The effects of biofeedback in diabetes and essential hypertension

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The effects of biofeedback in diabetes and essential hypertension

Type 2 diabetes, essential hypertension, obesity, and hyperlipidemia are the major components of the metabolic syndrome. Understanding the psychophysiologic basis of the metabolic syndrome is important since its prevalence has been increasing dramatically over the last decade. In the past, type 2 diabetes was diagnosed almost exclusively in persons in their 40s or older. Health care providers are now reporting emergence of type 2 diabetes and the metabolic syndrome in individuals in their 30s and even their late 20s.1,2

This article outlines the psychophysiologic bases for components of the metabolic syndrome and reviews the application of biofeedback and other psychophysiologic interventions on the two components for which such interventions have been most studied—diabetes and essential hypertension.

ETIOLOGY OF METABOLIC SYNDROME: THE INTERSECTION OF BIOLOGY, LIFESTYLE, STRESS

The disorders that constitute the metabolic syndrome share several etiologic factors. First, genetic predisposition increases the risk for diabetes, hypertension, hyperlipidemia, and obesity.3,4 Second, patients’ own behaviors—their choice of activity or inactivity, their food preferences, and their appetite—lead to gradual loss of control over body weight, blood glucose, blood pressure, and lipid levels. Third, chronic stress and its coincident psychological burden contribute to the etiology of various components of the metabolic syndrome.5 As life events accumulate and individuals lose their ability to cope, the stress response system maintains a higher than optimal level of activation.5–8

Chronic stress affects multiple organ systems, including the two master systems—nervous and endocrine. The biologic effects of stress include disordered breathing, increased activation of the renin-angiotension system, vascular constriction, tachycardia, decreased heart rate variability, inflammation, and sleep disruption.9 The mechanisms involved in acute stress responses are purpose-driven and adaptive. In contrast, chronically activated stress response systems involving increased sympathetic activity, decreased parasympathetic activity, and release of stress hormones have serious deleterious effects.10 Psychobiologic systems fail to adapt, delay recovery, or become exhausted.11

Role of psychological factors

As summarized in a review by Goldbacher and Matthews, 12 psychological factors have been related to increased risk for the metabolic syndrome. Depression has probably been most studied in the settings of cardiovascular disease and diabetes, whereas the psychological states of anger, hostility, and anxiety have been identified as salient etiologic factors in hypertension. In particular, depressed mood has been linked to decreased heart rate variability during the stress response.13 Anxiety affects blood pressure and blood glucose in normal individuals as part of the adaptive stress response, and the effects of anxiety are exacerbated in persons with the metabolic syndrome.14

Importance of sleep

Sleep disruption is often ignored in discussions of the mind-body interface in hypertension and diabetes. However, Knutson and Van Cauter15 suggested that sleep quality and sleep length have important effects on leptin levels and risk for diabetes. Very short sleepers have stronger appetites, as a result of lower leptin concentrations, and are much more likely to be obese compared with long sleepers (≥ 10 hours). This indicates that sleep length and quality affect metabolism. With regard to hypertension, a very important reduction of blood pressure occurs during the night, and a lack of nighttime blood pressure “dipping” is one of the markers for sustained blood pressure elevation.16

Factors overlap and begin to affect self-care

In addition to the effects of stress on mood and anxiety, repeated necessary demands for adaptation have marked effects on self-care behavior. Patients who suffer from anxiety are less efficient in managing their time and may be distracted from monitoring blood glucose and blood pressure. Anxious people often turn to the use of high-calorie comfort foods to soothe themselves during stressful times. Alcohol may be chosen as a means of reducing worry and tension. Depressed people lack the energy needed to maintain medical regimens and tend to be poor adherents to treatment recommendations. They also may choose comfort foods and addictive substances instead of nutritious, high-quality food and drink.17

Both anxiety and depression affect sleep routines and efficiency. Anxious people have trouble getting to sleep and may wake up often during the night, while depressed individuals frequently wake up early and cannot get back to sleep. Additionally, psychological distress influences social behaviors. Overt depressive and anxious symptoms tend not to foster social interactions with family and friends. Lack of social support and a scarcity of personal resources eventually contribute to the risk for diabetes and hypertension.18,19

In short, the metabolic syndrome is most likely to emerge when there is a combination of genetic factors, chronic stress, negative emotion, and unhealthy habits. The application of psychophysiologic interventions to diabetes and hypertension is based on our understanding of the etiology of these disorders, particularly the roles of psychological distress and behavior on blood glucose and blood pressure.

BIOFEEDBACK IN TYPE 2 DIABETES

Diabetes is characterized by elevated blood glucose and resistance of cell membranes to insulin, such that glucose is impeded from crossing from the blood into the cells. Standard treatment consists of oral antihyperglycemic agents, exogenous insulin, diet, and exercise.20 Type 2 diabetes may be the most behaviorally demanding of all chronic illnesses because patients must take an active role in daily management. Typical requirements are to measure blood glucose and take oral medicine, perhaps along with insulin, as well as to exercise, monitor diet, and adjust calories depending on activity level.

Therapy goals and a sampling of evidence

The goal of psychophysiologic therapy is not to replace standard treatment with relaxation training or biofeedback but rather to use biofeedback-assisted relaxation therapy to improve control of blood glucose. For example, McGinnis and colleagues compared the effects of 10 sessions of biofeedback (both surface electromyography and thermal feedback) and relaxation therapy versus three sessions of education in a sample of 30 patients with type 2 diabetes.21 No medicines were changed unless medically necessary. Patients kept daily logs of blood glucose, and had their hemoglobin A1c measured before and after treatment. Significant between-group differences in hemoglobin A1c and average blood glucose emerged in favor of the biofeedback group.21 However, patients with high scores on the Beck Depression Inventory22 (indicating more severe depressive symptoms) tended to drop out of the study or did not do as well as patients who were not symptomatic.

Another application of biofeedback in type 2 diabetes has been demonstrated by Rice and Schindler23 and Fiero et al.24 These investigators showed that patients with peripheral neuropathy, a common long-term complication of diabetes, were able to warm their hands and feet with the use of thermal biofeedback. Increased peripheral blood flow mediated the decrease in neuropathic pain.

Possible mechanisms of biofeedback in diabetes

Several explanations can be suggested to account for the results of biofeedback on blood glucose levels. Forehead muscle tension feedback (surface electromyography) helps patients to reduce facial tension and relax skeletal muscles, while increased finger temperature is an indicator of general relaxation. In the patients who completed the above study by McGinnis et al,21 both depression and anxiety scores decreased, which suggests a psychological mechanism for blood glucose reduction. Patients also reported improved sleep duration and quality with the use of relaxation therapy at bedtime.

