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Hi All,

A new look at the statistics of alcohol being good for heart health suggests

that it

is not of benefit to take even moderate amounts of alcohol, it seems.

The below article is pdf-available and not yet in Medline.

Lancet 2005 366 (9501):1911-1912

Alcohol and ischaemic heart disease: probably no free lunch

Rod , Joanna Broad, Jennie Connor and Wells

A quarter of a century ago, The Lancet published an ecological observation by St

Leger and colleagues of “a strong and specific negative association between

ischaemic heart disease (IHD) deaths and alcohol consumption”.1 The authors

attributed the association to wine consumption and concluded that: “If wine is

ever

found to contain a constituent protective against IHD then we consider it almost

sacrilege that this constituent be isolated. The medicine is already in a highly

palatable form.”

This study was among a number published during the 1970s and 1980s supporting a

rare

good-news public-health story. In 1990, Ellison's2 provocative editorial

entitled

“Cheers”, encapsulated what remains the dominant belief today that “small to

moderate amounts of alcohol are good for your health”. The benefit is attributed

mainly to a protective effect of light to moderate drinking on IHD risk that is

believed to outweigh adverse health effects in this window of modest

consumption. A

meta-analysis confirmed these earlier observations: self-reported consumption of

between one and three standard alcoholic drinks (a standard drink included about

10

g of alcohol) a day is associated with a 20–25% reduction in the risk of IHD.3

We believe it timely to challenge this belief in a “window of protection” given

the

increasing evidence of uncontrollable confounding in non-randomised studies of

IHD.4

and 5

The counter argument to the apparent coronary protection has attributed the

observed

protective association to misclassification and confounding. Shaper and

colleagues

proposed that ex-drinkers who stopped drinking because of cardiovascular-related

illness (sick quitters) were often misclassified with never drinkers,6 thus

artifactually raising the coronary risk in non-drinkers. This hypothesis has now

been discarded as new studies report a protective association after excluding

ex-drinkers.7

The more likely explanation for an artifactual association—uncontrolled

confounding—has been too readily dismissed by many researchers, including

ourselves.7 and 8 But this year, Naimi and colleagues have revived the

confounding hypothesis using data on cardiovascular risk factors from a

telephone

survey of over 200 000 adults in the USA.4 Of 30 cardiovascular-associated risk

factors or groups of factors assessed, 27 (90%) were significantly more

prevalent in

non-drinkers than in light to moderate drinkers. The authors suggest residual

confounding or unmeasured effect modification could account for some or all of

the

reported coronary protective associations.

The recent debacle over postmenopausal hormone therapy and IHD is another

sobering

reminder that non-randomised studies have their weaknesses. After adjusting for

multiple potential confounders, the non-randomised Nurses' Health Study reported

a

halving of IHD risk associated with hormone therapy.9 Randomised trials have now

shown that hormone therapy does not reduce IHD risk and uncontrolled confounding

is

the most likely explanation for the non-randomised observations.5 The Nurses'

Health

Study investigators reported a protective association of a similar size between

light to moderate alcohol consumption and IHD as they did for hormone therapy

and

IHD.10

So why have we not been more critical of observations suggesting as little as

one to

three drinks a week is associated with a halving of IHD risk?10 Perhaps we have

been

blinded by the plausible biological mechanisms. Alcohol raises

HDL-cholesterol—estimated to account for about half the coronary protective

effect—and also has “aspirin-like” thrombolytic effects.11 However, in our

opinion

the answer lies more in the way the debate has been framed as a dichotomy; you

are

either a believer in IHD protection or a non-believer. We think the debate needs

to

be reframed to consider a middle ground that addresses the likelihood of

bidirectional confounding.

Although less palatable, there is more compelling evidence for a

coronary-protective

effect of moderate to heavy drinking than for light to moderate drinking.3 and

12 In

heavy drinkers, confounding will obscure rather than exaggerate any coronary

protection because of their heart-unhealthy behaviours.8 and 12 The observations

of

relatively “clean” coronary arteries in autopsy studies of alcoholics are also

consistent with a coronary-protective effect of heavy drinking.13

So if the debate is framed as coronary protection versus no coronary protection,

we

remain believers in protection. But the believers, perhaps convinced by the

evidence

of coronary protection in moderate to heavy drinkers, are overlooking the

potential

for confounding to account for much of the protective association in lighter

drinkers. Similarly, the non-believers have underestimated the potential for

confounding (in the opposite direction) to obscure a real coronary-protective

effect

of heavier drinking.

