Re: Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies
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Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies
Re: Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies
Questioning the Evidence for the Dietary Fat-Heart Theory: Deja Vue All Over Again
As every journalist knows, to generate interest on a well-worn topic you have to be a contrarian. Now meta-analyses to question the diet-heart are the latest fad – as evidenced in this paper (1). Nutrition has the dubious distinction of providing the greatest volume of re-cycled discoveries that are contrary to conventional wisdom. Most can be safely disregarded as fads, but some potentially have great public health relevance. Coronary heart disease (CHD) is still the commonest cause of death in industrialized countries, so our understanding of the causal process is of paramount importance. The recent determined challenges to the veracity of the dietary fat-heart theory are therefore a serious cause for concern.
The structure of the dietary-fat-heart theory is elegant and comprehensive. First recognized a century ago in animal experimental research, dietary cholesterol and saturated fat raise serum LDL-cholesterol, in turn promoting atheroma and thrombosis. This diet-serum lipids relationship has been replicated in a large number of meticulously conducted nutrition trials in humans (2). In cohort studies, like Framingham, and international comparisons, like the Seven Countries Study, elevated LDL-C powerfully predicts events in groups, and less precisely in individuals. A relatively small set of other lifestyle factors interacts with genes to modulate that risk. Current LDL-C lowering agents reduce events in the magnitude predicted by observational studies.
Then why the resurgent controversy? Skepticism appears to be driven by three concerns. First, a chorus of objections to dietary fats instead suggest that refined carbohydrates, in particular sugar, are the key nutrient raising LDL-C. However, this concern has been repeatedly addressed since the 1980s. The body of evidence from metabolic ward studies, observational studies and RCTs consistently suggests that sugars may indeed contribute to the rising prevalence of obesity and diabetes; however, they are only a weak risk factor for CHD (3). Second, the obesity/diabetes epidemic has seized huge attention in the public health nutrition debate. So much, in fact, that we have lost sight of the larger impact of saturated fat on serum cholesterol. Finally, contrarians argue that the absence of randomized controlled trials (RCT) demonstrating lower intake in saturated fatty acids reduces CHD leaves the dietary-fat heart theory “unproven” (4).
This last objection is a form of analytic fundamentalism that perennially haunts epidemiology like a bad debt. While the RCT is an invaluable tool to study the benefits/risks of medical interventions it is hardly the only logical design for testing hypotheses. Randomized experiments form only a small fraction of the evidence base across scientific disciplines. In evolution, geology, astrophysics and many others, the RCT plays no role whatsoever, yet strong theories with enormous predictive power have emerged. Has anyone seen an RCT on sympatric speciation or plate tectonics? Worse yet, if data from an RCT was obligatory evidence on which to base judgments, we would still be at a total loss as how to address humanity’s biggest challenge – climate change. Biomedicine also has its own exemplars- RCTs played no role in proving that smoking causes lung cancer, and the impact of air pollution on CHD and asthma has never been “proven” by that standard. Instead inter-locking steps of a causal pathway, leading through a series of inferences, more often link cause to consequence (5). When we look for the etiology of common diseases, lowly observational data usually provide the crucial information.
But the dietary-fat-heart sceptics face an even bigger challenge. At the zenith of the CHD epidemic, mortality in the US among persons 25+ was 746 per 100,000. Preventive campaigns based on the precepts of the dietary-fat-heart theory initiated a sharp and continuous decline in CHD death rates - a public health phenomenon that even cardiovascular epidemiologists refused to believe for at least 10 years. In 2013, the age-adjusted CHD mortality was 159/100,000, 77% lower than in 1968. Thus 1.5 million fewer deaths occurred than if the 1968 rate had persisted. Clearly, several interventions each played a role. Fewer cigarettes smoked, kick-started the CHD decline, and the shift to low-fat dairy products helped drive cholesterol down from 220 to 200 mg/dl. As shown in numerous countries, the precipitous decline in CHD mortality fits a model quantifying powerful declines in cholesterol, smoking and hypertension, plus medical interventions in more recent decades (7). It is sobering to recognize that the widespread use of aspirin in the US accounted for a larger mortality decline than surgery and angioplasty combined (7).