 

 

BIOFEEDBACK IN ESSENTIAL HYPERTENSION

Biofeedback-assisted relaxation therapy has also been applied to control essential hypertension. The definition of hypertension, according to the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7),25 is systolic blood pressure greater than 139 mm Hg and diastolic blood pressure greater than 90 mm Hg. Prehypertension refers to systolic blood pressures between 130 and 139 mm Hg and diastolic pressures between 80 and 89 mm Hg. Standard treatment for established hypertension is antihypertensive medications, diet, and exercise. For patients in the prehypertensive blood pressure range, lifestyle changes are the primary intervention, unless the patient has multiple risk factors.25

Representative clinical evidence

Linden et al reported on the effects of 10 weeks of individualized psychophysiologic treatment on ambulatory blood pressure in patients with essential hypertension.26 Patients were initially screened for anxiety, depression, and anger, after which a program was designed for each patient based on his or her psychological risk factors. All patients received some form of relaxation therapy, and some received biofeedback. Over time significant reductions in ambulatory systolic and diastolic blood pressure were observed.26 In a separate study, Yucha et al provided a multimodal training program to hypertensive individuals and also reported significant decreases in blood pressure.27

Elliott et al trained hypertensive patients to use the RESPeRATE™ device to achieve the slow, deep breathing associated with the “relaxation response” sought in relaxation training.28 After initial training, patients were instructed to practice this device-guided breathing technique at home. Significant reductions in systolic blood pressure were observed over 8 weeks in the patients who used the device compared with controls who simply monitored their blood pressure at home. A maximum mean systolic blood pressure reduction of 15 mm Hg was achieved in the group of patients who practiced device-guided breathing for the greatest number of minutes during the 8-week study. Similar results with device-guided breathing using this device have been reported in two separate studies.29,30

More general stress reduction programs have also achieved success when offered to patients with essential hypertension in the clinic or the workplace. Studies of programs focusing on meditation and repeated practicing of centered breathing and relaxation responses, without use of biofeedback, have reported reductions of approximately 10.7 mm Hg in systolic pressure and 6.4 mm Hg in diastolic pressure.31,32 McCraty and colleagues provided a stress management program to hypertensive individuals at their place of work,33 based on the premise that individuals’ work demands are a source of chronic stress and thus create an ideal setting for the application of new coping skills. In this study, stress reduction training was associated with significant reductions both in blood pressure and in global measures of distress.33

Prehypertensive patients: An ideal target population

Although meta-analyses demonstrate that there is support for the efficacy of biofeedback in patients with essential hypertension,34,35 the field has been handicapped by the reality that most patients with hypertension are already being treated pharmacologically, which means that their blood pressure levels when starting biofeedback treatment are often low,36 limiting the potential effects of the intervention. The new category of patients with prehypertension may thus be the ideal population for stress management therapies, since their blood pressure is elevated, but not elevated enough to have prompted medication prescriptions in most cases. Lifestyle modifications, which could certainly include stress management, are the recommended first-line therapies for these prehypertensive patients.25

Possible mechanisms of biofeedback in hypertension

One can hypothesize on the mechanisms of action of relaxation-based therapies in hypertension. Relaxing the muscles of the face via electromyography biofeedback and increasing finger temperature facilitates whole-body relaxation and decreased sympathetic adrenergic activity. Parasympathetic dominance is facilitated by the use of breathing techniques to increase heart rate variability. 37,38 The improved deep sleep that results from relaxation may also reduce blood pressure by restoration of nighttime blood pressure dipping.16

IDENTIFYING THE BEST CANDIDATES IS NOT EASY

Some individuals are excellent candidates for biofeedback, while others do not benefit despite their best efforts.39,40 The likelihood of response is generally associated with adherence to medical recommendations and willingness and ability to follow instructions for home practice of relaxation. Nevertheless, some patients who attend sessions and practice still do not succeed, perhaps because they have few signs of overarousal in the system, such as a high degree of sympathetic activation, muscle tension, or low heart rate variability. Further, patients must be able to demonstrate that they learned the skill that was trained, such as consistent warming of the hands. If the training was for heart rate variability, the patient should be in the optimal range of heart rate variability and be able to demonstrate high-frequency waves.34 Patients with specific characteristics, such as stress sensitivity, may benefit more than those whose blood pressure and blood glucose are chronically elevated with few fluctuations.

CONCLUSIONS

The etiology of the metabolic syndrome is complex and multifactorial. Psychophysiologic interventions such as biofeedback and relaxation training are sometimes warranted for multiple aspects of metabolic syndrome, and they target several specific associated disruptions, particularly chronic stress, negative mood, and behavior. Initial patient evaluation should aim to assess the patient’s readiness for change, which must be present to a sufficient degree before continuing with biofeedback or relaxation techniques. Use of motivational interviewing techniques is recommended to increase patients’ preparedness for change.41 Understanding patients’ characteristic responses to stress will guide decisions on the type of biofeedback and relaxation therapies to use and whether or not psychotherapy will be necessary. Specific modalities of biofeedback or particular types of relaxation do not appear to be as critical as the total package of individualized psychophysiologic therapy.

