Saphenous Nerve Entrapment Neuropathy

By Brad McKechnie, DC, DACAN

Saphenous nerve neuropathy is an important consideration in the differential diagnosis of lumbar radiculopathy, medial knee pain, and lower extremity vascular insufficiency. The saphenous nerve is the largest cutaneous branch of the femoral nerve and is purely sensory, with branches of the L3 and L4 nerve root levels contributing to the nerve.

The nerve is comprised of two functional divisions; the infrapatellar branch, and the descending branch.¹

The saphenous nerve exits from the adductor canal (a.k.a. Hunter's canal, subsartorial canal), descends under the sartorius muscle, and then winds around the posterior edge of the sartorius muscle at its tendon portion. The infrapatellar branch pierces the sartorius muscle and courses anteriorly to the infrapatellar region. The descending branch passes down the medial aspect of the leg and, at the lower third of the leg, divides into two branches. One of the branches of the descending portion of the saphenous nerve courses along the medial border of the tibia and ends at the ankle while the other branch passes anterior to the ankle and is distributed to the medial aspect of the foot, sometimes reaching as far as the metatarsophalangeal joint of the great toe.¹

The adductor canal, the entrapment site for the saphenous nerve, is located approximately 10 centimeters (four finger widths) proximal to the medial femoral condyle. It is located by palpating along the anteromedial aspect of the vastus medialis muscle and then sliding posteriorly until the edge of the sartorius muscle is felt. The adductor canal is located directly beneath this point (See figure 1).^2,4

Chief complaints associated with saphenous nerve entrapment include medial knee and/or leg pain after prolonged walking or standing and pain in the distribution of the saphenous nerve following quadriceps exercise.⁵Pain associated with this entrapment syndrome is characterized as burning by most patients and may be present at rest. In one study,² two thirds of affected patients complained of pain at night. Additionally, stair climbing may aggravate symptoms associated with this entrapment neuropathy.

Clinical criteria for the diagnosis of saphenous nerve entrapment neuropathy includes pain in the distribution of the saphenous nerve, normal motor function, and tenderness to palpation over the entrapment site. The pain associated with this neuropathy may be referred to the lower medial aspect of the knee, mimicking orthopedic disorders of the knee, or it may radiate down the medial aspect of the lower extremity to the ankle and foot, mimicking symptoms of an L4 radiculopathy (See figure 2). Sensory symptoms noted in saphenous nerve neuropathy range from paresthesia to hypoesthesia, with variations due to the length of nerve compression at the entrapment site. The patient suffering from saphenous nerve entrapment neuropathy, as noted, has normal motor function of the affected lower extremity. This is one of the key distinctions between the saphenous nerve neuropathy and lumbar radiculopathy. The saphenous nerve neuropathy only demonstrates sensory alterations, while lumbar radiculopathy may have associated motor, sensory, and deep tendon reflex alterations. Entrapment site tenderness is a key feature of saphenous nerve neuropathy. In a series of 15 patients reported on by Worth, et al.,² and in a series of 30 patients reported by Romanoff, et al.;³ all patients demonstrated point tenderness over the exit site of the saphenous nerve from the adductor canal. Vigorous palpation at the exit point for the saphenous nerve may result in local pain and pain referred in the nerve's distribution.

Mechanisms for production of saphenous nerve neuropathy may be nontraumatic, traumatic, or post-surgical. Due to the angulation of the saphenous nerve over the sartorius muscle tendon after exiting from the adductor canal, traction on the nerve may be produced by limb movement leading to inflammation, edema, and paresthesia.³Additionally, patients may be over the age of 40, have a moderate amount of thigh obesity, and possible genu varum with accompanying internal tibial torsion, leading to more stress on the nerve.⁴ Direct trauma resulting from contact sports may cause saphenous nerve injury, but the force required must be sufficient to disrupt the medial support structures of the knee. Surgical trauma to the knee may result in saphenous nerve injury, and saphenous neuralgia has been reported as a possible complication of arterial surgery.^2,3 From the biomechanical standpoint, extension of the knee may aggravate symptoms associated with saphenous nerve neuropathy. To avoid the pain associated with knee extension, the patient may use the knee in the flexed posture, leading to compensatory shortening of the affected lower extremity. Thus, compensatory problems related to this functional alteration of lower extremity gait may manifest in disorders of the pelvis, spine, or foot.⁴ Treatment may be directed at release of the saphenous nerve from the entrapment site via transverse friction technique, functional biomechanical faults must be corrected, and TENS may be utilized to control pain associated with the entrapment syndrome.

References 

1. Williams PL and Warwick R. Gray's Anatomy, 36th Edition, W.B. Saunders, Philadelphia, 1980.
2. Worth RM et al. Saphenous nerve entrapment - A cause of medial knee pain. Am J. Sports Med, 12:80-81, 1984.
3. Romanoff ME et al. Saphenous nerve entrapment at the adductor canal", Am J. Sports Med, 17:478-481, 1989.
4. Kopell HP and Thompson W. Peripheral Entrapment Neuropathies, R.A. Krieger, Malabar, Florida, 1976.
5. Sunderland S. Nerves and Nerve Injuries, 2nd ed. Churchill-Livingstone, New York, 1978.

