gamble JG. Electromyographic differentiation of diplegic cerebral palsy from idiopathic toe walking: involuntary coactivation of the quadriceps and gastrocnemius. J Pediatr Orthop 1999;19:677-682.
7. Kelly IP, Jenkinson A, Stephens M, O’Brien T. The kinematic patterns of toe-walkers. J Pediatr Orthop 1997;17:478-480.
8. Hicks R, Durinick N, Gage JR. Differentiation of idiopathic toe-walking and cerebral palsy. J Pediatr Orthop 1988;8:160-163.
9. Stott NS, Walt SE, Lobb GA, Reynolds N, Nicol RO. Treatment for idiopathic toe-walking: results at skeletal maturity. J Pediatr Orthop 2004;24:63-69.
10. Eastwood DM, Menelaus MB, Dickens DR, Broughton NS, Cole WG. Idiopathic toe-walking: does treatment alter the natural history. J Pediatr Orthop B 2000;9:47-49.
11. Brouwer B, Davidson LK, Olney SJ. Serial casting in idiopathic toe-walkers and children with spastic cerebral palsy. J Pediatr Orthop 2000;20:221-225.
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