References
  1. Centers for Disease Control and Prevention. Prevalence of overweight and obesity among adults: United States, 2003–2004. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/nchs/products/pubs/pubd/hestats/overweight/overwghtadult_03.htm. Accessed August 11, 2009.
  2. Mayer-Davis EJ. Type 2 diabetes in youth: epidemiology and current research toward prevention and treatment. J Am Diet Assoc 2008; 108( 4 suppl 1):S45S51.
  3. Groop L. Genetics of the metabolic syndrome. Br J Nutr 2000; 83( suppl 1):S39S48.
  4. Pasquali R, Vicennati V. Activity of the hypothalamic-pituitary-adrenal axis in different obesity phenotypes. Int J Obes Relat Metab 2000; 24( suppl 2):S47S49.
  5. Chandola T, Brunner E, Marmot M. Chronic stress at work and the metabolic syndrome: prospective study. BMJ 2006; 332:521525.
  6. Jonas BS, Lando JF. Negative affect as a prospective risk factor for hypertension. Psychosom Med 2000; 62:188196.
  7. McGrady A, Bourey R, Bailey B. The metabolic syndrome: obesity, type 2 diabetes, hypertension, and hyperlipidemia. In:Moss D, McGrady A, Davies TC, Wickramasekera I, eds. Handbook of Mind-Body Medicine for Primary Care. Thousand Oaks, CA: Sage Publications; 2003:275297.
  8. Branth S, Ronquist G, Stridsberg M, et al Development of abdominal fat and incipient metabolic syndrome in young healthy men exposed to long-term stress. Nutr Metab Cardiovasc Dis 2007; 17:427435.
  9. Ganong WF. Review of Medical Physiology. 22nd ed. New York, NY: Lange Medical; 2005.
  10. McGrady A. Psychophysiological foundations of the mind-body therapies. In:Moss D, McGrady A, Davies TC, Wickramasekera I, eds. Handbook of Mind-Body Medicine for Primary Care. Thousand Oaks, CA: Sage Publications; 2003:4356.
  11. McEwen B. The End of Stress As We Know It. Washington, DC: Joseph Henry Press; 2002.
  12. Goldbacher EM, Matthews KA. Are psychological characteristics related to risk of the metabolic syndrome? A review of the literature. Ann Behav Med 2007; 34:240252.
  13. Hughes JW, Stoney CM. Depressed mood is related to high-frequency heart rate variability during stressors. Psychosom Med 2000; 62:796803.
  14. Brook RD, Julius S. Autonomic imbalance, hypertension, and cardiovascular risk. Am J Hypertens 2000; 13( 6 Pt 2):112S122S.
  15. Knutson KL, Van Cauter E. Associations between sleep loss and increased risk of obesity and diabetes. Ann N Y Acad Sci 2008; 1129:287304.
  16. Linden W, Klassen K, Phillips M. Can psychological factors account for a lack of nocturnal blood pressure dipping? Ann Behav Med 2008; 36:253258.
  17. Fisher EB, Thorpe CT, DeVellis BM, DeVellis RF. Healthy coping, negative emotions, and diabetes management: a systematic review and appraisal. Diabetes Educ 2007; 33:10801103.
  18. Vitaliano PP, Scanlan JM, Zhang J, Savage MV, Hirsch IB, Siegler IC. A path model of chronic stress, the metabolic syndrome, and coronary heart disease. Psychosom Med 2002; 64:418435.
  19. Flaa A, Aksnes TA, Kjeldsen SE, Eide I, Rostrup M. Increased sympathetic reactivity may predict insulin resistance: an 18-year follow-up study. Metab Clin Exp 2008; 57:14221427.
  20. American Diabetes Association. Standards of medical care in diabetes—2009. Diabetes Care 2009; 32( suppl 1):S13S61.
  21. McGinnis R, McGrady A, Cox S, Grower-Dowling K. Biofeedback-assisted relaxation in type 2 diabetes mellitus. Diabetes Care 2005; 28:21452149.
  22. Beck AT. Beck Depression Inventory. San Antonio, TX: Harcourt Brace & Co; 1978.
  23. Rice BI, Schindler JV. Effect of thermal biofeedback–assisted relaxation training on blood circulation in the lower extremities of a population with diabetes. Diabetes Care 1992; 15:853859.
  24. Fiero PL, Galper DI, Cox DJ, Phillips LH, Fryburg DA. Thermal biofeedback and lower extremity blood flow in adults with diabetes: is neuropathy a limiting factor? Appl Psychophysiol Biofeedback 2003; 28:193203.
  25. Chobanian AV, Bakris GL, Black HR, et al The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289:25602572.
  26. Linden W, Lenz JW, Con AH. Individualized stress management for primary hypertension: a randomized trial. Arch Intern Med 2001; 161:10711080.
  27. Yucha CB, Clark L, Smith M, Uris P, LaFleur B, Duval S. The effect of biofeedback in hypertension. Appl Nurs Res 2001; 14:2935.
  28. Elliott W, Izzo J, White WB, et al Graded blood pressure reduction in hypertensive outpatients associated with use of a device to assist with slow breathing. J Clin Hypertens 2004; 6:553559.
  29. Schein M, Gavish B, Herz M, et al Treating hypertension with a device that slows and regularizes breathing: a randomized double-blind controlled study. J Hum Hypertens 2001; 15:271278.
  30. Giannattasio C, Failla M, Meles E, Gentile G, Grappiolo A, Mancia G. Efficacy of self-treatment of hypertension at home with device-guided breathing. Am J Hypertens 2002; 15( 4 Pt 2):186A. Abstract P-425.
  31. Schneider RH, Alexander CN, Staggers F, et al Long-term effects of stress reduction on mortality in persons ≥ 55 years of age with systemic hypertension. Am J Cardiol 2005; 95:10601064.
  32. Paul-Labrador M, Polk D, Dwyer JH, et al Effects of randomized controlled trial of transcendental meditation on components of the metabolic syndrome in subjects with coronary heart disease. Arch Intern Med 2006; 166:12181224.
  33. McCraty R, Atkinson M, Tomasino D. Impact of a workplace stress reduction program on blood pressure and emotional health in hypertensive employees. J Altern Complement Med 2003; 9:355369.
  34. Rainforth MV, Schneider RH, Nidich SI, Gaylord-King C, Salerno JW, Anderson JW. Stress reduction programs in patients with elevated blood pressure: a systematic review and meta-analysis. Curr Hypertens Rep 2007; 9:520528.
  35. Nakao M, Yano E, Nomura S, Kuboki T. Blood pressure lowering effects of biofeedback treatment in hypertension: a meta-analysis of randomized controlled trials. Hypertens Res 2003; 26:3746.
  36. Linden W, Chambers LA. Clinical effectiveness of non-drug therapies for hypertension: a meta-analysis. Ann Behav Med 1994; 16:3545.
  37. McGrady AV, Linden W. Biobehavioral treatments of essential hypertension. In:Schwartz M, Andrasik F, eds. Biofeedback: A Practitioner’s Guide. New York, NY: Guilford Press; 2003:382408.
  38. Lehrer P. Biofeedback training to increase heart rate variability. In:Lehrer P, Woolfolk R, Sime W, eds. Principles and Practice of Stress Management. New York, NY: Guilford Press; 2007:227248.
  39. McGrady AV, Higgins JT. Prediction of response to biofeedback-assisted relaxation in hypertensives: development of a hypertensive predictor file (HYPP). Psychosom Med 1989; 51:277284.
  40. Yucha CB, Tsai PS, Calderson KS, Tian L. Biofeedback-assisted relaxation training for essential hypertension: who is most likely to benefit? J Cardiovasc Nurs 2005; 20:198205.
  41. Miller WR, Rollnick S. Motivational Interviewing. 2nd ed. New York, NY: Guilford Press; 2002.
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Correspondence: Angele McGrady, PhD, MEd, LPCC, Professor, Department of Psychiatry, University of Toledo, 3000 Arlington Avenue, MS #1193, Toledo, OH 43614–2598; [email protected]

Dr. McGrady reported that she has no financial relationships that pose a potential conflict of interest with this article.

 

 
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Professor, Department of Psychiatry, University of Toledo, Toledo, OH

Correspondence: Angele McGrady, PhD, MEd, LPCC, Professor, Department of Psychiatry, University of Toledo, 3000 Arlington Avenue, MS #1193, Toledo, OH 43614–2598; [email protected]

Dr. McGrady reported that she has no financial relationships that pose a potential conflict of interest with this article.

 

 
Author and Disclosure Information

Angele McGrady, PhD, MEd, LPCC
Professor, Department of Psychiatry, University of Toledo, Toledo, OH

Correspondence: Angele McGrady, PhD, MEd, LPCC, Professor, Department of Psychiatry, University of Toledo, 3000 Arlington Avenue, MS #1193, Toledo, OH 43614–2598; [email protected]

Dr. McGrady reported that she has no financial relationships that pose a potential conflict of interest with this article.

 

 
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Type 2 diabetes, essential hypertension, obesity, and hyperlipidemia are the major components of the metabolic syndrome. Understanding the psychophysiologic basis of the metabolic syndrome is important since its prevalence has been increasing dramatically over the last decade. In the past, type 2 diabetes was diagnosed almost exclusively in persons in their 40s or older. Health care providers are now reporting emergence of type 2 diabetes and the metabolic syndrome in individuals in their 30s and even their late 20s.1,2

This article outlines the psychophysiologic bases for components of the metabolic syndrome and reviews the application of biofeedback and other psychophysiologic interventions on the two components for which such interventions have been most studied—diabetes and essential hypertension.