Spinal Stabilization Exercises: The Low Cost Solution to Exercising Your Patients

By Craig Liebenson, DC and Jerry Hyman, DC

The goals of spinal stabilization exercise are to allow the patient to move pain-free using the least amount of effort possible. To successfully navigate through the activities of daily living the patient learns how to protect potentially vulnerable structures of the spine by recognizing and respecting the functional limitations dictated by their low back condition.

For example, a person caring for an infant must avoid the natural tendency to slump when lifting the baby in their charge. They learn the importance of stabilizing their back by performing a slight anterior pelvic tilt ("tail out") to avoid the "strain" of slumping when kneeling or squatting during a lift. Conversely, while carrying a baby, the tendency of the spine is to kyphose. The stable position is maintained by performing a slight posterior pelvic tilt ("squeeze buttocks"). In other words, the stable position or range of the spine varies depending on the task. It is the practitioner's responsibility to identify the unique needs of each patient and situation and prescribe exercises or postural advise accordingly.

This is a highly individualized approach. Each patient may have sensitivities that vary with gravity/weightbearing, position, or movement.¹ For example, disc patients are usually sensitive to flexion positions or movements, as well as to gravity. Conversely, stenotic patients are sensitive to extension positions. The majority of patients without clinically significant structural pathology will vary in their sensitivities: from those with extension movement sensitivity, if their facets are irritable, to those with weightbearing sensitivity whose posture is disturbed.

These intrinsic sensitivities of the patient function in much the same manner the extrinsic demands of different activities described above (lifting, carrying). They indicate that exercises must be customized to the needs of the patient and/or their activity. The disc patient will require a program of nonweightbearing exercises which avoid the flexion range. The stenotic patient will require posterior pelvic tilt exercises in all patients, particularly standing so that they can be trained to avoid the stenotic position. And the patient without structural pathology will need a varied program of exercises designed to protect their unique sensitivities and prepare them for the biomechanical demands of their activities.

This stabilization approach is not only a treatment but a strategy that allows a patient to function throughout the day within their prescribed limits. This is a very dynamic approach because these limits are constantly changing as the patient either improves or is faced with new challenges in their ADLs, occupation, or recreational activities. For example, when reaching overhead the patient will learn to produce a posterior pelvic tilt as a check rein to strenuous lumbar hyperextension. Conversely, during sitting and lifting, an anterior pelvic tilt will be taught to maintain the stable lordotic position of the spine during those activities where slumping is the natural tendency.

These particular movements are guidelines only. Movement involves the entire locomotor system not just one spinal segment or region. A chain of events is always involved which may start at the feet or the neck. For instance, hip extension may be restricted during gait and lead to overstress of the lumbar spine as compensatory hypermobility and trigger-points develop. But this problem may have stemmed from adaptations to hyperpronation of the foot. The key link may be a calcaneonavicular joint dysfunction or it may be a tight iliopsoas. The key dysfunctions must be addressed for our spinal adjustments, trigger point-therapy, or stabilization exercises to be truly effective.

The key to initiating stabilization exercises is recognition of the functional range of the patient. Dennis Morgan PT, DC, an originator of this functional approach says: "The functional position is the most stable and asymptomatic position of the spine for the task at hand."² This will therefore vary as described above, depending on the patients' activities (sitting, lifting, reaching) or sensitivities (gravity, positional, movement).

Early on in an acute patient or in a "kinesiophobic" chronic patient, the functional range may in fact be very narrow. In such cases isometric exercises, where little or no movement occurs, may be the best starting point. The skilled practitioner's task is to activate the patient as early as possible, and identify the proper functional range for initiating a progressive, therapeutic exercise regime. The initial functional range is their training range, and this is the seedling which if cared for will grow and expand into a wide repertoire of dynamic, stable, and pain-free activities.

A chiropractor's entire armamentarium of techniques and approaches will be challenged to unload and unstress the spine to "carve out" a training range. Neck or foot adjustments, postural muscle stretches, reflex therapies, etc., may all be incorporated as means to this end. The stabilization program starts by utilizing the position of least stress. For instance, exercises often will begin in a nonweightbearing supine position. Supportive devices (cushions, exercise balls) to help pre-position a patient in a pain-free posture will be utilized. Anything that can be done to help catalyze and initiate patient reactivation will be incorporated into this program.

Progression of exercises proceeds from simple to functional, nonweightbearing to weightbearing, stable to labile, etc. Attention is focused on the quality not the quantity of the movement. It is not the number of sets, repetitions, or weight that is performed, but the coordination and stability that is maintained during a course of repetitive and sustained exercises that is the goal. For example, strength gains at the sacrifice of proper pelvic positioning or lumbopelvic control will undo all the therapeutic good of our adjustments or other interventions. Sit-ups performed without lumbopelvic stability will overstrain the lumbar facets. Similarly, hip extension exercises on a standing hip machine or during bridges, if performed without enough posterior pelvic tilt, will overstress the lumbar spine causing irritation to facets and leading to myofascial trigger point formation in the lumbar extensor muscles.