Any coronary protection from light to moderate drinking will be very small and

unlikely to outweigh the harms. While moderate to heavy drinking is probably

coronary-protective, any benefit will be overwhelmed by the known harms.14 If

so,

the public-health message is clear. Do not assume there is a window in which the

health benefits of alcohol are greater than the harms—there is probably no free

lunch.

This paper was part of an investigator-initiated project on the burden of

alcohol-related disease and disability in New Zealand funded by the Alcohol

Advisory

Council of New Zealand (ALAC). ALAC is funded by a levy on alcohol produced and

imported for sale in New Zealand, and aims to encourage responsible use and

minimise

misuse. We declare that we have no conflict of interest.

Al Pater, PhD; email: old542000@...

__________________________________________

DSL – Something to write home about.

Just $16.99/mo. or less.

dsl.

Link to comment
Share on other sites

Hi folks:

It seems to me like this article is a poorly disguised effort to

raise funds (for their group) for a randomized study of alcoholic

beverage consumption and heart disease. I am sure such a study, if

well organized, would be helpful.

However, it seems to me they have a hypothesis, but do not, as far as

I can see, present any EVIDENCE to support it. Instead they lament

the absence of randomized studies to prove their point.

Also they repeatedly use the word 'alcohol' when there have been

serious studies that indicate it is probably not the alcohol that is

responsible. There are a number of (apparently unbiased) studies

that appear to indicate wine to be far preferable to other alcoholic

drinks. There is at least one study which showed that a wine

component, resveratrol, alone had an effect very similar to wine.

So, let's see, if they get the funding it appears they are looking

for, what their results show, whenever it is they get around to

publishing them. In the meantime I will be acting in response to the

data we already have, rather than the data this group wonders if it

might get X years down the road, if they can get funding.

I can see that arguing in favor of dealcoholized wine has much to be

said in its favor from the health viewpoint, if not in product

quality. I can also see some possible relevance to the view that

wine may principally help those at highest risk of CVD. Which would

not include most of us here. However these propositions have not

been seriously examined yet either, as far as I know.

Rodney.

--- In , Al Pater <old542000@y...>

wrote:

>

> Hi All,

>

> A new look at the statistics of alcohol being good for heart health

suggests that it

> is not of benefit to take even moderate amounts of alcohol, it

seems.

>

> The below article is pdf-available and not yet in Medline.

>

> Lancet 2005 366 (9501):1911-1912

> Alcohol and ischaemic heart disease: probably no free lunch

> Rod , Joanna Broad, Jennie Connor and Wells

>

> A quarter of a century ago, The Lancet published an ecological

observation by St

> Leger and colleagues of " a strong and specific negative association

between

> ischaemic heart disease (IHD) deaths and alcohol consumption " .1 The

authors

> attributed the association to wine consumption and concluded

that: " If wine is ever

> found to contain a constituent protective against IHD then we

consider it almost

> sacrilege that this constituent be isolated. The medicine is

already in a highly

> palatable form. "

