Prolonged heavy drinking is an established risk factor for pancreatitis, which may lead to the development of secondary diabetes. In addition, sustained alcohol use is associated with hypertriglyceridaemia, another factor implicated in pancreatic inflammation. However, for more modest drinkers, the evidence is conflicting with some studies showing that alcohol protects against diabetes whilst others suggest that alcohol may be an independent risk factor, at least in men. Abnormalities in glucose tolerance among heavy alcohol users usually resolve with abstention.
For patients with established diabetes, the consequences of alcohol use on peripheral blood glucose levels are variable and dependent upon a number of factors. Problems with hyper and hypoglycaemia are both possible and are influenced by both the amount and frequency ofalcohol use as well as the prevailing hormonal mileu. Alcohol effects glucose production by the liver by directly inhibiting hepatic gluconeogenesis. This can be balanced by reduced peripheral glucose uptake into muscle (i.e. insulin resistance) and therefore the overall effect on blood glucose levels may be neutral. To complicate matters further, alcohol has been shown, under laboratory conditions, to both enhance and impair insulin secretion and action!
The current consensus is that alcohol use within advised limits has no significant influence on long term glycaemic control. However, as it is well known that diabetes, per se, carries a 2-3 fold increased risk of premature death from cardiovascular disease, the putative benefits of alcohol in this area should not be ignored.
Alcohol and Oral hypoglycaemic agents
Alcohol can alter the metabolism of certain glucose lowering drugs (e.g. tolbutamide) and chlorpropamide can cause a Disulfiram-like reaction if used in combination with alcohol. There is also a risk of lactic acidosis with the biguanide metformin and this drug is contra-indicated inr patients with established liver disease or on-going alcohol misuse.
Alcohol and hypoglycaemia
In clinical practice, the major concern is the risk of hypoglycaemia with alcohol. Alcohol may! be associated with low blood glucose levels in aj number of ways:
• Alcohol-induced fasting hypoglycaemia
• Potentiation of drug-induced hypoglycaemia
• Reactive hypoglycaemia in susceptible individuals. After a prolonged fast, (6-36 hours), liver glycogen stores become depleted and an individual may become at risk from hypoglycaemia as a result of direct inhibition of hepatic gluconeogenesis by alcohol. Fortunately such a scenario is rare. More commonly alcohol has the ability to potentiate the effect of glucose lowering drugs such as insulin or sulphonylureas.
The brain is absolutely dependent upon a continuous supply of glucose from the peripheral circulation for normal function. Thus, as peripheral blood glucose levels begin to fall below normal, a complex and hierarchical system has evolved to protect glucose supply to neurones (Figure 1). Below 4.0 mmol/l, there is release of counter-regulatory (anti-insulin) hormones particularly glucagon, adrenaline, noradrenaline, cortisol and growth hormone. Between 3.5 and 3.0 mmol/l, patients develop characteristic warning symptoms (sweating, shaking and palpitations) as a consequence of activation of the autonomic nervous system. The perception of these symptoms which alert an individual to take appropriate action i.e. eat something. Unfortunately if blood glucose levels continue to fall, intellectual (cognitive) function deteriorates. At 2.5 mmol/l, blood flow to the brain increases in an attempt to enhance substrate delivery.
For patients with established diabetes, the consequences of alcohol use on peripheral blood glucose levels are variable and dependent upon a number of factors. Problems with hyper and hypoglycaemia are both possible and are influenced by both the amount and frequency ofalcohol use as well as the prevailing hormonal mileu. Alcohol effects glucose production by the liver by directly inhibiting hepatic gluconeogenesis. This can be balanced by reduced peripheral glucose uptake into muscle (i.e. insulin resistance) and therefore the overall effect on blood glucose levels may be neutral. To complicate matters further, alcohol has been shown, under laboratory conditions, to both enhance and impair insulin secretion and action!
The current consensus is that alcohol use within advised limits has no significant influence on long term glycaemic control. However, as it is well known that diabetes, per se, carries a 2-3 fold increased risk of premature death from cardiovascular disease, the putative benefits of alcohol in this area should not be ignored.
Alcohol and Oral hypoglycaemic agents
Alcohol can alter the metabolism of certain glucose lowering drugs (e.g. tolbutamide) and chlorpropamide can cause a Disulfiram-like reaction if used in combination with alcohol. There is also a risk of lactic acidosis with the biguanide metformin and this drug is contra-indicated inr patients with established liver disease or on-going alcohol misuse.