Therapeutic exercise concepts/principles allow us to identify improper movement patterns during the performance of activities of daily living, circuit training, etc. While our patients must exercise to fatigue to appreciate strength gains, fatiguing the desired parts is more important than sets and repetitions. This is one of the main contributions of the neuromuscular perspective. Gyms are full of individuals supposedly promoting their fitness through various exercises. However, poor quality or "trick" movements are epidemic in such settings and undermine the purpose of such a pursuit.³ For example, poor lumbopelvic control is commonly seen on stairmasters, treadmills, abdominal machines, lunge and squat exercises, and step aerobic classes. Cervicocranial hyperextension and a head forward position are seen during sit-ups, lat pull downs, squats/lunges, and rowing exercises. These are but a few examples to illustrate that quality of movement is usually ignored in health club settings. Chiropractors getting involved in rehabilitation will want to incorporate good biomechanical advise into their programs such as is emphasized in the stabilization program.

A recent study documented the effectiveness of stabilization exercises when combined with a McKenzie approach in failed lumbar laminectomy patients.⁴ Timm, in a randomized, controlled trial looking at exercise and passive care, concluded that low-tech exercises gave a greater benefit than high-tech exercises (Cybex), physical modalities, or joint mobilization.³ Previous work by Saal and Saal involved stabilization exercises for a presurgical group of patients with back and leg pain who were referred for surgery. They withheld the surgical intervention and concluded: "All patients had undergone an aggressive physical rehabilitation program consisting of back school and stabilization exercise training," and a "92 percent return to work rate."⁵

The stabilization exercise program consists of floor, exercise ball, proprioceptive, and strength training exercises. So long as the functional range is respected, very challenging exercises can be created which isolate the key spinal stabilizers; abdominals, gluteals and quadriceps muscles. The cardinal sign of successful stabilization exercise therapy is postexercise soreness in the targeted muscles without an increase in the patient's back or leg pain.

The most exciting tool is the exercise ball, which by virtue of its dynamic shape allows for precise isolation of the key trunk stabilizers while challenging one's balance. By working the muscles, while increasing the balance demand, a tremendous "burn" can be accomplished very quickly.

Stabilization exercises take very little office space, don't require any expensive equipment, and can be helpful to patients weather five or 50 minutes is spent with them. Chiropractors can learn to incorporate this skill into their practices within a short time. They have been proven to be effective for failed surgery and disc patients. While manipulation is now the "gold standard" for nonradicular patients in the acute and subacute stages, an approach such as this is the perfect complement to any chiropractor's practice style.

References 

1. Vollowitz E. Furniture prescription for the conservative management of low-back pain. Top Acute Care Trauma Rehabil 1988;2(4):18-37.
   
   
2. Morgan D. Concepts in functional training and postural stabilization for the low-back-injured. Top Acute Care Trauma Rehabil 1988;2:8-17.
   
   
3. Hyman J, Liebenson C. Spinal stabilization exercise program. In Liebenson C (ed) Spinal Rehabilitation: A Manual of Active Care Procedures. Williams and Wilkins, Baltimore 1995.
   4)Timm KE. A randomized-control study of active and passive treatments for chronic low back pain following L5 laminectomy. JOSPT 1994;20:276-286.
   5)Saal JA, Saal JS: Nonoperative treatment of herniated lumbar intervertebral disc with radiculopathy. Spine 1989;14:431-437.

This column will cover the integration of rehabilitation concepts in the chiropractic practice. Upcoming columns will include: "Rehabilitation: The Missing Link in Managing Headaches"; "Valid and Reliable Low-Tech Functional Capacity Tests"; "Duration and Frequency of Passive and Active Care for Complicated Patients." How to measure outcomes, find the correlation between muscle and joint dysfunction, and view regional complaints from a broad perspective of locomotor system dysfunction will be detailed in "DC".

Carpal Tunnel Syndrome: Provocative Maneuvers

By Brad McKechnie, DC, DACAN

Carpal tunnel syndrome is one of the most common peripheral entrapment neuropathies encountered in clinical practice. The following clinical tests may be useful to help confirm the diagnosis of carpal tunnel syndrome.

Phalen's test: The patient rests the elbows on a flat surface, holds the forearms vertically, and actively places the wrists in complete and forced flexion for at least one minute. This maneuver moderately increases the pressure in the carpal tunnel and has the effect of pinching the median nerve between the proximal edge of the transverse carpal ligament and the anterior border of the distal end of the radius.^1-3

Reverse Phalen's test: This test is performed by having the patient maintain full wrist and finger extension for two minutes. The reverse Phalen's test significantly increases pressure in the carpal tunnel within 10 seconds of the change in wrist posture and the carpal tunnel pressure has the tendency to increase throughout the test's duration. In contrast, the change in carpal tunnel pressure noted in the standard Phalen's test is modest and plateaus after 20 to 30 seconds. In a study comparing the changes in tunnel pressure with the Phalen's and reverse Phalen's test it was noted that the average pressure change for Phalen's test at one and two minutes was only 4 mm Hg. The average pressure changes in the carpal tunnel for the reverse Phalen's test were 34 mm Hg at one minute into the test and 42 mm Hg at the two minute point.⁴ Thus, the extended wrist posture significantly changes the pressure within the carpal tunnel and may be more useful as a provocative examination maneuver. In another study cited by Sunderland, flexion raised carpal tunnel pressure by 100 mm of water while extension raised the pressure in the tunnel to 300 mm.⁵