ETIOLOGY OF METABOLIC SYNDROME: THE INTERSECTION OF BIOLOGY, LIFESTYLE, STRESS

The disorders that constitute the metabolic syndrome share several etiologic factors. First, genetic predisposition increases the risk for diabetes, hypertension, hyperlipidemia, and obesity.3,4 Second, patients’ own behaviors—their choice of activity or inactivity, their food preferences, and their appetite—lead to gradual loss of control over body weight, blood glucose, blood pressure, and lipid levels. Third, chronic stress and its coincident psychological burden contribute to the etiology of various components of the metabolic syndrome.5 As life events accumulate and individuals lose their ability to cope, the stress response system maintains a higher than optimal level of activation.5–8

Chronic stress affects multiple organ systems, including the two master systems—nervous and endocrine. The biologic effects of stress include disordered breathing, increased activation of the renin-angiotension system, vascular constriction, tachycardia, decreased heart rate variability, inflammation, and sleep disruption.9 The mechanisms involved in acute stress responses are purpose-driven and adaptive. In contrast, chronically activated stress response systems involving increased sympathetic activity, decreased parasympathetic activity, and release of stress hormones have serious deleterious effects.10 Psychobiologic systems fail to adapt, delay recovery, or become exhausted.11

Role of psychological factors

As summarized in a review by Goldbacher and Matthews, 12 psychological factors have been related to increased risk for the metabolic syndrome. Depression has probably been most studied in the settings of cardiovascular disease and diabetes, whereas the psychological states of anger, hostility, and anxiety have been identified as salient etiologic factors in hypertension. In particular, depressed mood has been linked to decreased heart rate variability during the stress response.13 Anxiety affects blood pressure and blood glucose in normal individuals as part of the adaptive stress response, and the effects of anxiety are exacerbated in persons with the metabolic syndrome.14

Importance of sleep

Sleep disruption is often ignored in discussions of the mind-body interface in hypertension and diabetes. However, Knutson and Van Cauter15 suggested that sleep quality and sleep length have important effects on leptin levels and risk for diabetes. Very short sleepers have stronger appetites, as a result of lower leptin concentrations, and are much more likely to be obese compared with long sleepers (≥ 10 hours). This indicates that sleep length and quality affect metabolism. With regard to hypertension, a very important reduction of blood pressure occurs during the night, and a lack of nighttime blood pressure “dipping” is one of the markers for sustained blood pressure elevation.16

Factors overlap and begin to affect self-care

In addition to the effects of stress on mood and anxiety, repeated necessary demands for adaptation have marked effects on self-care behavior. Patients who suffer from anxiety are less efficient in managing their time and may be distracted from monitoring blood glucose and blood pressure. Anxious people often turn to the use of high-calorie comfort foods to soothe themselves during stressful times. Alcohol may be chosen as a means of reducing worry and tension. Depressed people lack the energy needed to maintain medical regimens and tend to be poor adherents to treatment recommendations. They also may choose comfort foods and addictive substances instead of nutritious, high-quality food and drink.17

Both anxiety and depression affect sleep routines and efficiency. Anxious people have trouble getting to sleep and may wake up often during the night, while depressed individuals frequently wake up early and cannot get back to sleep. Additionally, psychological distress influences social behaviors. Overt depressive and anxious symptoms tend not to foster social interactions with family and friends. Lack of social support and a scarcity of personal resources eventually contribute to the risk for diabetes and hypertension.18,19

In short, the metabolic syndrome is most likely to emerge when there is a combination of genetic factors, chronic stress, negative emotion, and unhealthy habits. The application of psychophysiologic interventions to diabetes and hypertension is based on our understanding of the etiology of these disorders, particularly the roles of psychological distress and behavior on blood glucose and blood pressure.

BIOFEEDBACK IN TYPE 2 DIABETES

Diabetes is characterized by elevated blood glucose and resistance of cell membranes to insulin, such that glucose is impeded from crossing from the blood into the cells. Standard treatment consists of oral antihyperglycemic agents, exogenous insulin, diet, and exercise.20 Type 2 diabetes may be the most behaviorally demanding of all chronic illnesses because patients must take an active role in daily management. Typical requirements are to measure blood glucose and take oral medicine, perhaps along with insulin, as well as to exercise, monitor diet, and adjust calories depending on activity level.

Therapy goals and a sampling of evidence

The goal of psychophysiologic therapy is not to replace standard treatment with relaxation training or biofeedback but rather to use biofeedback-assisted relaxation therapy to improve control of blood glucose. For example, McGinnis and colleagues compared the effects of 10 sessions of biofeedback (both surface electromyography and thermal feedback) and relaxation therapy versus three sessions of education in a sample of 30 patients with type 2 diabetes.21 No medicines were changed unless medically necessary. Patients kept daily logs of blood glucose, and had their hemoglobin A1c measured before and after treatment. Significant between-group differences in hemoglobin A1c and average blood glucose emerged in favor of the biofeedback group.21 However, patients with high scores on the Beck Depression Inventory22 (indicating more severe depressive symptoms) tended to drop out of the study or did not do as well as patients who were not symptomatic.

Another application of biofeedback in type 2 diabetes has been demonstrated by Rice and Schindler23 and Fiero et al.24 These investigators showed that patients with peripheral neuropathy, a common long-term complication of diabetes, were able to warm their hands and feet with the use of thermal biofeedback. Increased peripheral blood flow mediated the decrease in neuropathic pain.

Possible mechanisms of biofeedback in diabetes

Several explanations can be suggested to account for the results of biofeedback on blood glucose levels. Forehead muscle tension feedback (surface electromyography) helps patients to reduce facial tension and relax skeletal muscles, while increased finger temperature is an indicator of general relaxation. In the patients who completed the above study by McGinnis et al,21 both depression and anxiety scores decreased, which suggests a psychological mechanism for blood glucose reduction. Patients also reported improved sleep duration and quality with the use of relaxation therapy at bedtime.

 

 

BIOFEEDBACK IN ESSENTIAL HYPERTENSION

Biofeedback-assisted relaxation therapy has also been applied to control essential hypertension. The definition of hypertension, according to the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7),25 is systolic blood pressure greater than 139 mm Hg and diastolic blood pressure greater than 90 mm Hg. Prehypertension refers to systolic blood pressures between 130 and 139 mm Hg and diastolic pressures between 80 and 89 mm Hg. Standard treatment for established hypertension is antihypertensive medications, diet, and exercise. For patients in the prehypertensive blood pressure range, lifestyle changes are the primary intervention, unless the patient has multiple risk factors.25

Representative clinical evidence

Linden et al reported on the effects of 10 weeks of individualized psychophysiologic treatment on ambulatory blood pressure in patients with essential hypertension.26 Patients were initially screened for anxiety, depression, and anger, after which a program was designed for each patient based on his or her psychological risk factors. All patients received some form of relaxation therapy, and some received biofeedback. Over time significant reductions in ambulatory systolic and diastolic blood pressure were observed.26 In a separate study, Yucha et al provided a multimodal training program to hypertensive individuals and also reported significant decreases in blood pressure.27

Elliott et al trained hypertensive patients to use the RESPeRATE™ device to achieve the slow, deep breathing associated with the “relaxation response” sought in relaxation training.28 After initial training, patients were instructed to practice this device-guided breathing technique at home. Significant reductions in systolic blood pressure were observed over 8 weeks in the patients who used the device compared with controls who simply monitored their blood pressure at home. A maximum mean systolic blood pressure reduction of 15 mm Hg was achieved in the group of patients who practiced device-guided breathing for the greatest number of minutes during the 8-week study. Similar results with device-guided breathing using this device have been reported in two separate studies.29,30

More general stress reduction programs have also achieved success when offered to patients with essential hypertension in the clinic or the workplace. Studies of programs focusing on meditation and repeated practicing of centered breathing and relaxation responses, without use of biofeedback, have reported reductions of approximately 10.7 mm Hg in systolic pressure and 6.4 mm Hg in diastolic pressure.31,32 McCraty and colleagues provided a stress management program to hypertensive individuals at their place of work,33 based on the premise that individuals’ work demands are a source of chronic stress and thus create an ideal setting for the application of new coping skills. In this study, stress reduction training was associated with significant reductions both in blood pressure and in global measures of distress.33

