Diabetes and its complications: Blood glucose control vs. genetic susceptibility

J. Rosenstock, Philip Raskin

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Which hypothesis of the cause of microvascular complications of diabetes, the genetic or the metabolic, is better supported? Choosing between the two remains difficult. Alternatively, we propose that the small blood vessel complications of diabetes are related to both genetic and metabolic influences. Although hyperglycemia is needed for the microvascular complications of diabetes to develop, it is not a sufficient cause in itself. In addition to hyperglycemia, some 'genetic predisposition' is also required. In approximately 20% of diabetic patients, the genetic predisposition to develop diabetic complications is very low. Thus, regardless of the severity of the metabolic abnormality (how much hyperglycemia occurs for the duration of their illness), these patients rarely develop significant complications. If we could identify this subset of patients at the onset of disease, our treatment recommendations would be simple: Keep them free of symptoms and avoid hypoglycemia, severe hyperglycemia, and ketoacidosis. These patients would not need expensive, intensive diabetes management that would significantly affect their lifestyles. In another 5% of patients, the genetic predisposition to develop microvascular complications is so great that even a slight degree of hyperglycemia results in severe microvascular complications. Unfortunately, present treatment techniques may not have the capacity to normalize the blood glucose level sufficiently to help this group of patients. Finally, we have the greatest number of diabetic patients who have varying degrees of the genetic predisposition to develop microvascular complications. We believe that in this group, improved diabetes control that results in lowering of the overall blood glucose level might reduce the severity or progression of the microvascular complications. It may well be that there is a blood glucose threshold for the development of complications. The ideal situation would be to get the HbA1c lower than this threshold without necessarily having to achieve normoglycemia. Although the data appear to support our hypothesis, it has yet to be proved.

Original languageEnglish (US)
Pages (from-to)417-435
Number of pages19
JournalDiabetes/Metabolism Reviews
Volume4
Issue number5
StatePublished - 1988

Fingerprint

Diabetes Complications
Genetic Predisposition to Disease
Medical problems
Blood Glucose
Hyperglycemia
Blood vessels
Ketosis
Hypoglycemia
Blood Vessels
Life Style
Therapeutics

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Diabetes and its complications : Blood glucose control vs. genetic susceptibility. / Rosenstock, J.; Raskin, Philip.

In: Diabetes/Metabolism Reviews, Vol. 4, No. 5, 1988, p. 417-435.

Research output: Contribution to journalArticle

@article{05daa23ab02b4cc6af3cfdfd7a10074f,
title = "Diabetes and its complications: Blood glucose control vs. genetic susceptibility",
abstract = "Which hypothesis of the cause of microvascular complications of diabetes, the genetic or the metabolic, is better supported? Choosing between the two remains difficult. Alternatively, we propose that the small blood vessel complications of diabetes are related to both genetic and metabolic influences. Although hyperglycemia is needed for the microvascular complications of diabetes to develop, it is not a sufficient cause in itself. In addition to hyperglycemia, some 'genetic predisposition' is also required. In approximately 20{\%} of diabetic patients, the genetic predisposition to develop diabetic complications is very low. Thus, regardless of the severity of the metabolic abnormality (how much hyperglycemia occurs for the duration of their illness), these patients rarely develop significant complications. If we could identify this subset of patients at the onset of disease, our treatment recommendations would be simple: Keep them free of symptoms and avoid hypoglycemia, severe hyperglycemia, and ketoacidosis. These patients would not need expensive, intensive diabetes management that would significantly affect their lifestyles. In another 5{\%} of patients, the genetic predisposition to develop microvascular complications is so great that even a slight degree of hyperglycemia results in severe microvascular complications. Unfortunately, present treatment techniques may not have the capacity to normalize the blood glucose level sufficiently to help this group of patients. Finally, we have the greatest number of diabetic patients who have varying degrees of the genetic predisposition to develop microvascular complications. We believe that in this group, improved diabetes control that results in lowering of the overall blood glucose level might reduce the severity or progression of the microvascular complications. It may well be that there is a blood glucose threshold for the development of complications. The ideal situation would be to get the HbA1c lower than this threshold without necessarily having to achieve normoglycemia. Although the data appear to support our hypothesis, it has yet to be proved.",
author = "J. Rosenstock and Philip Raskin",
year = "1988",
language = "English (US)",
volume = "4",
pages = "417--435",
journal = "Diabetes/Metabolism Research and Reviews",
issn = "1520-7552",
publisher = "John Wiley and Sons Ltd",
number = "5",

}

TY - JOUR

T1 - Diabetes and its complications

T2 - Blood glucose control vs. genetic susceptibility

AU - Rosenstock, J.