Tethered median nerve stress test: This test may be useful in detecting chronic, low grade median nerve compression in the carpal tunnel and may be most useful when sensory complaints predominate and motor signs are minimal. To perform the test, the doctor grasps the distal phalanx of the patient's index finger and pulls the index finger into forced extension and holds that position. This maneuver produces the greatest amount of median nerve distal excursion in the tunnel and combines the effects generated by the reverse Phalen's test with those of tractioning of the median nerve. The median nerve is bound, in some patients, to the tendon of the flexor digitorum profundus muscle to the index finger. Thus, by extending the index finger from the distal phalanx, the median nerve may be tractioned distally due to connective tissue attachments between the tendon and the nerve. The test produces discomfort as its most common provocative complaint which is characterized as aching and myalgic and increases the longer the test position is held. There may also be proximal radiation of pain from the carpal tunnel to the pronator teres muscle which may persist post-test.⁶

Direct pressure over the tunnel: Pressure of the examiner's thumbs applied directly versus the median nerve running deep to the transverse carpal ligament may produce pain, tingling, or numbness in the median nerve's field in the hand related to the carpal tunnel (Figure I). This test is specific for the carpal tunnel syndrome and has elicited symptoms in 87 percent of a bona fide group of carpal tunnel syndrome patients. The average time to the onset of symptoms with direct compression of the median nerve is between 16 seconds and 29 seconds. In contrast, the standard Phalen's test elicited symptoms in approximately 70 percent of patients with the average onset of symptoms taking approximately 25 seconds following the initiation of the flexed hand position.

Tinel's sign: Light percussion over the median nerve as it passes under the transverse carpal ligament may elicit a shock-like sensation which radiates into the median field of the hand. Percussion should begin distally and progress proximally. For future comparison, a measurement should be made from a bony prominence to the point of maximum response once that site has been identified. This test is the least sensitive of the median nerve provocative maneuvers but is the most specific test for median neuropathy at the carpal tunnel.^5,7

Tourniquet test: A blood pressure cuff is applied proximal to the elbow and cuff pressure is taken beyond systolic pressure.^5,7 The pressure induced ischemia in the distal limb may cause damaged nerve fibers to react to the ischemia by discharging spontaneously, aggravating the condition. The test is considered to be positive if symptoms occur within one minute, however the test does have an abnormally high false positive rate (upwards of 40 percent).

References 

1. Phalen GS, Gardner WJ, and La Londe A. Neuropathy of the median nerve due to compression beneath the transverse carpal ligament. JBJS, 32A:109-112, 1950.
   
   
2. Phalen GS and Kendrick JI. Compression neuropathy of the median nerve in the carpal tunnel. JAMA, 164:524-530, 1957.
   
   
3. Phalen GS. The carpal tunnel syndrome. JBJS, 48A:211-228, 1966.
   
   
4. Werner RA, Bir C, and Armstrong TJ. Reverse Phalen's maneuver as an aid in diagnosing carpal tunnel syndrome. Arch Phys Med Rehabil, 75:783-786, 1994.
   
   
5. Sunderland S. Nerves and Nerve Injuries.
   Churchill-Livingstone, New York, 1978.
   
   
6. LaBan MM, MacKenzie JR, and Zemenick, GA. Anatomic observations in carpal tunnel syndrome as they relate to the tethered median nerve stress test. Arch Phys Med Rehabil, 70:44-46, 1989.
   
   
7. Gellman H et al. Carpal tunnel syndrome: An evaluation of the provocative diagnostic tests. JBJS, 68A:735-737, 1986.

Physical Activity and Television Watching in Relation to Risk for Type 2 Diabetes Mellitus in MenFREE

Frank B. Hu, MD; Michael F. 

Leitzmann, MD; Meir J. Stampfer, MD; 

Graham A. Colditz, MD; Walter C.

 Willett, MD; Eric B. Rimm, ScD

ABSTRACT

ABSTRACT | SUBJECTS AND METHODS | RESULTS | COMMENT | CONCLUSIONS |ARTICLE INFORMATION | REFERENCES

Background  Television (TV) watching, a major sedentary behavior in the United States, has been associated with obesity. We hypothesized that prolonged TV watching may increase risk for type 2 diabetes.

Methods  In 1986, 37 918 men aged 40 to 75 years and free of diabetes, cardiovascular disease, and cancer completed a detailed physical activity questionnaire. Starting from 1988, participants reported their average weekly time spent watching TV on biennial questionnaires.