>

> This study was among a number published during the 1970s and 1980s

supporting a rare

> good-news public-health story. In 1990, Ellison's2 provocative

editorial entitled

> " Cheers " , encapsulated what remains the dominant belief today

that " small to

> moderate amounts of alcohol are good for your health " . The benefit

is attributed

> mainly to a protective effect of light to moderate drinking on IHD

risk that is

> believed to outweigh adverse health effects in this window of

modest consumption. A

> meta-analysis confirmed these earlier observations: self-reported

consumption of

> between one and three standard alcoholic drinks (a standard drink

included about 10

> g of alcohol) a day is associated with a 20–25% reduction in the

risk of IHD.3

>

> We believe it timely to challenge this belief in a " window of

protection " given the

> increasing evidence of uncontrollable confounding in non-randomised

studies of IHD.4

> and 5

>

> The counter argument to the apparent coronary protection has

attributed the observed

> protective association to misclassification and confounding. Shaper

and colleagues

> proposed that ex-drinkers who stopped drinking because of

cardiovascular-related

> illness (sick quitters) were often misclassified with never

drinkers,6 thus

> artifactually raising the coronary risk in non-drinkers. This

hypothesis has now

> been discarded as new studies report a protective association after

excluding

> ex-drinkers.7

>

> The more likely explanation for an artifactual association—

uncontrolled

> confounding—has been too readily dismissed by many researchers,

including

> ourselves.7 and 8 But this year, Naimi and colleagues have

revived the

> confounding hypothesis using data on cardiovascular risk factors

from a telephone

> survey of over 200 000 adults in the USA.4 Of 30 cardiovascular-

associated risk

> factors or groups of factors assessed, 27 (90%) were significantly

more prevalent in

> non-drinkers than in light to moderate drinkers. The authors

suggest residual

> confounding or unmeasured effect modification could account for

some or all of the

> reported coronary protective associations.

>

> The recent debacle over postmenopausal hormone therapy and IHD is

another sobering

> reminder that non-randomised studies have their weaknesses. After

adjusting for

> multiple potential confounders, the non-randomised Nurses' Health

Study reported a

> halving of IHD risk associated with hormone therapy.9 Randomised

trials have now

> shown that hormone therapy does not reduce IHD risk and

uncontrolled confounding is

> the most likely explanation for the non-randomised observations.5

The Nurses' Health

> Study investigators reported a protective association of a similar

size between

> light to moderate alcohol consumption and IHD as they did for

hormone therapy and

> IHD.10

>

> So why have we not been more critical of observations suggesting as

little as one to

> three drinks a week is associated with a halving of IHD risk?10

Perhaps we have been

> blinded by the plausible biological mechanisms. Alcohol raises

> HDL-cholesterol—estimated to account for about half the coronary

protective

> effect—and also has " aspirin-like " thrombolytic effects.11 However,

in our opinion

> the answer lies more in the way the debate has been framed as a

dichotomy; you are

> either a believer in IHD protection or a non-believer. We think the

debate needs to

> be reframed to consider a middle ground that addresses the

likelihood of

> bidirectional confounding.

>

> Although less palatable, there is more compelling evidence for a

coronary-protective

> effect of moderate to heavy drinking than for light to moderate

drinking.3 and 12 In

> heavy drinkers, confounding will obscure rather than exaggerate any

coronary

> protection because of their heart-unhealthy behaviours.8 and 12 The

observations of

> relatively " clean " coronary arteries in autopsy studies of

alcoholics are also

> consistent with a coronary-protective effect of heavy drinking.13

>

> So if the debate is framed as coronary protection versus no

coronary protection, we

> remain believers in protection. But the believers, perhaps

convinced by the evidence

> of coronary protection in moderate to heavy drinkers, are

overlooking the potential

> for confounding to account for much of the protective association

in lighter

> drinkers. Similarly, the non-believers have underestimated the

potential for

> confounding (in the opposite direction) to obscure a real coronary-

protective effect

> of heavier drinking.

>

> Any coronary protection from light to moderate drinking will be

very small and

> unlikely to outweigh the harms. While moderate to heavy drinking is

probably

> coronary-protective, any benefit will be overwhelmed by the known

harms.14 If so,

> the public-health message is clear. Do not assume there is a window

in which the

> health benefits of alcohol are greater than the harms—there is

probably no free

> lunch.

>

> This paper was part of an investigator-initiated project on the

burden of

> alcohol-related disease and disability in New Zealand funded by the

Alcohol Advisory

> Council of New Zealand (ALAC). ALAC is funded by a levy on alcohol

produced and

> imported for sale in New Zealand, and aims to encourage responsible

use and minimise

> misuse. We declare that we have no conflict of interest.

>

> Al Pater, PhD; email: old542000@y...

>

>

>

> __________________________________________

> DSL – Something to write home about.

> Just $16.99/mo. or less.

> dsl.