AU - Raskin, Philip

PY - 1988

Y1 - 1988

N2 - Which hypothesis of the cause of microvascular complications of diabetes, the genetic or the metabolic, is better supported? Choosing between the two remains difficult. Alternatively, we propose that the small blood vessel complications of diabetes are related to both genetic and metabolic influences. Although hyperglycemia is needed for the microvascular complications of diabetes to develop, it is not a sufficient cause in itself. In addition to hyperglycemia, some 'genetic predisposition' is also required. In approximately 20% of diabetic patients, the genetic predisposition to develop diabetic complications is very low. Thus, regardless of the severity of the metabolic abnormality (how much hyperglycemia occurs for the duration of their illness), these patients rarely develop significant complications. If we could identify this subset of patients at the onset of disease, our treatment recommendations would be simple: Keep them free of symptoms and avoid hypoglycemia, severe hyperglycemia, and ketoacidosis. These patients would not need expensive, intensive diabetes management that would significantly affect their lifestyles. In another 5% of patients, the genetic predisposition to develop microvascular complications is so great that even a slight degree of hyperglycemia results in severe microvascular complications. Unfortunately, present treatment techniques may not have the capacity to normalize the blood glucose level sufficiently to help this group of patients. Finally, we have the greatest number of diabetic patients who have varying degrees of the genetic predisposition to develop microvascular complications. We believe that in this group, improved diabetes control that results in lowering of the overall blood glucose level might reduce the severity or progression of the microvascular complications. It may well be that there is a blood glucose threshold for the development of complications. The ideal situation would be to get the HbA1c lower than this threshold without necessarily having to achieve normoglycemia. Although the data appear to support our hypothesis, it has yet to be proved.

AB - Which hypothesis of the cause of microvascular complications of diabetes, the genetic or the metabolic, is better supported? Choosing between the two remains difficult. Alternatively, we propose that the small blood vessel complications of diabetes are related to both genetic and metabolic influences. Although hyperglycemia is needed for the microvascular complications of diabetes to develop, it is not a sufficient cause in itself. In addition to hyperglycemia, some 'genetic predisposition' is also required. In approximately 20% of diabetic patients, the genetic predisposition to develop diabetic complications is very low. Thus, regardless of the severity of the metabolic abnormality (how much hyperglycemia occurs for the duration of their illness), these patients rarely develop significant complications. If we could identify this subset of patients at the onset of disease, our treatment recommendations would be simple: Keep them free of symptoms and avoid hypoglycemia, severe hyperglycemia, and ketoacidosis. These patients would not need expensive, intensive diabetes management that would significantly affect their lifestyles. In another 5% of patients, the genetic predisposition to develop microvascular complications is so great that even a slight degree of hyperglycemia results in severe microvascular complications. Unfortunately, present treatment techniques may not have the capacity to normalize the blood glucose level sufficiently to help this group of patients. Finally, we have the greatest number of diabetic patients who have varying degrees of the genetic predisposition to develop microvascular complications. We believe that in this group, improved diabetes control that results in lowering of the overall blood glucose level might reduce the severity or progression of the microvascular complications. It may well be that there is a blood glucose threshold for the development of complications. The ideal situation would be to get the HbA1c lower than this threshold without necessarily having to achieve normoglycemia. Although the data appear to support our hypothesis, it has yet to be proved.

UR - http://www.scopus.com/inward/record.url?scp=0023724620&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023724620&partnerID=8YFLogxK

M3 - Article

C2 - 3061755

AN - SCOPUS:0023724620

VL - 4

SP - 417

EP - 435

JO - Diabetes/Metabolism Research and Reviews

JF - Diabetes/Metabolism Research and Reviews

SN - 1520-7552

IS - 5

ER -