Results  A total of 1058 cases of type 2 diabetes were diagnosed during 10 years (347 040 person-years) of follow-up. After adjustment for age, smoking, alcohol use, and other covariates, the relative risks (RRs) for type 2 diabetes across increasing quintiles of metabolic equivalent hours (MET-hours) per week were 1.00, 0.78, 0.65, 0.58, and 0.51 (P for trend, <.001). Time spent watching TV was significantly associated with higher risk for diabetes. After adjustment for age, smoking, physical activity levels, and other covariates, the RRs of diabetes across categories of average hours spent watching TV per week (0-1, 2-10, 11-20, 21-40, and >40) were 1.00, 1.66, 1.64, 2.16, and 2.87, respectively (P for trend, <.001). This association was somewhat attenuated after adjustment for body mass index, but a significant positive gradient persisted (RR comparing extreme categories, 2.31; P for trend, .01).

Conclusions  Increasing physical activity is associated with a significant reduction in risk for diabetes, whereas a sedentary lifestyle indicated by prolonged TV watching is directly related to risk. Our findings suggest the importance of reducing sedentary behavior in the prevention of type 2 diabetes.

EPIDEMIOLOGICAL evidence strongly supports a role of exercise in the prevention of type 2 diabetes mellitus.1- 8 However, less attention has focused on sedentary behaviors in relation to risk for diabetes. Television (TV) watching represents a major sedentary behavior in the United States; on average, a male adult spends approximately 29 hours per week watching TV, and a female adult, 34 hours per week.9Television watching results in lower metabolic rate compared with other sedentary activities such as sewing, playing board games, reading, writing, and driving a car.10 In several studies, time spent watching TV has been strongly associated with weight gain and obesity in children11,12 and adults.13- 15 The purpose of this study is to examine whether prolonged TV watching predicts subsequent diabetes risk independent of physical activity in a prospective cohort of men. We also examined total physical activity, vigorous exercise, and moderate-intensity activity in relation to risk for type 2 diabetes in this cohort.

SUBJECTS AND METHODS

ABSTRACT | SUBJECTS AND METHODS | RESULTS | COMMENT | CONCLUSIONS |ARTICLE INFORMATION | REFERENCES

SUBJECTS

The Health Professional's Follow-up Study (HPFS) began in 1986 when 51 529 US health professionals (dentists, optometrists, pharmacists, podiatrists, osteopaths, and veterinarians), aged 40 to 75 years, answered a detailed questionnaire that included a comprehensive diet survey and items on lifestyle practice and medical history.16 Follow-up questionnaires were sent in 1988, 1990, 1992, 1994, and 1996 to update information on potential risk factors and to identify newly diagnosed cases of diabetes and other diseases. We excluded from the present analysis men with a previous diagnosis of cardiovascular disease (n = 4639), cancer (n = 1638), or diabetes (n = 1796) at baseline. Participants with diagnosed cardiovascular disease or cancer at baseline were excluded because these diagnoses may lead to change in physical activity levels. Participants who had missing information on activity questions or reported implausible total energy intake on the food frequency questionnaire17 (<3347 or >17 572 kJ/d) were also excluded (n = 5538). We followed up the remaining 37 918 men for incidence of type 2 diabetes during the subsequent 10 years of the study.

ASSESSMENT OF PHYSICAL ACTIVITY

Physical activity was assessed using mailed questionnaires at baseline and every 2 years thereafter. Subjects were asked to report the average amount of time they spent per week on each of the following activities: walking, jogging, running, bicycling, calisthenics or use of a rowing machine, lap swimming, squash or racquetball, and tennis. They were also asked about their usual walking pace, specified as easy or casual (<2 miles/h), normal (2-2.9 miles/h), brisk (3-3.9 miles/h), or striding (≥4 miles/h). From this information, weekly energy expenditure in metabolic equivalent hours (MET-hours) was calculated.10 We defined any physical activity requiring 6 MET-hours or greater (a 6-fold or greater increase above resting metabolic rate) as vigorous. These activities included jogging, running, bicycling, calisthenics or use of a rowing machine, lap swimming, squash or racquetball, and tennis. In contrast, walking requires an energy expenditure of only 2 to 4.5 MET-hours, depending on pace, and was therefore considered to be a moderate-intensity activity.

The reproducibility and validity of the physical activity questionnaire was evaluated in a subsample (n = 238) of participants in the HPFS cohort.18 The Pearson correlation between moderate plus vigorous physical activity, assessed by means of diaries for 4 weeks across different seasons, and that reported on the questionnaire was 0.58. The correlation between vigorous activity score, assessed by means of the questionnaire, and resting pulse was −0.45; for pulse after stopping, the correlation was −0.41. In a separate study on a population aged 20 to 59 years recruited from a university community (n = 103), the correlation between physical activity score on a similar questionnaire and maximum oxygen consumption was 0.54.19 In a subsample of participants in the HPFS cohort (n = 466), high-density lipoprotein (HDL) cholesterol level increased by 0.06 mmol/L (2.4 mg/dL) for each increment of 20 MET-hours per week (P<.01).20