Alcohol and hypoglycaemia
In clinical practice, the major concern is the risk of hypoglycaemia with alcohol. Alcohol may! be associated with low blood glucose levels in aj number of ways:
• Alcohol-induced fasting hypoglycaemia
• Potentiation of drug-induced hypoglycaemia
• Reactive hypoglycaemia in susceptible individuals. After a prolonged fast, (6-36 hours), liver glycogen stores become depleted and an individual may become at risk from hypoglycaemia as a result of direct inhibition of hepatic gluconeogenesis by alcohol. Fortunately such a scenario is rare. More commonly alcohol has the ability to potentiate the effect of glucose lowering drugs such as insulin or sulphonylureas.
The brain is absolutely dependent upon a continuous supply of glucose from the peripheral circulation for normal function. Thus, as peripheral blood glucose levels begin to fall below normal, a complex and hierarchical system has evolved to protect glucose supply to neurones (Figure 1). Below 4.0 mmol/l, there is release of counter-regulatory (anti-insulin) hormones particularly glucagon, adrenaline, noradrenaline, cortisol and growth hormone. Between 3.5 and 3.0 mmol/l, patients develop characteristic warning symptoms (sweating, shaking and palpitations) as a consequence of activation of the autonomic nervous system. The perception of these symptoms which alert an individual to take appropriate action i.e. eat something. Unfortunately if blood glucose levels continue to fall, intellectual (cognitive) function deteriorates. At 2.5 mmol/l, blood flow to the brain increases in an attempt to enhance substrate delivery.
For patients with established diabetes, the consequences of alcohol use on peripheral blood glucose levels are variable and dependent upon a number of factors. Problems with hyper and hypoglycaemia are both possible and are influenced by both the amount and frequency ofalcohol use as well as the prevailing hormonal mileu. Alcohol effects glucose production by the liver by directly inhibiting hepatic gluconeogenesis. This can be balanced by reduced peripheral glucose uptake into muscle (i.e. insulin resistance) and therefore the overall effect on blood glucose levels may be neutral. To complicate matters further, alcohol has been shown, under laboratory conditions, to both enhance and impair insulin secretion and action!
The current consensus is that alcohol use within advised limits has no significant influence on long term glycaemic control. However, as it is well known that diabetes, per se, carries a 2-3 fold increased risk of premature death from cardiovascular disease, the putative benefits of alcohol in this area should not be ignored.
Alcohol and Oral hypoglycaemic agents
Alcohol can alter the metabolism of certain glucose lowering drugs (e.g. tolbutamide) and chlorpropamide can cause a Disulfiram-like reaction if used in combination with alcohol. There is also a risk of lactic acidosis with the biguanide metformin and this drug is contra-indicated inr patients with established liver disease or on-going alcohol misuse.
Alcohol and hypoglycaemia
In clinical practice, the major concern is the risk of hypoglycaemia with alcohol. Alcohol may! be associated with low blood glucose levels in aj number of ways:
• Alcohol-induced fasting hypoglycaemia
• Potentiation of drug-induced hypoglycaemia
• Reactive hypoglycaemia in susceptible individuals. After a prolonged fast, (6-36 hours), liver glycogen stores become depleted and an individual may become at risk from hypoglycaemia as a result of direct inhibition of hepatic gluconeogenesis by alcohol. Fortunately such a scenario is rare. More commonly alcohol has the ability to potentiate the effect of glucose lowering drugs such as insulin or sulphonylureas.
The brain is absolutely dependent upon a continuous supply of glucose from the peripheral circulation for normal function. Thus, as peripheral blood glucose levels begin to fall below normal, a complex and hierarchical system has evolved to protect glucose supply to neurones (Figure 1). Below 4.0 mmol/l, there is release of counter-regulatory (anti-insulin) hormones particularly glucagon, adrenaline, noradrenaline, cortisol and growth hormone. Between 3.5 and 3.0 mmol/l, patients develop characteristic warning symptoms (sweating, shaking and palpitations) as a consequence of activation of the autonomic nervous system. The perception of these symptoms which alert an individual to take appropriate action i.e. eat something. Unfortunately if blood glucose levels continue to fall, intellectual (cognitive) function deteriorates. At 2.5 mmol/l, blood flow to the brain increases in an attempt to enhance substrate delivery.
For patients with established diabetes, the consequences of alcohol use on peripheral blood glucose levels are variable and dependent upon a number of factors. Problems with hyper and hypoglycaemia are both possible and are influenced by both the amount and frequency ofalcohol use as well as the prevailing hormonal mileu. Alcohol effects glucose production by the liver by directly inhibiting hepatic gluconeogenesis. This can be balanced by reduced peripheral glucose uptake into muscle (i.e. insulin resistance) and therefore the overall effect on blood glucose levels may be neutral. To complicate matters further, alcohol has been shown, under laboratory conditions, to both enhance and impair insulin secretion and action!
The current consensus is that alcohol use within advised limits has no significant influence on long term glycaemic control. However, as it is well known that diabetes, per se, carries a 2-3 fold increased risk of premature death from cardiovascular disease, the putative benefits of alcohol in this area should not be ignored.
