0
Letters |

Effects of Counterregulatory Hormones in a High–Glycemic Index Diet

Daniel J. Brotman, MD
[+] Author Affiliations

Stephen J. Lurie, MD, PhDSenior Editor: IndividualAuthor

Copyright 2002 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.

More Author Information
JAMA. 2002;288(6):695-695. doi:10-1001/pubs.JAMA-ISSN-0098-7484-288-6-jlt0814
Text Size: A A A
Published online

To the Editor: Dr Ludwig reviewed the glycemic index and its possible role in the establishment and maintenance of insulin resistance.1 However, in the section addressing the mechanisms by which a high–glycemic index diet may precipitate cardiovascular disease, he did not address the cardiovascular effects of counterregulatory hormones and fatty acids. Such substances may be related to chronically increased autonomic tone,2 which has many of the same long-term consequences as insulin resistance.

Ludwig notes that consumption of a meal with a high glycemic index results in a postprandial surge of counterregulatory hormones and free fatty acids that "resembles a state of fasting normally reached only after many hours without food." In contrast to insulin, which is vasodilatory, all the counterregulatory hormones (glucocorticoids, catecholamines, glucagon, and growth hormone) increase cardiovascular tone. There is recent evidence that fatty acids do so, as well.3 Thus, this response itself may confer increased risk for cardiovascular disease.

In the metabolic syndrome, urinary norepinephrine levels are elevated, likely reflecting increased sympathetic tone.4 Clinically, this may be responsible for higher resting heart rate, decreased heart rate variability, impaired heart rate recovery after exertion, and increased mortality.2 The recent observation that fatty acid infusion increases blood pressure, norepinephrine levels, and heart rate while decreasing heart rate variability3 suggests that increased circulating free fatty acids may contribute to abnormal sympathetic tone in the metabolic syndrome. Fatty acids may also impair endothelial function directly.5 Similarly, cortisol and growth hormone may increase cardiovascular tone through potentiation of catecholamine effects6 and perhaps by stimulating lipolysis, leading to increased concentrations of circulating fatty acids. Finally, glucagon increases cardiac inotropy and chronotropy.7

Thus, it is possible that any type of hormone-induced carbohydrate insulin resistance might also increase cardiovascular tone, especially when insulin production is compromised and its vasodilatory effects are overwhelmed. If the insulin resistance associated with the consumption of high–glycemic index meals is due in part to a counterregulatory hormone surge, as Ludwig suggests, then the hemodynamic effects of these hormones may be as important as hyperglycemia or oxidative stress in precipitating cardiovascular morbidity and mortality.

REFERENCES

Ludwig  DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA. 2002;287:2414-2423.
Curtis  BM, O'Keefe Jr  JH. Autonomic tone as a cardiovascular risk factor: the dangers of chronic fight or flight. Mayo Clin Proc. 2002;77:45-54.
Manzella  D, Barbieri  M, Rizzo  MR.  et al.  Role of free fatty acids on cardiac autonomic nervous system in noninsulin-dependent diabetic patients: effects of metabolic control. J Clin Endocrinol Metab. 2001;86:2769-2774.
Reaven  GM, Lithell  H, Landsberg  L. Hypertension and associated metabolic abnormalities—the role of insulin resistance and the sympathoadrenal system. N Engl J Med. 1996;334:374-381.
Lundman  P, Eriksson  M, Schenck-Gustafsson  K, Karpe  F, Tornvall  P. Transient triglyceridemia decreases vascular reactivity in young, healthy men without risk factors for coronary heart disease. Circulation. 1997;96:3266-3268.
Maison  P, Demolis  P, Young  J, Schaison  G, Giudicelli  JF, Chanson  P. Vascular reactivity in acromegalic patients: preliminary evidence for regional endothelial dysfunction and increased sympathetic vasoconstriction. Clin Endocrinol (Oxf). 2000;53:445-451.
Peterson  CD, Leeder  JS, Sterner  S. Glucagon therapy for beta-blocker overdose. Drug Intell Clin Pharm. 1984;18:394-398.

First Page Preview

First page PDF preview

Figures

Tables

Interactive Graphics

Video

Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature

Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal

Ludwig  DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA. 2002;287:2414-2423.
Curtis  BM, O'Keefe Jr  JH. Autonomic tone as a cardiovascular risk factor: the dangers of chronic fight or flight. Mayo Clin Proc. 2002;77:45-54.
Manzella  D, Barbieri  M, Rizzo  MR.  et al.  Role of free fatty acids on cardiac autonomic nervous system in noninsulin-dependent diabetic patients: effects of metabolic control. J Clin Endocrinol Metab. 2001;86:2769-2774.
Reaven  GM, Lithell  H, Landsberg  L. Hypertension and associated metabolic abnormalities—the role of insulin resistance and the sympathoadrenal system. N Engl J Med. 1996;334:374-381.
Lundman  P, Eriksson  M, Schenck-Gustafsson  K, Karpe  F, Tornvall  P. Transient triglyceridemia decreases vascular reactivity in young, healthy men without risk factors for coronary heart disease. Circulation. 1997;96:3266-3268.
Maison  P, Demolis  P, Young  J, Schaison  G, Giudicelli  JF, Chanson  P. Vascular reactivity in acromegalic patients: preliminary evidence for regional endothelial dysfunction and increased sympathetic vasoconstriction. Clin Endocrinol (Oxf). 2000;53:445-451.
Peterson  CD, Leeder  JS, Sterner  S. Glucagon therapy for beta-blocker overdose. Drug Intell Clin Pharm. 1984;18:394-398.
CME Course for:


You need to register in order to view this quiz.


To understand the clinical management of acute heart failure syndromes.
Accreditation Information The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
To view and print your certificate and access a summary of your CME courses go to My CME.
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s “Cited By” API will populate this tab (http://www.crossref.org/citedby.html).
Submit a Response

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.