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SNOWMASS, COLO. – Cutting dietary fat intake remains a highly effective strategy for reducing coronary heart disease risk – but only so long as the replacement nutrients aren’t even bigger offenders, Dr. Robert A. Vogel said at the Annual Cardiovascular Conference at Snowmass.
In the face of decades of public health admonitions to reduce saturated fat intake, most Americans have increased their consumption of trans fats and simple carbohydrates, especially sugar. And therein lies a problem. Trans fats are far more harmful than saturated fats in terms of cardiovascular risk. And excessive sugar consumption is a major contributor to abdominal obesity, metabolic syndrome, hypertension, and endothelial dysfunction.
“In the United States, sugar is a bigger source of hypertension than is salt,” asserted Dr. Vogel, a cardiologist at the University of Colorado, Denver.
The editors of Time magazine ignited a public controversy last year with a cover story arrestingly titled, “Eat Butter – Scientists labelled fat the enemy. Why they were wrong.” The editors were picking up on a British meta-analysis of 32 observational studies that concluded there is no clear evidence to support the notion that saturated fats are harmful to cardiovascular health and that swapping them out for consumption of polyunsaturated fatty acids (PUFAs) is beneficial (Ann. Intern. Med. 2014;160:398-406).
Dr. Vogel said those investigators are in fact correct: Many of the observational studies – going all the way back to the pioneering work by Dr. Ancel Keys in the 1950s – are flawed. They don’t convincingly prove the case for PUFAs as a healthier alternative. But there is persuasive evidence from well-conducted, randomized, controlled trials that this is indeed so, he added.
Several of these studies were done in an earlier era when it was possible to slip around the challenges and limitations of dietary studies in free-living populations. These trials wouldn’t be possible today for ethical reasons involving lack of informed consent.
For example, in the Finnish Mental Hospital Study conducted during 1959-1971, the food served at two mental institutions was altered. Patients at one hospital got 6 years of a diet high in PUFAs, then were crossed over to a typical Finnish diet. At the other mental hospital, patients were fed a normal Finnish diet for 6 years, then crossed over to the high-PUFA diet for 6 years. During the experimental-diet years, the coronary heart disease event rate was reduced by nearly 60% (Int. J. Epidemiol. 1979;8:99-118).
Similarly, in a prospective randomized trial conducted at a Los Angeles Veterans Affairs institution for older, cognitively impaired men, a no-choice shift to a diet high in PUFAs with reduced saturated fats resulted in roughly a 30% reduction in CHD events compared to the usual institutional diet (Lancet 1968;2:1060-2). A similar magnitude of CHD event reduction was seen with a high-PUFA dietary intervention in the Oslo Diet-Heart Study, a prospective secondary prevention trial (Circulation 1970;42:935-42).
In the contemporary era, the standout randomized dietary intervention trial is the Lyon Diet Heart Study, a 46-month prospective secondary prevention trial in which a Mediterranean diet low in saturated fat and high in alpha-linoleic acid, a PUFA, reduced the combined endpoint of cardiac death and nonfatal MI by 70%, compared with the usual post-MI prudent diet recommended at that time. Yet total cholesterol levels in the two study arms did not differ (Circulation 1999;99:779-85).
To put these results into context, Dr. Vogel noted that the Cholesterol Treatment Trialists Collaboration headquartered at the University of Oxford (England) has shown that for every 40 mg/dL of LDL-lowering achieved with statin therapy, the result is roughly a 20% reduction in CHD. In contrast, the classic nonpharmacologic diet studies resulted in 30%-70% relative risk reductions.
“Heart disease is a dietary disease,” the cardiologist emphasized. “When you compare diet intervention to LDL lowering with statins, you see that diet is very, very effective. But you have to know the details of the diet. You can’t take something out and put just anything in. It doesn’t work like that.”
For example, an analysis of data from the National Health and Nutrition Examination Survey concluded that individuals who consumed 25% of their calories from added sugar – that’s the equivalent of three 12-oz cans of a sugary cola per day – had a 175% increased risk of cardiovascular mortality during a median 14.6 years of follow-up, compared with those who got less than 10% of their calories from added sugar (JAMA Intern. Med. 2014;174:516-24).
And as for the impact of the trans fat that’s liberally present in many processed foods, the Nurses Health Study showed that for every 5% increase in energy intake from saturated fat – that’s equivalent to one 8-oz steak per day – the relative risk for CHD rose by a relatively modest 17%, while for a 5% increase in energy intake from trans fat – the equivalent of 4 oz of butter – CHD risk shot up by 382% (N. Engl. J. Med. 1997;337:1491-9).
Dr. Vogel reported serving as a paid consultant to the National Football League and the Pritikin Longevity Center and receiving a research grant from Sanofi.