Alcohol and Oral hypoglycaemic agents
Alcohol can alter the metabolism of certain glucose lowering drugs (e.g. tolbutamide) and chlorpropamide can cause a Disulfiram-like reaction if used in combination with alcohol. There is also a risk of lactic acidosis with the biguanide metformin and this drug is contra-indicated inr patients with established liver disease or on-going alcohol misuse.
Alcohol and hypoglycaemia
In clinical practice, the major concern is the risk of hypoglycaemia with alcohol. Alcohol may! be associated with low blood glucose levels in aj number of ways:
• Alcohol-induced fasting hypoglycaemia
• Potentiation of drug-induced hypoglycaemia
• Reactive hypoglycaemia in susceptible individuals. After a prolonged fast, (6-36 hours), liver glycogen stores become depleted and an individual may become at risk from hypoglycaemia as a result of direct inhibition of hepatic gluconeogenesis by alcohol. Fortunately such a scenario is rare. More commonly alcohol has the ability to potentiate the effect of glucose lowering drugs such as insulin or sulphonylureas.
The brain is absolutely dependent upon a continuous supply of glucose from the peripheral circulation for normal function. Thus, as peripheral blood glucose levels begin to fall below normal, a complex and hierarchical system has evolved to protect glucose supply to neurones (Figure 1). Below 4.0 mmol/l, there is release of counter-regulatory (anti-insulin) hormones particularly glucagon, adrenaline, noradrenaline, cortisol and growth hormone. Between 3.5 and 3.0 mmol/l, patients develop characteristic warning symptoms (sweating, shaking and palpitations) as a consequence of activation of the autonomic nervous system. The perception of these symptoms which alert an individual to take appropriate action i.e. eat something. Unfortunately if blood glucose levels continue to fall, intellectual (cognitive) function deteriorates. At 2.5 mmol/l, blood flow to the brain increases in an attempt to enhance substrate delivery.
For patients with established diabetes, the consequences of alcohol use on peripheral blood glucose levels are variable and dependent upon a number of factors. Problems with hyper and hypoglycaemia are both possible and are influenced by both the amount and frequency ofalcohol use as well as the prevailing hormonal mileu. Alcohol effects glucose production by the liver by directly inhibiting hepatic gluconeogenesis. This can be balanced by reduced peripheral glucose uptake into muscle (i.e. insulin resistance) and therefore the overall effect on blood glucose levels may be neutral. To complicate matters further, alcohol has been shown, under laboratory conditions, to both enhance and impair insulin secretion and action!
The current consensus is that alcohol use within advised limits has no significant influence on long term glycaemic control. However, as it is well known that diabetes, per se, carries a 2-3 fold increased risk of premature death from cardiovascular disease, the putative benefits of alcohol in this area should not be ignored.
Alcohol and Oral hypoglycaemic agents
Alcohol can alter the metabolism of certain glucose lowering drugs (e.g. tolbutamide) and chlorpropamide can cause a Disulfiram-like reaction if used in combination with alcohol. There is also a risk of lactic acidosis with the biguanide metformin and this drug is contra-indicated inr patients with established liver disease or on-going alcohol misuse.
Alcohol and hypoglycaemia
In clinical practice, the major concern is the risk of hypoglycaemia with alcohol. Alcohol may! be associated with low blood glucose levels in aj number of ways:
• Alcohol-induced fasting hypoglycaemia
• Potentiation of drug-induced hypoglycaemia
• Reactive hypoglycaemia in susceptible individuals. After a prolonged fast, (6-36 hours), liver glycogen stores become depleted and an individual may become at risk from hypoglycaemia as a result of direct inhibition of hepatic gluconeogenesis by alcohol. Fortunately such a scenario is rare. More commonly alcohol has the ability to potentiate the effect of glucose lowering drugs such as insulin or sulphonylureas.
The brain is absolutely dependent upon a continuous supply of glucose from the peripheral circulation for normal function. Thus, as peripheral blood glucose levels begin to fall below normal, a complex and hierarchical system has evolved to protect glucose supply to neurones (Figure 1). Below 4.0 mmol/l, there is release of counter-regulatory (anti-insulin) hormones particularly glucagon, adrenaline, noradrenaline, cortisol and growth hormone. Between 3.5 and 3.0 mmol/l, patients develop characteristic warning symptoms (sweating, shaking and palpitations) as a consequence of activation of the autonomic nervous system. The perception of these symptoms which alert an individual to take appropriate action i.e. eat something. Unfortunately if blood glucose levels continue to fall, intellectual (cognitive) function deteriorates. At 2.5 mmol/l, blood flow to the brain increases in an attempt to enhance substrate delivery.