>

Link to comment
Share on other sites

Hi folks:

It seems to me like this article is a poorly disguised effort to

raise funds (for their group) for a randomized study of alcoholic

beverage consumption and heart disease. I am sure such a study, if

well organized, would be helpful.

However, it seems to me they have a hypothesis, but do not, as far as

I can see, present any EVIDENCE to support it. Instead they lament

the absence of randomized studies to prove their point.

Also they repeatedly use the word 'alcohol' when there have been

serious studies that indicate it is probably not the alcohol that is

responsible. There are a number of (apparently unbiased) studies

that appear to indicate wine to be far preferable to other alcoholic

drinks. There is at least one study which showed that a wine

component, resveratrol, alone had an effect very similar to wine.

So, let's see, if they get the funding it appears they are looking

for, what their results show, whenever it is they get around to

publishing them. In the meantime I will be acting in response to the

data we already have, rather than the data this group wonders if it

might get X years down the road, if they can get funding.

I can see that arguing in favor of dealcoholized wine has much to be

said in its favor from the health viewpoint, if not in product

quality. I can also see some possible relevance to the view that

wine may principally help those at highest risk of CVD. Which would

not include most of us here. However these propositions have not

been seriously examined yet either, as far as I know.

Rodney.

--- In , Al Pater <old542000@y...>

wrote:

>

> Hi All,

>

> A new look at the statistics of alcohol being good for heart health

suggests that it

> is not of benefit to take even moderate amounts of alcohol, it

seems.

>

> The below article is pdf-available and not yet in Medline.

>

> Lancet 2005 366 (9501):1911-1912

> Alcohol and ischaemic heart disease: probably no free lunch

> Rod , Joanna Broad, Jennie Connor and Wells

>

> A quarter of a century ago, The Lancet published an ecological

observation by St

> Leger and colleagues of " a strong and specific negative association

between

> ischaemic heart disease (IHD) deaths and alcohol consumption " .1 The

authors

> attributed the association to wine consumption and concluded

that: " If wine is ever

> found to contain a constituent protective against IHD then we

consider it almost

> sacrilege that this constituent be isolated. The medicine is

already in a highly

> palatable form. "

>

> This study was among a number published during the 1970s and 1980s

supporting a rare

> good-news public-health story. In 1990, Ellison's2 provocative

editorial entitled

> " Cheers " , encapsulated what remains the dominant belief today

that " small to

> moderate amounts of alcohol are good for your health " . The benefit

is attributed

> mainly to a protective effect of light to moderate drinking on IHD

risk that is

> believed to outweigh adverse health effects in this window of

modest consumption. A

> meta-analysis confirmed these earlier observations: self-reported

consumption of

> between one and three standard alcoholic drinks (a standard drink

included about 10

> g of alcohol) a day is associated with a 20–25% reduction in the

risk of IHD.3

>

> We believe it timely to challenge this belief in a " window of

protection " given the

> increasing evidence of uncontrollable confounding in non-randomised

studies of IHD.4

> and 5

>

> The counter argument to the apparent coronary protection has

attributed the observed

> protective association to misclassification and confounding. Shaper

and colleagues

> proposed that ex-drinkers who stopped drinking because of

cardiovascular-related

> illness (sick quitters) were often misclassified with never

drinkers,6 thus

> artifactually raising the coronary risk in non-drinkers. This

hypothesis has now

> been discarded as new studies report a protective association after

excluding

> ex-drinkers.7

>

> The more likely explanation for an artifactual association—

uncontrolled

> confounding—has been too readily dismissed by many researchers,

including

> ourselves.7 and 8 But this year, Naimi and colleagues have

revived the

> confounding hypothesis using data on cardiovascular risk factors

from a telephone

> survey of over 200 000 adults in the USA.4 Of 30 cardiovascular-

associated risk

> factors or groups of factors assessed, 27 (90%) were significantly

more prevalent in

> non-drinkers than in light to moderate drinkers. The authors

suggest residual

> confounding or unmeasured effect modification could account for

some or all of the

> reported coronary protective associations.