If the dietary-fat-heart theory was wrong, why, despite a steep increase in sugar consumption and obesity, have CHD mortality rates continued to drop 5% / year through 2013?
Health professionals have two essential social functions – to improve the quality of life of their patients and to reduce mortality. Over the last half century, the dietary-fat-heart theory has arguably contributed more to the health of the US population than any other single “theory” apart from tobacco control (another theory equally “unproven” by RCTs). We should continue to bet on the winners.
References
1. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies BMJ 2015; 351 doi: http://dx.doi.org/10.1136/
2. Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997;314:112-7.
3. Stanhope K, Medici V, Bremer AA, Lee V, Lam HD, Nunez MV, Guoxia X Chen GX, Nancy L Keim NL, Havel PJ. A dose-response study of consuming high-fructose corn syrup–sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults. Am J Clin Nutr 2015:10.3945 ; doi:10.3945/ajcn.114.100461
4. Zoë H, Julien SB, Stephen MC, Bruce Davies3, Nicholas S, James J D, Fergal G. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart 2015;2: doi:10.1136/openhrt-2014-000196.
5. Hill AB. The environment and disease: Association or causation? Proceedings Roy Soc Med 1965;58:295-300.
6. Cooper R, Stamler J, Dyer A, Garside D. The decline in mortality from coronary heart disease, U.S.A., 1968-1975. J Chron Dis 1978;31:709-720.
7. Ford ES1, Ajani UA, Croft JB, Critchley JA, Labarthe DR, Kottke TE, Giles WH, Capewell S. Explaining the decrease in U.S. deaths from coronary disease, 1980-2000. N Engl J Med. 2007;356:2388-98.
Rapid Response:
Re: Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies
Questioning the Evidence for the Dietary Fat-Heart Theory: Deja Vue All Over Again
As every journalist knows, to generate interest on a well-worn topic you have to be a contrarian. Now meta-analyses to question the diet-heart are the latest fad – as evidenced in this paper (1). Nutrition has the dubious distinction of providing the greatest volume of re-cycled discoveries that are contrary to conventional wisdom. Most can be safely disregarded as fads, but some potentially have great public health relevance. Coronary heart disease (CHD) is still the commonest cause of death in industrialized countries, so our understanding of the causal process is of paramount importance. The recent determined challenges to the veracity of the dietary fat-heart theory are therefore a serious cause for concern.
The structure of the dietary-fat-heart theory is elegant and comprehensive. First recognized a century ago in animal experimental research, dietary cholesterol and saturated fat raise serum LDL-cholesterol, in turn promoting atheroma and thrombosis. This diet-serum lipids relationship has been replicated in a large number of meticulously conducted nutrition trials in humans (2). In cohort studies, like Framingham, and international comparisons, like the Seven Countries Study, elevated LDL-C powerfully predicts events in groups, and less precisely in individuals. A relatively small set of other lifestyle factors interacts with genes to modulate that risk. Current LDL-C lowering agents reduce events in the magnitude predicted by observational studies.
Then why the resurgent controversy? Skepticism appears to be driven by three concerns. First, a chorus of objections to dietary fats instead suggest that refined carbohydrates, in particular sugar, are the key nutrient raising LDL-C. However, this concern has been repeatedly addressed since the 1980s. The body of evidence from metabolic ward studies, observational studies and RCTs consistently suggests that sugars may indeed contribute to the rising prevalence of obesity and diabetes; however, they are only a weak risk factor for CHD (3). Second, the obesity/diabetes epidemic has seized huge attention in the public health nutrition debate. So much, in fact, that we have lost sight of the larger impact of saturated fat on serum cholesterol. Finally, contrarians argue that the absence of randomized controlled trials (RCT) demonstrating lower intake in saturated fatty acids reduces CHD leaves the dietary-fat heart theory “unproven” (4).