Prehypertensive patients: An ideal target population

Although meta-analyses demonstrate that there is support for the efficacy of biofeedback in patients with essential hypertension,34,35 the field has been handicapped by the reality that most patients with hypertension are already being treated pharmacologically, which means that their blood pressure levels when starting biofeedback treatment are often low,36 limiting the potential effects of the intervention. The new category of patients with prehypertension may thus be the ideal population for stress management therapies, since their blood pressure is elevated, but not elevated enough to have prompted medication prescriptions in most cases. Lifestyle modifications, which could certainly include stress management, are the recommended first-line therapies for these prehypertensive patients.25

Possible mechanisms of biofeedback in hypertension

One can hypothesize on the mechanisms of action of relaxation-based therapies in hypertension. Relaxing the muscles of the face via electromyography biofeedback and increasing finger temperature facilitates whole-body relaxation and decreased sympathetic adrenergic activity. Parasympathetic dominance is facilitated by the use of breathing techniques to increase heart rate variability. 37,38 The improved deep sleep that results from relaxation may also reduce blood pressure by restoration of nighttime blood pressure dipping.16

IDENTIFYING THE BEST CANDIDATES IS NOT EASY

Some individuals are excellent candidates for biofeedback, while others do not benefit despite their best efforts.39,40 The likelihood of response is generally associated with adherence to medical recommendations and willingness and ability to follow instructions for home practice of relaxation. Nevertheless, some patients who attend sessions and practice still do not succeed, perhaps because they have few signs of overarousal in the system, such as a high degree of sympathetic activation, muscle tension, or low heart rate variability. Further, patients must be able to demonstrate that they learned the skill that was trained, such as consistent warming of the hands. If the training was for heart rate variability, the patient should be in the optimal range of heart rate variability and be able to demonstrate high-frequency waves.34 Patients with specific characteristics, such as stress sensitivity, may benefit more than those whose blood pressure and blood glucose are chronically elevated with few fluctuations.

CONCLUSIONS

The etiology of the metabolic syndrome is complex and multifactorial. Psychophysiologic interventions such as biofeedback and relaxation training are sometimes warranted for multiple aspects of metabolic syndrome, and they target several specific associated disruptions, particularly chronic stress, negative mood, and behavior. Initial patient evaluation should aim to assess the patient’s readiness for change, which must be present to a sufficient degree before continuing with biofeedback or relaxation techniques. Use of motivational interviewing techniques is recommended to increase patients’ preparedness for change.41 Understanding patients’ characteristic responses to stress will guide decisions on the type of biofeedback and relaxation therapies to use and whether or not psychotherapy will be necessary. Specific modalities of biofeedback or particular types of relaxation do not appear to be as critical as the total package of individualized psychophysiologic therapy.

Type 2 diabetes, essential hypertension, obesity, and hyperlipidemia are the major components of the metabolic syndrome. Understanding the psychophysiologic basis of the metabolic syndrome is important since its prevalence has been increasing dramatically over the last decade. In the past, type 2 diabetes was diagnosed almost exclusively in persons in their 40s or older. Health care providers are now reporting emergence of type 2 diabetes and the metabolic syndrome in individuals in their 30s and even their late 20s.1,2

This article outlines the psychophysiologic bases for components of the metabolic syndrome and reviews the application of biofeedback and other psychophysiologic interventions on the two components for which such interventions have been most studied—diabetes and essential hypertension.

ETIOLOGY OF METABOLIC SYNDROME: THE INTERSECTION OF BIOLOGY, LIFESTYLE, STRESS

The disorders that constitute the metabolic syndrome share several etiologic factors. First, genetic predisposition increases the risk for diabetes, hypertension, hyperlipidemia, and obesity.3,4 Second, patients’ own behaviors—their choice of activity or inactivity, their food preferences, and their appetite—lead to gradual loss of control over body weight, blood glucose, blood pressure, and lipid levels. Third, chronic stress and its coincident psychological burden contribute to the etiology of various components of the metabolic syndrome.5 As life events accumulate and individuals lose their ability to cope, the stress response system maintains a higher than optimal level of activation.5–8

Chronic stress affects multiple organ systems, including the two master systems—nervous and endocrine. The biologic effects of stress include disordered breathing, increased activation of the renin-angiotension system, vascular constriction, tachycardia, decreased heart rate variability, inflammation, and sleep disruption.9 The mechanisms involved in acute stress responses are purpose-driven and adaptive. In contrast, chronically activated stress response systems involving increased sympathetic activity, decreased parasympathetic activity, and release of stress hormones have serious deleterious effects.10 Psychobiologic systems fail to adapt, delay recovery, or become exhausted.11

Role of psychological factors

As summarized in a review by Goldbacher and Matthews, 12 psychological factors have been related to increased risk for the metabolic syndrome. Depression has probably been most studied in the settings of cardiovascular disease and diabetes, whereas the psychological states of anger, hostility, and anxiety have been identified as salient etiologic factors in hypertension. In particular, depressed mood has been linked to decreased heart rate variability during the stress response.13 Anxiety affects blood pressure and blood glucose in normal individuals as part of the adaptive stress response, and the effects of anxiety are exacerbated in persons with the metabolic syndrome.14

Importance of sleep

Sleep disruption is often ignored in discussions of the mind-body interface in hypertension and diabetes. However, Knutson and Van Cauter15 suggested that sleep quality and sleep length have important effects on leptin levels and risk for diabetes. Very short sleepers have stronger appetites, as a result of lower leptin concentrations, and are much more likely to be obese compared with long sleepers (≥ 10 hours). This indicates that sleep length and quality affect metabolism. With regard to hypertension, a very important reduction of blood pressure occurs during the night, and a lack of nighttime blood pressure “dipping” is one of the markers for sustained blood pressure elevation.16

Factors overlap and begin to affect self-care

In addition to the effects of stress on mood and anxiety, repeated necessary demands for adaptation have marked effects on self-care behavior. Patients who suffer from anxiety are less efficient in managing their time and may be distracted from monitoring blood glucose and blood pressure. Anxious people often turn to the use of high-calorie comfort foods to soothe themselves during stressful times. Alcohol may be chosen as a means of reducing worry and tension. Depressed people lack the energy needed to maintain medical regimens and tend to be poor adherents to treatment recommendations. They also may choose comfort foods and addictive substances instead of nutritious, high-quality food and drink.17

Both anxiety and depression affect sleep routines and efficiency. Anxious people have trouble getting to sleep and may wake up often during the night, while depressed individuals frequently wake up early and cannot get back to sleep. Additionally, psychological distress influences social behaviors. Overt depressive and anxious symptoms tend not to foster social interactions with family and friends. Lack of social support and a scarcity of personal resources eventually contribute to the risk for diabetes and hypertension.18,19

In short, the metabolic syndrome is most likely to emerge when there is a combination of genetic factors, chronic stress, negative emotion, and unhealthy habits. The application of psychophysiologic interventions to diabetes and hypertension is based on our understanding of the etiology of these disorders, particularly the roles of psychological distress and behavior on blood glucose and blood pressure.

BIOFEEDBACK IN TYPE 2 DIABETES

Diabetes is characterized by elevated blood glucose and resistance of cell membranes to insulin, such that glucose is impeded from crossing from the blood into the cells. Standard treatment consists of oral antihyperglycemic agents, exogenous insulin, diet, and exercise.20 Type 2 diabetes may be the most behaviorally demanding of all chronic illnesses because patients must take an active role in daily management. Typical requirements are to measure blood glucose and take oral medicine, perhaps along with insulin, as well as to exercise, monitor diet, and adjust calories depending on activity level.