>

> The recent debacle over postmenopausal hormone therapy and IHD is

another sobering

> reminder that non-randomised studies have their weaknesses. After

adjusting for

> multiple potential confounders, the non-randomised Nurses' Health

Study reported a

> halving of IHD risk associated with hormone therapy.9 Randomised

trials have now

> shown that hormone therapy does not reduce IHD risk and

uncontrolled confounding is

> the most likely explanation for the non-randomised observations.5

The Nurses' Health

> Study investigators reported a protective association of a similar

size between

> light to moderate alcohol consumption and IHD as they did for

hormone therapy and

> IHD.10

>

> So why have we not been more critical of observations suggesting as

little as one to

> three drinks a week is associated with a halving of IHD risk?10

Perhaps we have been

> blinded by the plausible biological mechanisms. Alcohol raises

> HDL-cholesterol—estimated to account for about half the coronary

protective

> effect—and also has " aspirin-like " thrombolytic effects.11 However,

in our opinion

> the answer lies more in the way the debate has been framed as a

dichotomy; you are

> either a believer in IHD protection or a non-believer. We think the

debate needs to

> be reframed to consider a middle ground that addresses the

likelihood of

> bidirectional confounding.

>

> Although less palatable, there is more compelling evidence for a

coronary-protective

> effect of moderate to heavy drinking than for light to moderate

drinking.3 and 12 In

> heavy drinkers, confounding will obscure rather than exaggerate any

coronary

> protection because of their heart-unhealthy behaviours.8 and 12 The

observations of

> relatively " clean " coronary arteries in autopsy studies of

alcoholics are also

> consistent with a coronary-protective effect of heavy drinking.13

>

> So if the debate is framed as coronary protection versus no

coronary protection, we

> remain believers in protection. But the believers, perhaps

convinced by the evidence

> of coronary protection in moderate to heavy drinkers, are

overlooking the potential

> for confounding to account for much of the protective association

in lighter

> drinkers. Similarly, the non-believers have underestimated the

potential for

> confounding (in the opposite direction) to obscure a real coronary-

protective effect

> of heavier drinking.

>

> Any coronary protection from light to moderate drinking will be

very small and

> unlikely to outweigh the harms. While moderate to heavy drinking is

probably

> coronary-protective, any benefit will be overwhelmed by the known

harms.14 If so,

> the public-health message is clear. Do not assume there is a window

in which the

> health benefits of alcohol are greater than the harms—there is

probably no free

> lunch.

>

> This paper was part of an investigator-initiated project on the

burden of

> alcohol-related disease and disability in New Zealand funded by the

Alcohol Advisory

> Council of New Zealand (ALAC). ALAC is funded by a levy on alcohol

produced and

> imported for sale in New Zealand, and aims to encourage responsible

use and minimise

> misuse. We declare that we have no conflict of interest.

>

> Al Pater, PhD; email: old542000@y...

>

>

>

> __________________________________________

> DSL – Something to write home about.

> Just $16.99/mo. or less.

> dsl.