This last objection is a form of analytic fundamentalism that perennially haunts epidemiology like a bad debt. While the RCT is an invaluable tool to study the benefits/risks of medical interventions it is hardly the only logical design for testing hypotheses. Randomized experiments form only a small fraction of the evidence base across scientific disciplines. In evolution, geology, astrophysics and many others, the RCT plays no role whatsoever, yet strong theories with enormous predictive power have emerged. Has anyone seen an RCT on sympatric speciation or plate tectonics? Worse yet, if data from an RCT was obligatory evidence on which to base judgments, we would still be at a total loss as how to address humanity’s biggest challenge – climate change. Biomedicine also has its own exemplars- RCTs played no role in proving that smoking causes lung cancer, and the impact of air pollution on CHD and asthma has never been “proven” by that standard. Instead inter-locking steps of a causal pathway, leading through a series of inferences, more often link cause to consequence (5). When we look for the etiology of common diseases, lowly observational data usually provide the crucial information.
But the dietary-fat-heart sceptics face an even bigger challenge. At the zenith of the CHD epidemic, mortality in the US among persons 25+ was 746 per 100,000. Preventive campaigns based on the precepts of the dietary-fat-heart theory initiated a sharp and continuous decline in CHD death rates - a public health phenomenon that even cardiovascular epidemiologists refused to believe for at least 10 years. In 2013, the age-adjusted CHD mortality was 159/100,000, 77% lower than in 1968. Thus 1.5 million fewer deaths occurred than if the 1968 rate had persisted. Clearly, several interventions each played a role. Fewer cigarettes smoked, kick-started the CHD decline, and the shift to low-fat dairy products helped drive cholesterol down from 220 to 200 mg/dl. As shown in numerous countries, the precipitous decline in CHD mortality fits a model quantifying powerful declines in cholesterol, smoking and hypertension, plus medical interventions in more recent decades (7). It is sobering to recognize that the widespread use of aspirin in the US accounted for a larger mortality decline than surgery and angioplasty combined (7).
If the dietary-fat-heart theory was wrong, why, despite a steep increase in sugar consumption and obesity, have CHD mortality rates continued to drop 5% / year through 2013?
Health professionals have two essential social functions – to improve the quality of life of their patients and to reduce mortality. Over the last half century, the dietary-fat-heart theory has arguably contributed more to the health of the US population than any other single “theory” apart from tobacco control (another theory equally “unproven” by RCTs). We should continue to bet on the winners.
References
1. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies BMJ 2015; 351 doi: http://dx.doi.org/10.1136/
2. Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997;314:112-7.
3. Stanhope K, Medici V, Bremer AA, Lee V, Lam HD, Nunez MV, Guoxia X Chen GX, Nancy L Keim NL, Havel PJ. A dose-response study of consuming high-fructose corn syrup–sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults. Am J Clin Nutr 2015:10.3945 ; doi:10.3945/ajcn.114.100461
4. Zoë H, Julien SB, Stephen MC, Bruce Davies3, Nicholas S, James J D, Fergal G. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart 2015;2: doi:10.1136/openhrt-2014-000196.
5. Hill AB. The environment and disease: Association or causation? Proceedings Roy Soc Med 1965;58:295-300.
6. Cooper R, Stamler J, Dyer A, Garside D. The decline in mortality from coronary heart disease, U.S.A., 1968-1975. J Chron Dis 1978;31:709-720.
7. Ford ES1, Ajani UA, Croft JB, Critchley JA, Labarthe DR, Kottke TE, Giles WH, Capewell S. Explaining the decrease in U.S. deaths from coronary disease, 1980-2000. N Engl J Med. 2007;356:2388-98.
Source: CDC; WONDER. Accessed May 7, 2015
Competing interests: No competing interests