Starting from 1988, participants reported their average weekly time spent watching TV (including videotapes) on the biennial questionnaires. The 1988 questionnaire included 6 response categories (ranging from 0-1 to >40 h/wk). Subsequent questionnaires included 13 response categories (ranging from 0 to >40 h/wk). In the present analyses, 5 categories were coded consistently across all questionnaires (0-1, 2-10, 11-20, 21-40, and >40 h/wk). In a subsample of participants in the HPFS (n = 466), average hours of TV watching were significantly associated with higher levels of leptin and low-density lipoprotein (LDL) cholesterol and with lower levels of HDL cholesterol and apolipoprotein A-I.20

DIAGNOSIS OF TYPE 2 DIABETES

A supplementary questionnaire regarding symptoms, diagnostic tests, and hypoglycemic therapy was mailed to men who indicated on any biennial questionnaire that they had been diagnosed with diabetes. A case of diabetes was considered confirmed if at least 1 of the following was reported on the supplementary questionnaire: (1) 1 or more classic symptoms (excessive thirst, polyuria, weight loss, hunger) plus 1 fasting plasma glucose level of at least 7.8 mmol/L (140 mg/dL) or random plasma glucose of at least 11.1 mmol/L (200 mg/dL); (2) at least 2 elevated plasma glucose concentrations on different occasions (fasting, ≥7.8 mmol/L [≥140 mg/dL]; random, ≥11.1 mmol/L [≥200 mg/dL]; and/or ≥11.1 mmol/L [≥200 mg/dL] after ≥2 hours of oral glucose tolerance testing) in the absence of symptoms; or (3) treatment with hypoglycemic medication (insulin or oral hypoglycemic agent). Because of potential associations between weight and physical activity, no body weight criteria were used in the classification of type of diabetes for these analyses. Our criteria for diabetes classification are consistent with those proposed by the National Diabetes Data Group21 for 1986-1996. The validity of self-report of diabetes has been verified in a subsample of 71 men from the HPFS cohort. A physician blinded to the information reported on the supplementary questionnaire and reviewed the medical records according to the diagnostic criteria. Of the 71 patients, 12 had incomplete records, eg, absent laboratory data (n = 2), or 1 set only of laboratory data (n = 9). Among the remaining 59 cases, the diagnosis of type 2 diabetes was confirmed in 57 (97%). One patient denied the diagnosis and another lacked evidence of diabetes in his submitted records. Similarly, 98% of diabetic cases reported by the supplementary questionnaire were confirmed by medical record review in a subsample of participants (n = 62) in the Nurses' Health Study.22

STATISTICAL ANALYSIS

Person-time for each participant was calculated from the date of return of the 1986 (physical activity) or 1988 (TV watching) questionnaires to the date of confirmed type 2 diabetes, death due to any cause, or January 1, 1996, whichever came first. Incidence rates of type 2 diabetes were obtained by dividing the number of cases by person-years in each category of physical activity or average time spent on watching TV. Relative risks (RRs) were computed as the incidence rate in a specific category of MET score (ie, MET-hours per week) or TV watching divided by that in the reference category, with adjustment for 5-year age categories. Tests for linear trend across increasing categories of MET score or average time spent watching TV were conducted by treating the categories as a continuous variable and assigning the median score for the category as its value. Both MET score or time spent watching TV were updated every 2 years.

We used pooled logistic regression to adjust estimated incidence rate ratios simultaneously for potential confounding variables. In this approach, independent 2-year blocks of person-time of follow-up are pooled for regression analysis, and the dependence of the incidence rates on time is modeled nonparametrically with indicator variables. D'Agostino et al23 have shown that the pooled logistic model is asymptotically equivalent to the Cox regression when the time intervals are short and the probability of outcome in the intervals is low. Our covariates included age (40-44, 45-49, 50-54, 55-59, 60-64, 65-69, and ≥70 years), smoking (never, past, or current [1-14, 15-24, and ≥25 cigarettes per day]), alcohol consumption (0-4, 5-9, 10-14, 15-29, and ≥30 g/d), parental history of diabetes, and history of hypercholesterolemia or hypertension at baseline. In additional analyses, we included body mass index (BMI [calculated as weight in kilograms divided by the square of height in meters], in quintiles) in the model to examine the degree to which the relation with physical activity was mediated through BMI.

To examine whether the effects of physical activity on diabetes were modified by important covariates, we conducted multivariate analyses according to categories of age (<65 or ≥65 years), family history of diabetes (no or yes), smoking (never or ever), and BMI (<25.0, 25.0-29.9, or ≥30.0 kg/m2). To examine independent effects of physical activity and TV watching, we estimated RRs of diabetes according to joint classifications of these 2 variables. In this analysis, both variables were classified into quartiles rather than 5 categories to have sufficient power.

RESULTS

ABSTRACT | SUBJECTS AND METHODS | RESULTS | COMMENT | CONCLUSIONS |ARTICLE INFORMATION | REFERENCES

During 10 years (347 040 person-years) of follow-up, we documented 1058 newly diagnosed cases of type 2 diabetes. As described elsewhere,15 physically more active men tended to be leaner and were less likely to be current smokers. Increasing total physical activity score was strongly associated with progressively reduced risk for type 2 diabetes (Table 1). The age-adjusted RRs across quintiles of MET score from total physical activity were 1.00, 0.76, 0.61, 0.55, and 0.47 (P for trend, <.001). Further adjustment for smoking, parental history of diabetes, and other covariates did not appreciably change these RRs. This inverse gradient remained strong even after adjusting for BMI (RRs across quintiles of MET score were 1.00, 0.82, 0.72, 0.66, and 0.62; P for trend, <.001). Adjustment for dietary intakes of fats and cereal fiber did not appreciably change the results.