Therapy goals and a sampling of evidence

The goal of psychophysiologic therapy is not to replace standard treatment with relaxation training or biofeedback but rather to use biofeedback-assisted relaxation therapy to improve control of blood glucose. For example, McGinnis and colleagues compared the effects of 10 sessions of biofeedback (both surface electromyography and thermal feedback) and relaxation therapy versus three sessions of education in a sample of 30 patients with type 2 diabetes.21 No medicines were changed unless medically necessary. Patients kept daily logs of blood glucose, and had their hemoglobin A1c measured before and after treatment. Significant between-group differences in hemoglobin A1c and average blood glucose emerged in favor of the biofeedback group.21 However, patients with high scores on the Beck Depression Inventory22 (indicating more severe depressive symptoms) tended to drop out of the study or did not do as well as patients who were not symptomatic.

Another application of biofeedback in type 2 diabetes has been demonstrated by Rice and Schindler23 and Fiero et al.24 These investigators showed that patients with peripheral neuropathy, a common long-term complication of diabetes, were able to warm their hands and feet with the use of thermal biofeedback. Increased peripheral blood flow mediated the decrease in neuropathic pain.

Possible mechanisms of biofeedback in diabetes

Several explanations can be suggested to account for the results of biofeedback on blood glucose levels. Forehead muscle tension feedback (surface electromyography) helps patients to reduce facial tension and relax skeletal muscles, while increased finger temperature is an indicator of general relaxation. In the patients who completed the above study by McGinnis et al,21 both depression and anxiety scores decreased, which suggests a psychological mechanism for blood glucose reduction. Patients also reported improved sleep duration and quality with the use of relaxation therapy at bedtime.

 

 

BIOFEEDBACK IN ESSENTIAL HYPERTENSION

Biofeedback-assisted relaxation therapy has also been applied to control essential hypertension. The definition of hypertension, according to the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7),25 is systolic blood pressure greater than 139 mm Hg and diastolic blood pressure greater than 90 mm Hg. Prehypertension refers to systolic blood pressures between 130 and 139 mm Hg and diastolic pressures between 80 and 89 mm Hg. Standard treatment for established hypertension is antihypertensive medications, diet, and exercise. For patients in the prehypertensive blood pressure range, lifestyle changes are the primary intervention, unless the patient has multiple risk factors.25

Representative clinical evidence

Linden et al reported on the effects of 10 weeks of individualized psychophysiologic treatment on ambulatory blood pressure in patients with essential hypertension.26 Patients were initially screened for anxiety, depression, and anger, after which a program was designed for each patient based on his or her psychological risk factors. All patients received some form of relaxation therapy, and some received biofeedback. Over time significant reductions in ambulatory systolic and diastolic blood pressure were observed.26 In a separate study, Yucha et al provided a multimodal training program to hypertensive individuals and also reported significant decreases in blood pressure.27

Elliott et al trained hypertensive patients to use the RESPeRATE™ device to achieve the slow, deep breathing associated with the “relaxation response” sought in relaxation training.28 After initial training, patients were instructed to practice this device-guided breathing technique at home. Significant reductions in systolic blood pressure were observed over 8 weeks in the patients who used the device compared with controls who simply monitored their blood pressure at home. A maximum mean systolic blood pressure reduction of 15 mm Hg was achieved in the group of patients who practiced device-guided breathing for the greatest number of minutes during the 8-week study. Similar results with device-guided breathing using this device have been reported in two separate studies.29,30

More general stress reduction programs have also achieved success when offered to patients with essential hypertension in the clinic or the workplace. Studies of programs focusing on meditation and repeated practicing of centered breathing and relaxation responses, without use of biofeedback, have reported reductions of approximately 10.7 mm Hg in systolic pressure and 6.4 mm Hg in diastolic pressure.31,32 McCraty and colleagues provided a stress management program to hypertensive individuals at their place of work,33 based on the premise that individuals’ work demands are a source of chronic stress and thus create an ideal setting for the application of new coping skills. In this study, stress reduction training was associated with significant reductions both in blood pressure and in global measures of distress.33

Prehypertensive patients: An ideal target population

Although meta-analyses demonstrate that there is support for the efficacy of biofeedback in patients with essential hypertension,34,35 the field has been handicapped by the reality that most patients with hypertension are already being treated pharmacologically, which means that their blood pressure levels when starting biofeedback treatment are often low,36 limiting the potential effects of the intervention. The new category of patients with prehypertension may thus be the ideal population for stress management therapies, since their blood pressure is elevated, but not elevated enough to have prompted medication prescriptions in most cases. Lifestyle modifications, which could certainly include stress management, are the recommended first-line therapies for these prehypertensive patients.25

Possible mechanisms of biofeedback in hypertension

One can hypothesize on the mechanisms of action of relaxation-based therapies in hypertension. Relaxing the muscles of the face via electromyography biofeedback and increasing finger temperature facilitates whole-body relaxation and decreased sympathetic adrenergic activity. Parasympathetic dominance is facilitated by the use of breathing techniques to increase heart rate variability. 37,38 The improved deep sleep that results from relaxation may also reduce blood pressure by restoration of nighttime blood pressure dipping.16

IDENTIFYING THE BEST CANDIDATES IS NOT EASY

Some individuals are excellent candidates for biofeedback, while others do not benefit despite their best efforts.39,40 The likelihood of response is generally associated with adherence to medical recommendations and willingness and ability to follow instructions for home practice of relaxation. Nevertheless, some patients who attend sessions and practice still do not succeed, perhaps because they have few signs of overarousal in the system, such as a high degree of sympathetic activation, muscle tension, or low heart rate variability. Further, patients must be able to demonstrate that they learned the skill that was trained, such as consistent warming of the hands. If the training was for heart rate variability, the patient should be in the optimal range of heart rate variability and be able to demonstrate high-frequency waves.34 Patients with specific characteristics, such as stress sensitivity, may benefit more than those whose blood pressure and blood glucose are chronically elevated with few fluctuations.

CONCLUSIONS

The etiology of the metabolic syndrome is complex and multifactorial. Psychophysiologic interventions such as biofeedback and relaxation training are sometimes warranted for multiple aspects of metabolic syndrome, and they target several specific associated disruptions, particularly chronic stress, negative mood, and behavior. Initial patient evaluation should aim to assess the patient’s readiness for change, which must be present to a sufficient degree before continuing with biofeedback or relaxation techniques. Use of motivational interviewing techniques is recommended to increase patients’ preparedness for change.41 Understanding patients’ characteristic responses to stress will guide decisions on the type of biofeedback and relaxation therapies to use and whether or not psychotherapy will be necessary. Specific modalities of biofeedback or particular types of relaxation do not appear to be as critical as the total package of individualized psychophysiologic therapy.