SNOWMASS, COLO. – Cutting dietary fat intake remains a highly effective strategy for reducing coronary heart disease risk – but only so long as the replacement nutrients aren’t even bigger offenders, Dr. Robert A. Vogel said at the Annual Cardiovascular Conference at Snowmass.
In the face of decades of public health admonitions to reduce saturated fat intake, most Americans have increased their consumption of trans fats and simple carbohydrates, especially sugar. And therein lies a problem. Trans fats are far more harmful than saturated fats in terms of cardiovascular risk. And excessive sugar consumption is a major contributor to abdominal obesity, metabolic syndrome, hypertension, and endothelial dysfunction.
“In the United States, sugar is a bigger source of hypertension than is salt,” asserted Dr. Vogel, a cardiologist at the University of Colorado, Denver.
The editors of Time magazine ignited a public controversy last year with a cover story arrestingly titled, “Eat Butter – Scientists labelled fat the enemy. Why they were wrong.” The editors were picking up on a British meta-analysis of 32 observational studies that concluded there is no clear evidence to support the notion that saturated fats are harmful to cardiovascular health and that swapping them out for consumption of polyunsaturated fatty acids (PUFAs) is beneficial (Ann. Intern. Med. 2014;160:398-406).
Dr. Vogel said those investigators are in fact correct: Many of the observational studies – going all the way back to the pioneering work by Dr. Ancel Keys in the 1950s – are flawed. They don’t convincingly prove the case for PUFAs as a healthier alternative. But there is persuasive evidence from well-conducted, randomized, controlled trials that this is indeed so, he added.
Several of these studies were done in an earlier era when it was possible to slip around the challenges and limitations of dietary studies in free-living populations. These trials wouldn’t be possible today for ethical reasons involving lack of informed consent.
For example, in the Finnish Mental Hospital Study conducted during 1959-1971, the food served at two mental institutions was altered. Patients at one hospital got 6 years of a diet high in PUFAs, then were crossed over to a typical Finnish diet. At the other mental hospital, patients were fed a normal Finnish diet for 6 years, then crossed over to the high-PUFA diet for 6 years. During the experimental-diet years, the coronary heart disease event rate was reduced by nearly 60% (Int. J. Epidemiol. 1979;8:99-118).
Similarly, in a prospective randomized trial conducted at a Los Angeles Veterans Affairs institution for older, cognitively impaired men, a no-choice shift to a diet high in PUFAs with reduced saturated fats resulted in roughly a 30% reduction in CHD events compared to the usual institutional diet (Lancet 1968;2:1060-2). A similar magnitude of CHD event reduction was seen with a high-PUFA dietary intervention in the Oslo Diet-Heart Study, a prospective secondary prevention trial (Circulation 1970;42:935-42).
In the contemporary era, the standout randomized dietary intervention trial is the Lyon Diet Heart Study, a 46-month prospective secondary prevention trial in which a Mediterranean diet low in saturated fat and high in alpha-linoleic acid, a PUFA, reduced the combined endpoint of cardiac death and nonfatal MI by 70%, compared with the usual post-MI prudent diet recommended at that time. Yet total cholesterol levels in the two study arms did not differ (Circulation 1999;99:779-85).
To put these results into context, Dr. Vogel noted that the Cholesterol Treatment Trialists Collaboration headquartered at the University of Oxford (England) has shown that for every 40 mg/dL of LDL-lowering achieved with statin therapy, the result is roughly a 20% reduction in CHD. In contrast, the classic nonpharmacologic diet studies resulted in 30%-70% relative risk reductions.
“Heart disease is a dietary disease,” the cardiologist emphasized. “When you compare diet intervention to LDL lowering with statins, you see that diet is very, very effective. But you have to know the details of the diet. You can’t take something out and put just anything in. It doesn’t work like that.”
For example, an analysis of data from the National Health and Nutrition Examination Survey concluded that individuals who consumed 25% of their calories from added sugar – that’s the equivalent of three 12-oz cans of a sugary cola per day – had a 175% increased risk of cardiovascular mortality during a median 14.6 years of follow-up, compared with those who got less than 10% of their calories from added sugar (JAMA Intern. Med. 2014;174:516-24).
And as for the impact of the trans fat that’s liberally present in many processed foods, the Nurses Health Study showed that for every 5% increase in energy intake from saturated fat – that’s equivalent to one 8-oz steak per day – the relative risk for CHD rose by a relatively modest 17%, while for a 5% increase in energy intake from trans fat – the equivalent of 4 oz of butter – CHD risk shot up by 382% (N. Engl. J. Med. 1997;337:1491-9).
Dr. Vogel reported serving as a paid consultant to the National Football League and the Pritikin Longevity Center and receiving a research grant from Sanofi.