Table 1. Relative Risks for Type 2 Diabetes According to Quintiles of Total Physical Activity Score Among US Male Health Professionals, 1986-1996*

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To minimize potential bias from subclinical disease, we conducted additional analyses in which we excluded cases of type 2 diabetes that occurred during the first 2 years of follow-up. The multivariate RRs (without BMI) across quintiles of physical activity score were 1.00, 0.88, 0.75, 0.69, and 0.57 (P for trend, <.001). The inverse association between total physical activity score and diabetes risk was persistent in subgroup analyses according to age (<65 or ≥65 years), family history of diabetes, smoking (never or ever), and BMI (<25.0, 25.0-29.9, or ≥30.0 kg/m2) (Table 2). In particular, the increased risks associated with family history of diabetes and obesity were substantially mitigated by increasing physical activity levels. To address the possibility that medical surveillance may have varied according to physical activity level, we conducted an analysis restricted to subjects reporting at least 1 symptom of diabetes at diagnosis (n = 595). Results from this subgroup were similar to those for the entire cohort (multivariate RRs without BMI in the model across quintiles of MET score were 1.00, 0.66, 0.65, 0.57, and 0.49; P for trend, <.001).

Table 2. Relative Risks of Type 2 Diabetes According to Quintiles of MET-Hours from Total Physical Activity Among Various Subpopulations of US Male Health Professionals, 1986-1996*

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After adjustment for age and other covariates, we observed a significant inverse association between MET score for walking and risk for type 2 diabetes. The multivariate RRs across quintiles of walking score were 1.00, 1.02, 0.80, 0.76, and 0.72 (P for trend, <.001). This inverse association remained significant after adjustment for vigorous exercise (RRs were 1.00, 1.06, 0.86, 0.82, and 0.80; P for trend, .006). Independent of the number of hours spent walking, walking pace was strongly associated with risk for diabetes. Compared with men whose usual walking pace was easy or casual, multivariate RRs were 0.68 for normal pace, 0.46 for brisk pace, and 0.39 for very brisk pace (P for trend, <.001).

Walking and vigorous exercise were associated with comparable risk reductions for equivalent energy expenditure. When the walking and vigorous activity scores were entered into the model as continuous variables simultaneously, RRs associated with an increase in energy expenditures of 10 MET-hours per week were 0.89 (95% confidence interval [CI], 0.82-0.96) for walking and 0.88 (95% CI, 0.85-0.92) for vigorous exercise.

Men who spent more time watching TV were more likely to smoke and drink alcohol and less likely to exercise (Table 3). They were substantially heavier and more likely to have hypertension and hypercholesterolemia. These men also had higher intake of total energy, total and saturated fats, red meat, processed meat, French fries, refined grain products, snacks, and sweets or desserts and lower intakes of fish, vegetables, fruits, and whole grains.

Table 3. Age-Standardized Characteristics According to Average Number of Hours Watching Television per Week in the HPFS at Baseline in 1988*

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After adjustment for age, average time spent watching TV was strongly associated with increased risk for diabetes (Table 4). The RRs across categories of average hours spent watching TV per week (0-1, 2-10, 11-20, 21-40, and >40) were 1.00, 1.62, 1.61, 2.22, and 3.35 (95% CI, 1.71-6.55, respectively; P for trend, <.001). After further adjustment for smoking, alcohol use, physical activity, and other covariates, the positive association persisted (RR comparing extreme categories, 2.87; 95% CI, 1.46-5.65; P for trend, <.001). The significant positive association persisted even after adjustment for BMI (RR comparing extreme categories, 2.31; 95% CI, 1.17-4.56; P for trend, .01). Further simultaneous adjustment for intakes of saturated fat, monounsaturated fat, polyunsaturated fat, trans-fatty acids, and cereal fiber did not appreciably change the results (Table 4).

Table 4. Relative Risks for Type 2 Diabetes According to Categories of Television Watching, HPFS 1988-1996

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In multivariate analyses, we observed independent effects of TV watching and physical activity levels (Figure 1). Compared with men who were in the most active (>46 MET-hours per week) and the lowest TV watching category (<3.5 h/wk), those who were in the least active (<10 MET-hours per week) and most sedentary category (>15 h/wk watching TV) had a significantly increased risk for type 2 diabetes (RR, 2.92; 95% CI, 1.87-4.55; P for interaction, .90). When total physical activity score and time spent watching TV were simultaneously included in a multivariate model (without BMI), an increment of 2 h/d spent watching TV was associated with a 20% (95% CI, 8%-32%) increase in risk for diabetes, whereas an increment of 18 MET-hours per week (equivalent to very brisk walking for 40 minutes per day) was associated with a 19% (95% CI, 13%-24%) reduction in risk.