References
  1. Centers for Disease Control and Prevention. Prevalence of overweight and obesity among adults: United States, 2003–2004. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/nchs/products/pubs/pubd/hestats/overweight/overwghtadult_03.htm. Accessed August 11, 2009.
  2. Mayer-Davis EJ. Type 2 diabetes in youth: epidemiology and current research toward prevention and treatment. J Am Diet Assoc 2008; 108( 4 suppl 1):S45S51.
  3. Groop L. Genetics of the metabolic syndrome. Br J Nutr 2000; 83( suppl 1):S39S48.
  4. Pasquali R, Vicennati V. Activity of the hypothalamic-pituitary-adrenal axis in different obesity phenotypes. Int J Obes Relat Metab 2000; 24( suppl 2):S47S49.
  5. Chandola T, Brunner E, Marmot M. Chronic stress at work and the metabolic syndrome: prospective study. BMJ 2006; 332:521525.
  6. Jonas BS, Lando JF. Negative affect as a prospective risk factor for hypertension. Psychosom Med 2000; 62:188196.
  7. McGrady A, Bourey R, Bailey B. The metabolic syndrome: obesity, type 2 diabetes, hypertension, and hyperlipidemia. In:Moss D, McGrady A, Davies TC, Wickramasekera I, eds. Handbook of Mind-Body Medicine for Primary Care. Thousand Oaks, CA: Sage Publications; 2003:275297.
  8. Branth S, Ronquist G, Stridsberg M, et al Development of abdominal fat and incipient metabolic syndrome in young healthy men exposed to long-term stress. Nutr Metab Cardiovasc Dis 2007; 17:427435.
  9. Ganong WF. Review of Medical Physiology. 22nd ed. New York, NY: Lange Medical; 2005.
  10. McGrady A. Psychophysiological foundations of the mind-body therapies. In:Moss D, McGrady A, Davies TC, Wickramasekera I, eds. Handbook of Mind-Body Medicine for Primary Care. Thousand Oaks, CA: Sage Publications; 2003:4356.
  11. McEwen B. The End of Stress As We Know It. Washington, DC: Joseph Henry Press; 2002.
  12. Goldbacher EM, Matthews KA. Are psychological characteristics related to risk of the metabolic syndrome? A review of the literature. Ann Behav Med 2007; 34:240252.
  13. Hughes JW, Stoney CM. Depressed mood is related to high-frequency heart rate variability during stressors. Psychosom Med 2000; 62:796803.
  14. Brook RD, Julius S. Autonomic imbalance, hypertension, and cardiovascular risk. Am J Hypertens 2000; 13( 6 Pt 2):112S122S.
  15. Knutson KL, Van Cauter E. Associations between sleep loss and increased risk of obesity and diabetes. Ann N Y Acad Sci 2008; 1129:287304.
  16. Linden W, Klassen K, Phillips M. Can psychological factors account for a lack of nocturnal blood pressure dipping? Ann Behav Med 2008; 36:253258.
  17. Fisher EB, Thorpe CT, DeVellis BM, DeVellis RF. Healthy coping, negative emotions, and diabetes management: a systematic review and appraisal. Diabetes Educ 2007; 33:10801103.
  18. Vitaliano PP, Scanlan JM, Zhang J, Savage MV, Hirsch IB, Siegler IC. A path model of chronic stress, the metabolic syndrome, and coronary heart disease. Psychosom Med 2002; 64:418435.
  19. Flaa A, Aksnes TA, Kjeldsen SE, Eide I, Rostrup M. Increased sympathetic reactivity may predict insulin resistance: an 18-year follow-up study. Metab Clin Exp 2008; 57:14221427.
  20. American Diabetes Association. Standards of medical care in diabetes—2009. Diabetes Care 2009; 32( suppl 1):S13S61.
  21. McGinnis R, McGrady A, Cox S, Grower-Dowling K. Biofeedback-assisted relaxation in type 2 diabetes mellitus. Diabetes Care 2005; 28:21452149.
  22. Beck AT. Beck Depression Inventory. San Antonio, TX: Harcourt Brace & Co; 1978.
  23. Rice BI, Schindler JV. Effect of thermal biofeedback–assisted relaxation training on blood circulation in the lower extremities of a population with diabetes. Diabetes Care 1992; 15:853859.
  24. Fiero PL, Galper DI, Cox DJ, Phillips LH, Fryburg DA. Thermal biofeedback and lower extremity blood flow in adults with diabetes: is neuropathy a limiting factor? Appl Psychophysiol Biofeedback 2003; 28:193203.
  25. Chobanian AV, Bakris GL, Black HR, et al The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289:25602572.
  26. Linden W, Lenz JW, Con AH. Individualized stress management for primary hypertension: a randomized trial. Arch Intern Med 2001; 161:10711080.
  27. Yucha CB, Clark L, Smith M, Uris P, LaFleur B, Duval S. The effect of biofeedback in hypertension. Appl Nurs Res 2001; 14:2935.
  28. Elliott W, Izzo J, White WB, et al Graded blood pressure reduction in hypertensive outpatients associated with use of a device to assist with slow breathing. J Clin Hypertens 2004; 6:553559.
  29. Schein M, Gavish B, Herz M, et al Treating hypertension with a device that slows and regularizes breathing: a randomized double-blind controlled study. J Hum Hypertens 2001; 15:271278.
  30. Giannattasio C, Failla M, Meles E, Gentile G, Grappiolo A, Mancia G. Efficacy of self-treatment of hypertension at home with device-guided breathing. Am J Hypertens 2002; 15( 4 Pt 2):186A. Abstract P-425.
  31. Schneider RH, Alexander CN, Staggers F, et al Long-term effects of stress reduction on mortality in persons ≥ 55 years of age with systemic hypertension. Am J Cardiol 2005; 95:10601064.
  32. Paul-Labrador M, Polk D, Dwyer JH, et al Effects of randomized controlled trial of transcendental meditation on components of the metabolic syndrome in subjects with coronary heart disease. Arch Intern Med 2006; 166:12181224.
  33. McCraty R, Atkinson M, Tomasino D. Impact of a workplace stress reduction program on blood pressure and emotional health in hypertensive employees. J Altern Complement Med 2003; 9:355369.
  34. Rainforth MV, Schneider RH, Nidich SI, Gaylord-King C, Salerno JW, Anderson JW. Stress reduction programs in patients with elevated blood pressure: a systematic review and meta-analysis. Curr Hypertens Rep 2007; 9:520528.
  35. Nakao M, Yano E, Nomura S, Kuboki T. Blood pressure lowering effects of biofeedback treatment in hypertension: a meta-analysis of randomized controlled trials. Hypertens Res 2003; 26:3746.
  36. Linden W, Chambers LA. Clinical effectiveness of non-drug therapies for hypertension: a meta-analysis. Ann Behav Med 1994; 16:3545.
  37. McGrady AV, Linden W. Biobehavioral treatments of essential hypertension. In:Schwartz M, Andrasik F, eds. Biofeedback: A Practitioner’s Guide. New York, NY: Guilford Press; 2003:382408.
  38. Lehrer P. Biofeedback training to increase heart rate variability. In:Lehrer P, Woolfolk R, Sime W, eds. Principles and Practice of Stress Management. New York, NY: Guilford Press; 2007:227248.
  39. McGrady AV, Higgins JT. Prediction of response to biofeedback-assisted relaxation in hypertensives: development of a hypertensive predictor file (HYPP). Psychosom Med 1989; 51:277284.
  40. Yucha CB, Tsai PS, Calderson KS, Tian L. Biofeedback-assisted relaxation training for essential hypertension: who is most likely to benefit? J Cardiovasc Nurs 2005; 20:198205.
  41. Miller WR, Rollnick S. Motivational Interviewing. 2nd ed. New York, NY: Guilford Press; 2002.
References