>

Link to comment
Share on other sites

Hi Rodney,I think the study highlighted a major problem with many of the human-based studies that we must rely on (e.g., green tea benefits, etc.). The inherent confounding factors are especially troubling when comparing groups of people from different countries (such as is often done, for example, in assessing the effects of dairy intake on health).TomOn Dec 2, 2005, at 2:09 PM, Rodney wrote: Hi folks: It seems to me like this article is a poorly disguised effort to raise funds (for their group) for a randomized study of alcoholic beverage consumption and heart disease.   I am sure such a study, if well organized, would be helpful. However, it seems to me they have a hypothesis, but do not, as far as I can see, present any EVIDENCE to support it.  Instead they lament the absence of randomized studies to prove their point. Also they repeatedly use the word 'alcohol' when there have been serious studies that indicate it is probably not the alcohol that is responsible.  There are a number of (apparently unbiased) studies that appear to indicate wine to be far preferable to other alcoholic drinks.  There is at least one study which showed that a wine component, resveratrol, alone had an effect very similar to wine. So, let's see, if they get the funding it appears they are looking for, what their results show, whenever it is they get around to publishing them.  In the meantime I will be acting in response to the data we already have, rather than the data this group wonders if it might get X years down the road, if they can get funding. I can see that arguing in favor of dealcoholized wine has much to be said in its favor from the health viewpoint, if not in product quality.  I can also see some possible relevance to the view that wine may principally help those at highest risk of CVD.  Which would not include most of us here.  However these propositions have not been seriously examined yet either, as far as I know. Rodney. > > Hi All, > > A new look at the statistics of alcohol being good for heart health suggests that it > is not of benefit to take even moderate amounts of alcohol, it seems. > > The below article is pdf-available and not yet in Medline. > > Lancet 2005 366 (9501):1911-1912 > Alcohol and ischaemic heart disease: probably no free lunch > Rod , Joanna Broad, Jennie Connor and Wells >  > A quarter of a century ago, The Lancet published an ecological observation by St > Leger and colleagues of "a strong and specific negative association between > ischaemic heart disease (IHD) deaths and alcohol consumption".1 The authors > attributed the association to wine consumption and concluded that: "If wine is ever > found to contain a constituent protective against IHD then we consider it almost > sacrilege that this constituent be isolated. The medicine is already in a highly > palatable form." > > This study was among a number published during the 1970s and 1980s supporting a rare > good-news public-health story. In 1990, Ellison's2 provocative editorial entitled > "Cheers", encapsulated what remains the dominant belief today that "small to > moderate amounts of alcohol are good for your health". The benefit is attributed > mainly to a protective effect of light to moderate drinking on IHD risk that is > believed to outweigh adverse health effects in this window of modest consumption. A > meta-analysis confirmed these earlier observations: self-reported consumption of > between one and three standard alcoholic drinks (a standard drink included about 10 > g of alcohol) a day is associated with a 20–25% reduction in the risk of IHD.3 > > We believe it timely to challenge this belief in a "window of protection" given the > increasing evidence of uncontrollable confounding in non-randomised studies of IHD.4 > and 5 > > The counter argument to the apparent coronary protection has attributed the observed > protective association to misclassification and confounding. Shaper and colleagues > proposed that ex-drinkers who stopped drinking because of cardiovascular-related > illness (sick quitters) were often misclassified with never drinkers,6 thus > artifactually raising the coronary risk