Multivariate relative risks (RRs) for type 2 diabetes mellitus according to categories of metabolic equivalent hours (MET-hours) per week and average weekly time spent watching television (TV). Adjusted for the same covariates as in Table 1 (body mass index not included in the model).

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COMMENT

ABSTRACT | SUBJECTS AND METHODS | RESULTS | COMMENT | CONCLUSIONS |ARTICLE INFORMATION | REFERENCES

In this large prospective cohort of men, greater leisure time physical activity was associated with reduced risk for type 2 diabetes. In contrast, a sedentary lifestyle, as indicated by time spent watching TV, was significantly associated with an increased risk for diabetes, independent of the effects of physical activity and body weight.

Our findings extend the literature showing that regular physical activity is associated with a substantial reduction in risk for type 2 diabetes.1- 5,7,22 Our results also suggest that the apparent beneficial effect of exercise is not confined to high-risk groups (eg, subjects with ≥1 risk factors such as obesity and family history of diabetes). Contrary to the belief that fitness and physical activity might offset the adverse effects of obesity,24 we found that men who were obese and physically active had a substantially increased risk for diabetes compared with those who were lean and inactive (Table 2), although obese and inactive men were at highest risk. In addition, we found that equivalent energy expenditure from brisk walking or vigorous exercise may confer comparable benefits. These findings are consistent with emerging evidence to support the benefits of moderate-intensity activities in the prevention of diabetes and cardiovascular disease.8,25- 27Since walking is an activity that is highly accessible, readily adopted, and rarely associated with exercise-related injury, these findings may have important public health implications.

The beneficial effects of vigorous exercise and walking on risk for type 2 diabetes are partly mediated by body weight and body fat distribution. Leaner individuals have a reduced risk for diabetes,28- 30 and physical activity facilitates weight loss and weight maintenance.31 Furthermore, exercise may lead to loss in visceral fat,32 which is strongly associated with insulin resistance and the related metabolic syndrome. To the extent that exercise causes individuals to have lower BMI than they would otherwise, adjustment for BMI in regression models constitutes statistical overcorrection and results in underestimation of the true beneficial effect of physical activity.

In our study, prolonged TV watching was strongly associated with risk for diabetes. These findings do not necessarily imply that TV watching per se causes type 2 diabetes; rather, they suggest that a sedentary lifestyle substantially affects future risk for diabetes. There are at least 2 explanations for the observed positive association between TV watching and diabetes risk. First, TV watching is directly related to obesity and weight gain,11- 15,33 probably due to lower energy expenditure (ie, less physical activity) and higher caloric intake. Second, participants who spent more time watching TV tended to eat more red meat, processed meat, snacks, refined grains, and sweets and fewer vegetables, fruits, and whole grains. Such an eating pattern, which is directly related to commercial advertisements and food cues appearing on TV,34,35may adversely affect diabetes risk. In our previous study of 466 men in the HPFS, average hours of TV watching was significantly associated with increased levels of leptin and LDL cholesterol and lower levels of HDL cholesterol and apolipoprotein A-I, independent of physical activity levels.20

Because our cohort did not undergo uniform screening for glucose intolerance, some diabetes cases may have been undiagnosed. However, misclassification would be expected to be small compared with that in the general population because of health professionals' ready access to medical care. For example, more than 85% of men in our study visited a physician for a physical examination, sigmoidoscopy, or colonoscopy at least once between 1988 and 1990. In addition, when the analyses were restricted to symptomatic cases of type 2 diabetes, the findings were similar, suggesting that surveillance bias according to activity level is unlikely. The diagnostic criteria for type 2 diabetes have recently changed36 such that lower fasting glucose levels (>7.0 mmol/L [>126 mg/dL]) would now be considered diabetic. We used the criteria proposed by the National Diabetes Data Group21 because all of our cases were diagnosed before January 1996. If new criteria were used, some nondiabetic subjects would have been classified as diabetic. However, this is unlikely to explain our results, because inclusion of diabetics in the nondiabetic group would have attenuated the associations we observed.

CONCLUSIONS

ABSTRACT | SUBJECTS AND METHODS | RESULTS | COMMENT | CONCLUSIONS |ARTICLE INFORMATION | REFERENCES

Our data provide further evidence that higher levels of physical activity, including moderate-intensity exercise such as walking, are associated with a substantial reduction in risk for diabetes. In contrast, sedentary lifestyle indicated by prolonged TV watching is directly related to diabetes risk. Although these findings lend further support to current guidelines37,38 that promote physical activity, they also suggest the importance of reducing sedentary behavior in the prevention of diabetes.

ARTICLE INFORMATION

ABSTRACT | SUBJECTS AND METHODS | RESULTS | COMMENT | CONCLUSIONS |ARTICLE INFORMATION | REFERENCES

Accepted for publication October 3, 2000.

Supported by research grants CA 55075 and HL 35464 from the National Institutes of Health, Bethesda, Md, and partly by a Research Award from the American Diabetes Association, Alexandria, Va (Dr Hu).

Corresponding author: Frank B. Hu, MD, Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 (e-mail: frank.hu@channing.harvard.edu).

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