  1. Centers for Disease Control and Prevention. Prevalence of overweight and obesity among adults: United States, 2003–2004. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/nchs/products/pubs/pubd/hestats/overweight/overwghtadult_03.htm. Accessed August 11, 2009.
  2. Mayer-Davis EJ. Type 2 diabetes in youth: epidemiology and current research toward prevention and treatment. J Am Diet Assoc 2008; 108( 4 suppl 1):S45S51.
  3. Groop L. Genetics of the metabolic syndrome. Br J Nutr 2000; 83( suppl 1):S39S48.
  4. Pasquali R, Vicennati V. Activity of the hypothalamic-pituitary-adrenal axis in different obesity phenotypes. Int J Obes Relat Metab 2000; 24( suppl 2):S47S49.
  5. Chandola T, Brunner E, Marmot M. Chronic stress at work and the metabolic syndrome: prospective study. BMJ 2006; 332:521525.
  6. Jonas BS, Lando JF. Negative affect as a prospective risk factor for hypertension. Psychosom Med 2000; 62:188196.
  7. McGrady A, Bourey R, Bailey B. The metabolic syndrome: obesity, type 2 diabetes, hypertension, and hyperlipidemia. In:Moss D, McGrady A, Davies TC, Wickramasekera I, eds. Handbook of Mind-Body Medicine for Primary Care. Thousand Oaks, CA: Sage Publications; 2003:275297.
  8. Branth S, Ronquist G, Stridsberg M, et al Development of abdominal fat and incipient metabolic syndrome in young healthy men exposed to long-term stress. Nutr Metab Cardiovasc Dis 2007; 17:427435.
  9. Ganong WF. Review of Medical Physiology. 22nd ed. New York, NY: Lange Medical; 2005.
  10. McGrady A. Psychophysiological foundations of the mind-body therapies. In:Moss D, McGrady A, Davies TC, Wickramasekera I, eds. Handbook of Mind-Body Medicine for Primary Care. Thousand Oaks, CA: Sage Publications; 2003:4356.
  11. McEwen B. The End of Stress As We Know It. Washington, DC: Joseph Henry Press; 2002.
  12. Goldbacher EM, Matthews KA. Are psychological characteristics related to risk of the metabolic syndrome? A review of the literature. Ann Behav Med 2007; 34:240252.
  13. Hughes JW, Stoney CM. Depressed mood is related to high-frequency heart rate variability during stressors. Psychosom Med 2000; 62:796803.
  14. Brook RD, Julius S. Autonomic imbalance, hypertension, and cardiovascular risk. Am J Hypertens 2000; 13( 6 Pt 2):112S122S.
  15. Knutson KL, Van Cauter E. Associations between sleep loss and increased risk of obesity and diabetes. Ann N Y Acad Sci 2008; 1129:287304.
  16. Linden W, Klassen K, Phillips M. Can psychological factors account for a lack of nocturnal blood pressure dipping? Ann Behav Med 2008; 36:253258.
  17. Fisher EB, Thorpe CT, DeVellis BM, DeVellis RF. Healthy coping, negative emotions, and diabetes management: a systematic review and appraisal. Diabetes Educ 2007; 33:10801103.
  18. Vitaliano PP, Scanlan JM, Zhang J, Savage MV, Hirsch IB, Siegler IC. A path model of chronic stress, the metabolic syndrome, and coronary heart disease. Psychosom Med 2002; 64:418435.
  19. Flaa A, Aksnes TA, Kjeldsen SE, Eide I, Rostrup M. Increased sympathetic reactivity may predict insulin resistance: an 18-year follow-up study. Metab Clin Exp 2008; 57:14221427.
  20. American Diabetes Association. Standards of medical care in diabetes—2009. Diabetes Care 2009; 32( suppl 1):S13S61.
  21. McGinnis R, McGrady A, Cox S, Grower-Dowling K. Biofeedback-assisted relaxation in type 2 diabetes mellitus. Diabetes Care 2005; 28:21452149.
  22. Beck AT. Beck Depression Inventory. San Antonio, TX: Harcourt Brace & Co; 1978.
  23. Rice BI, Schindler JV. Effect of thermal biofeedback–assisted relaxation training on blood circulation in the lower extremities of a population with diabetes. Diabetes Care 1992; 15:853859.
  24. Fiero PL, Galper DI, Cox DJ, Phillips LH, Fryburg DA. Thermal biofeedback and lower extremity blood flow in adults with diabetes: is neuropathy a limiting factor? Appl Psychophysiol Biofeedback 2003; 28:193203.
  25. Chobanian AV, Bakris GL, Black HR, et al The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289:25602572.
  26. Linden W, Lenz JW, Con AH. Individualized stress management for primary hypertension: a randomized trial. Arch Intern Med 2001; 161:10711080.
  27. Yucha CB, Clark L, Smith M, Uris P, LaFleur B, Duval S. The effect of biofeedback in hypertension. Appl Nurs Res 2001; 14:2935.
  28. Elliott W, Izzo J, White WB, et al Graded blood pressure reduction in hypertensive outpatients associated with use of a device to assist with slow breathing. J Clin Hypertens 2004; 6:553559.
  29. Schein M, Gavish B, Herz M, et al Treating hypertension with a device that slows and regularizes breathing: a randomized double-blind controlled study. J Hum Hypertens 2001; 15:271278.
  30. Giannattasio C, Failla M, Meles E, Gentile G, Grappiolo A, Mancia G. Efficacy of self-treatment of hypertension at home with device-guided breathing. Am J Hypertens 2002; 15( 4 Pt 2):186A. Abstract P-425.
  31. Schneider RH, Alexander CN, Staggers F, et al Long-term effects of stress reduction on mortality in persons ≥ 55 years of age with systemic hypertension. Am J Cardiol 2005; 95:10601064.
  32. Paul-Labrador M, Polk D, Dwyer JH, et al Effects of randomized controlled trial of transcendental meditation on components of the metabolic syndrome in subjects with coronary heart disease. Arch Intern Med 2006; 166:12181224.
  33. McCraty R, Atkinson M, Tomasino D. Impact of a workplace stress reduction program on blood pressure and emotional health in hypertensive employees. J Altern Complement Med 2003; 9:355369.
  34. Rainforth MV, Schneider RH, Nidich SI, Gaylord-King C, Salerno JW, Anderson JW. Stress reduction programs in patients with elevated blood pressure: a systematic review and meta-analysis. Curr Hypertens Rep 2007; 9:520528.
  35. Nakao M, Yano E, Nomura S, Kuboki T. Blood pressure lowering effects of biofeedback treatment in hypertension: a meta-analysis of randomized controlled trials. Hypertens Res 2003; 26:3746.
  36. Linden W, Chambers LA. Clinical effectiveness of non-drug therapies for hypertension: a meta-analysis. Ann Behav Med 1994; 16:3545.
  37. McGrady AV, Linden W. Biobehavioral treatments of essential hypertension. In:Schwartz M, Andrasik F, eds. Biofeedback: A Practitioner’s Guide. New York, NY: Guilford Press; 2003:382408.
  38. Lehrer P. Biofeedback training to increase heart rate variability. In:Lehrer P, Woolfolk R, Sime W, eds. Principles and Practice of Stress Management. New York, NY: Guilford Press; 2007:227248.
  39. McGrady AV, Higgins JT. Prediction of response to biofeedback-assisted relaxation in hypertensives: development of a hypertensive predictor file (HYPP). Psychosom Med 1989; 51:277284.
  40. Yucha CB, Tsai PS, Calderson KS, Tian L. Biofeedback-assisted relaxation training for essential hypertension: who is most likely to benefit? J Cardiovasc Nurs 2005; 20:198205.
  41. Miller WR, Rollnick S. Motivational Interviewing. 2nd ed. New York, NY: Guilford Press; 2002.
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