SNOWMASS, COLO. – Cutting dietary fat intake remains a highly effective strategy for reducing coronary heart disease risk – but only so long as the replacement nutrients aren’t even bigger offenders, Dr. Robert A. Vogel said at the Annual Cardiovascular Conference at Snowmass.
In the face of decades of public health admonitions to reduce saturated fat intake, most Americans have increased their consumption of trans fats and simple carbohydrates, especially sugar. And therein lies a problem. Trans fats are far more harmful than saturated fats in terms of cardiovascular risk. And excessive sugar consumption is a major contributor to abdominal obesity, metabolic syndrome, hypertension, and endothelial dysfunction.
“In the United States, sugar is a bigger source of hypertension than is salt,” asserted Dr. Vogel, a cardiologist at the University of Colorado, Denver.
The editors of Time magazine ignited a public controversy last year with a cover story arrestingly titled, “Eat Butter – Scientists labelled fat the enemy. Why they were wrong.” The editors were picking up on a British meta-analysis of 32 observational studies that concluded there is no clear evidence to support the notion that saturated fats are harmful to cardiovascular health and that swapping them out for consumption of polyunsaturated fatty acids (PUFAs) is beneficial (Ann. Intern. Med. 2014;160:398-406).
Dr. Vogel said those investigators are in fact correct: Many of the observational studies – going all the way back to the pioneering work by Dr. Ancel Keys in the 1950s – are flawed. They don’t convincingly prove the case for PUFAs as a healthier alternative. But there is persuasive evidence from well-conducted, randomized, controlled trials that this is indeed so, he added.
Several of these studies were done in an earlier era when it was possible to slip around the challenges and limitations of dietary studies in free-living populations. These trials wouldn’t be possible today for ethical reasons involving lack of informed consent.
For example, in the Finnish Mental Hospital Study conducted during 1959-1971, the food served at two mental institutions was altered. Patients at one hospital got 6 years of a diet high in PUFAs, then were crossed over to a typical Finnish diet. At the other mental hospital, patients were fed a normal Finnish diet for 6 years, then crossed over to the high-PUFA diet for 6 years. During the experimental-diet years, the coronary heart disease event rate was reduced by nearly 60% (Int. J. Epidemiol. 1979;8:99-118).
Similarly, in a prospective randomized trial conducted at a Los Angeles Veterans Affairs institution for older, cognitively impaired men, a no-choice shift to a diet high in PUFAs with reduced saturated fats resulted in roughly a 30% reduction in CHD events compared to the usual institutional diet (Lancet 1968;2:1060-2). A similar magnitude of CHD event reduction was seen with a high-PUFA dietary intervention in the Oslo Diet-Heart Study, a prospective secondary prevention trial (Circulation 1970;42:935-42).
In the contemporary era, the standout randomized dietary intervention trial is the Lyon Diet Heart Study, a 46-month prospective secondary prevention trial in which a Mediterranean diet low in saturated fat and high in alpha-linoleic acid, a PUFA, reduced the combined endpoint of cardiac death and nonfatal MI by 70%, compared with the usual post-MI prudent diet recommended at that time. Yet total cholesterol levels in the two study arms did not differ (Circulation 1999;99:779-85).
To put these results into context, Dr. Vogel noted that the Cholesterol Treatment Trialists Collaboration headquartered at the University of Oxford (England) has shown that for every 40 mg/dL of LDL-lowering achieved with statin therapy, the result is roughly a 20% reduction in CHD. In contrast, the classic nonpharmacologic diet studies resulted in 30%-70% relative risk reductions.
“Heart disease is a dietary disease,” the cardiologist emphasized. “When you compare diet intervention to LDL lowering with statins, you see that diet is very, very effective. But you have to know the details of the diet. You can’t take something out and put just anything in. It doesn’t work like that.”
For example, an analysis of data from the National Health and Nutrition Examination Survey concluded that individuals who consumed 25% of their calories from added sugar – that’s the equivalent of three 12-oz cans of a sugary cola per day – had a 175% increased risk of cardiovascular mortality during a median 14.6 years of follow-up, compared with those who got less than 10% of their calories from added sugar (JAMA Intern. Med. 2014;174:516-24).
And as for the impact of the trans fat that’s liberally present in many processed foods, the Nurses Health Study showed that for every 5% increase in energy intake from saturated fat – that’s equivalent to one 8-oz steak per day – the relative risk for CHD rose by a relatively modest 17%, while for a 5% increase in energy intake from trans fat – the equivalent of 4 oz of butter – CHD risk shot up by 382% (N. Engl. J. Med. 1997;337:1491-9).
Dr. Vogel reported serving as a paid consultant to the National Football League and the Pritikin Longevity Center and receiving a research grant from Sanofi.
EXPERT ANALYSIS FROM THE CARDIOVASCULAR CONFERENCE AT SNOWMASS