in non-drinkers. This hypothesis has now > been discarded as new studies report a protective association after excluding > ex-drinkers.7 > > The more likely explanation for an artifactual association— uncontrolled > confounding—has been too readily dismissed by many researchers, including > ourselves.7 and 8 But this year, Naimi and colleagues have revived the > confounding hypothesis using data on cardiovascular risk factors from a telephone > survey of over 200 000 adults in the USA.4 Of 30 cardiovascular- associated risk > factors or groups of factors assessed, 27 (90%) were significantly more prevalent in > non-drinkers than in light to moderate drinkers. The authors suggest residual > confounding or unmeasured effect modification could account for some or all of the > reported coronary protective associations. > > The recent debacle over postmenopausal hormone therapy and IHD is another sobering > reminder that non-randomised studies have their weaknesses. After adjusting for > multiple potential confounders, the non-randomised Nurses' Health Study reported a > halving of IHD risk associated with hormone therapy.9 Randomised trials have now > shown that hormone therapy does not reduce IHD risk and uncontrolled confounding is > the most likely explanation for the non-randomised observations.5 The Nurses' Health > Study investigators reported a protective association of a similar size between > light to moderate alcohol consumption and IHD as they did for hormone therapy and > IHD.10 > > So why have we not been more critical of observations suggesting as little as one to > three drinks a week is associated with a halving of IHD risk?10 Perhaps we have been > blinded by the plausible biological mechanisms. Alcohol raises > HDL-cholesterol—estimated to account for about half the coronary protective > effect—and also has "aspirin-like" thrombolytic effects.11 However, in our opinion > the answer lies more in the way the debate has been framed as a dichotomy; you are > either a believer in IHD protection or a non-believer. We think the debate needs to > be reframed to consider a middle ground that addresses the likelihood of > bidirectional confounding. > > Although less palatable, there is more compelling evidence for a coronary-protective > effect of moderate to heavy drinking than for light to moderate drinking.3 and 12 In > heavy drinkers, confounding will obscure rather than exaggerate any coronary > protection because of their heart-unhealthy behaviours.8 and 12 The observations of > relatively "clean" coronary arteries in autopsy studies of alcoholics are also > consistent with a coronary-protective effect of heavy drinking.13 > > So if the debate is framed as coronary protection versus no coronary protection, we > remain believers in protection. But the believers, perhaps convinced by the evidence > of coronary protection in moderate to heavy drinkers, are overlooking the potential > for confounding to account for much of the protective association in lighter > drinkers. Similarly, the non-believers have underestimated the potential for > confounding (in the opposite direction) to obscure a real coronary- protective effect > of heavier drinking. > > Any coronary protection from light to moderate drinking will be very small and > unlikely to outweigh the harms. While moderate to heavy drinking is probably > coronary-protective, any benefit will be overwhelmed by the known harms.14 If so, > the public-health message is clear. Do not assume there is a window in which the > health benefits of alcohol are greater than the harms—there is probably no free > lunch. > > This paper was part of an investigator-initiated project on the burden of > alcohol-related disease and disability in New Zealand funded by the Alcohol Advisory > Council of New Zealand (ALAC). ALAC is funded by a levy on alcohol produced and > imported for sale in New Zealand, and aims to encourage responsible use and minimise > misuse. We declare that we have no conflict of interest. > > Al Pater, PhD; email: old542000@y... > > >             > __________________________________________ > DSL – Something to write home about. > Just $16.99/mo. or less. > dsl. >

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Hi Rodney,I think the study highlighted a major problem with many of the human-based studies that we must rely on (e.g., green tea benefits, etc.). The inherent confounding factors are especially troubling when comparing groups of people from different countries (such as is often done, for example, in assessing the effects of dairy intake on health).TomOn Dec 2, 2005, at 2:09 PM, Rodney wrote: Hi folks: It seems to me like this article is a poorly disguised effort to raise funds (for their group) for a randomized study of alcoholic beverage consumption and heart disease.   I am sure such a study, if well organized, would be helpful. However, it seems to me they have a hypothesis, but do not, as far as I can see, present any EVIDENCE to support it.  Instead they lament the absence of randomized studies to prove their point. Also they repeatedly use the word 'alcohol' when there have been serious studies that indicate it is probably not the alcohol that is responsible.  There are a number of (apparently unbiased) studies that appear to indicate wine to be far preferable to other alcoholic drinks.  There is at least one study which showed that a wine component, resveratrol, alone had an effect very similar to wine. So, let's see, if they get the funding it appears they are looking for, what their results show, whenever it is they get around to publishing them.  In the meantime I will be acting in response to the data we already have, rather than the data this group wonders if it might get X years down the road, if they can get funding. I can see that arguing in favor of dealcoholized wine has much to be said in its favor from the health viewpoint, if not in product quality.  I can also see some possible relevance to the view that wine may principally help those at highest risk of CVD.  Which would not include most of us here.  However these propositions have not been seriously examined yet either, as far as I know. Rodney. > > Hi All, > > A new look at the statistics of alcohol being good for heart health suggests that it > is not of benefit to take even moderate amounts of alcohol, it seems. > > The below article is pdf-available and not yet in Medline. > > Lancet 2005 366 (9501):1911-1912 > Alcohol and ischaemic heart disease: probably no free lunch > Rod , Joanna Broad, Jennie Connor and Wells >  > A quarter of a century ago, The Lancet published an ecological observation by St > Leger and colleagues of "a strong and specific negative association between > ischaemic heart disease (IHD) deaths and alcohol consumption".1 The authors > attributed the association to wine consumption and concluded that: "If wine is ever > found to contain a constituent protective against IHD then we consider it almost > sacrilege that this constituent be isolated. The medicine is already in a highly > palatable form." > > This study was among a number published during the 1970s and 1980s supporting a rare > good-news public-health story. In 1990, Ellison's2 provocative editorial entitled > "Cheers", encapsulated what remains the dominant belief today that "small to > moderate amounts of alcohol are good for your health". The benefit is attributed > mainly to a protective effect of light to moderate drinking on IHD risk that is > believed to outweigh adverse health effects in this window of modest consumption. A > meta-analysis confirmed these earlier observations: self-reported consumption of > between one and three standard alcoholic drinks (a standard drink included about 10 > g of alcohol) a day is associated with a 20–25% reduction in the risk of IHD.3 > > We believe it timely to challenge this belief in a "window of protection" given the > increasing evidence of uncontrollable confounding in non-randomised studies of IHD.4 > and 5 > > The counter argument to the apparent coronary protection has attributed the observed > protective association to misclassification and confounding. Shaper and colleagues > proposed that ex-drinkers who stopped drinking because of cardiovascular-related > illness (sick quitters) were often misclassified with never drinkers,6 thus > artifactually raising the coronary risk in non-drinkers. This hypothesis has now > been discarded as new studies report a protective association after excluding > ex-drinkers.7 > > The more likely explanation for an artifactual association— uncontrolled > confounding—has been too readily dismissed by many researchers, including > ourselves.7 and 8 But this year, Naimi and colleagues have revived the > confounding hypothesis using data on cardiovascular risk factors from a telephone > survey of over 200 000 adults in the USA.4 Of 30 cardiovascular- associated risk > factors or groups of factors assessed, 27 (90%) were significantly more prevalent in > non-drinkers than in light to moderate drinkers. The authors suggest residual > confounding or unmeasured effect modification could account for some or all of the > reported coronary protective associations. > > The recent debacle over postmenopausal hormone therapy and IHD is another sobering > reminder that non-randomised studies have their weaknesses. After adjusting for > multiple potential confounders, the non-randomised Nurses' Health Study reported a > halving of IHD risk associated with hormone therapy.9 Randomised trials have now > shown that hormone therapy does not reduce IHD risk and uncontrolled confounding is > the most likely explanation for the non-randomised observations.5 The Nurses' Health > Study investigators reported a protective association of a similar size between > light to moderate alcohol consumption and IHD as they did for hormone therapy and > IHD.10 > > So why have we not been more critical of observations suggesting as little as one to > three drinks a week is associated with a halving of IHD risk?10 Perhaps we have been > blinded by the plausible biological mechanisms. Alcohol raises > HDL-cholesterol—estimated to account for about half the coronary protective > effect—and also has "aspirin-like" thrombolytic effects.11 However, in our opinion > the answer lies more in the way the debate has been framed as a dichotomy; you are > either a believer in IHD protection or a non-believer. We think the debate needs to > be reframed to consider a middle ground that addresses the likelihood of > bidirectional confounding. > > Although less palatable, there is more compelling evidence for a coronary-protective > effect of moderate to heavy drinking than for light to moderate drinking.3 and 12 In > heavy drinkers, confounding will obscure rather than exaggerate any coronary > protection because of their heart-unhealthy behaviours.8 and 12 The observations of > relatively "clean" coronary arteries in autopsy studies of alcoholics are also > consistent with a coronary-protective effect of heavy drinking.13 > > So if the debate is framed as coronary protection versus no coronary protection, we > remain believers in protection. But the believers, perhaps convinced by the evidence > of coronary protection in moderate to heavy drinkers, are overlooking the potential > for confounding to account for much of the protective association in lighter > drinkers. Similarly, the non-believers have underestimated the potential for > confounding (in the opposite direction) to obscure a real coronary- protective effect > of heavier drinking. > > Any coronary protection from light to moderate drinking will be very small and > unlikely to outweigh the harms. While moderate to heavy drinking is probably > coronary-protective, any benefit will be overwhelmed by the known harms.14 If so, > the public-health message is clear. Do not assume there is a window in which the > health benefits of alcohol are greater than the harms—there is probably no free > lunch. > > This paper was part of an investigator-initiated project on the burden of > alcohol-related disease and disability in New Zealand funded by the Alcohol Advisory > Council of New Zealand (ALAC). ALAC is funded by a levy on alcohol produced and > imported for sale in New Zealand, and aims to encourage responsible use and minimise > misuse. We declare that we have no conflict of interest. > > Al Pater, PhD; email: old542000@y... > > >             > __________________________________________ > DSL – Something to write home about. > Just $16.99/mo. or less. > dsl. >

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