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Coronary Heart Disease Research: Sugar Industry influenced national conversation on heart disease – Adoption of Low Fat Diet vs Low Carbohydrates Diet


Coronary Heart Disease Research: Sugar Industry influenced national conversation on heart disease – Adoption of Low Fat Diet vs Low Carbohydrates Diet

Public Health Outcome:

  • Uncontrolled consumption of sugar prevailed 1965 – 2005 – role of sugar in CVD was played down

while

  • Consumption of fat become the diet factor to be control and monitored in the Medical community – role of Fat was the main focus and its management by Statins

and

  • FDA Food Pyramid evolution

USDA Food Pyramid History

In January 1977, after listening to the testimony of Ancel Keys and other doctors and scientists intent on promoting the unsupported Dietary Fat-Heart hypothesis, the Committee published the “Dietary Goals for the United States” recommending that all Americans reduce their fat, saturated fat and cholesterol consumption, and increase their carbohydrate consumption to 55-60% of daily calories.

http://www.healthy-eating-politics.com/usda-food-pyramid.html

Concerns that were raised with the first dietary recommendations 30 y ago have yet to be adequately addressed. The initial Dietary Goals for Americans (1977) proposed increases in carbohydrate intake and decreases in fat, saturated fat, cholesterol, and salt consumption that are carried further in the 2010 Dietary Guidelines Advisory Committee (DGAC) Report. Important aspects of these recommendations remain unproven, yet a dietary shift in this direction has already taken place even as overweight/obesity and diabetes have increased. Although appealing to an evidence-based methodology, the DGAC Report demonstrates several critical weaknesses, including use of an incomplete body of relevant science; inaccurately representing, interpreting, or summarizing the literature; and drawing conclusions and/or making recommendations that do not reflect the limitations or controversies in the science. An objective assessment of evidence in the DGAC Report does not suggest a conclusive proscription against low-carbohydrate diets. The DGAC Report does not provide sufficient evidence to conclude that increases in whole grain and fiber and decreases in dietary saturated fat, salt, and animal protein will lead to positive health outcomes. Lack of supporting evidence limits the value of the proposed recommendations as guidance for consumers or as the basis for public health policy. It is time to reexamine how US dietary guidelines are created and ask whether the current process is still appropriate for our needs.

http://www.nutritionjrnl.com/article/S0899-9007(10)00289-3/abstract

 

Curator: Aviva Lev-Ari, PhD, RN

 

UCSF reveals how sugar industry influenced national conversation on heart disease

 

Special Communication |

Sugar Industry and Coronary Heart Disease Research – A Historical Analysis of Internal Industry Documents

Cristin E. Kearns, DDS, MBA1,2; Laura A. Schmidt, PhD, MSW, MPH1,3,4; Stanton A. Glantz, PhD1,5,6,7,8
JAMA Intern Med. Published online September 12, 2016. doi:10.1001/jamainternmed.2016.5394

Corresponding Author: Stanton A. Glantz, PhD, UCSF Center for Tobacco Control Research and Education, 530 Parnassus Ave, Ste 366, San Francisco, CA 94143-1390 (glantz@medicine.ucsf.edu).

Accepted for Publication: July 2, 2016.

Published Online: September 12, 2016. doi:10.1001/jamainternmed.2016.5394

Author Contributions: Drs Kearns and Glantz had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of data analysis.

Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in the New England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review’s objective, contributed articles for inclusion, and received drafts. The SRF’s funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry–funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development.

These internal documents show that the SRF initiated CHD research in 1965 to protect market share and that its first project, a literature review, was published in NEJM in 1967 without disclosure of the sugar industry’s funding or role. The NEJM review served the sugar industry’s interests by arguing that epidemiologic, animal, and mechanistic studies associating sucrose with CHD were limited, implying they should not be included in an evidentiary assessment of the CHD risks of sucrose. Instead, the review argued that the only evidence modality needed to yield a definitive answer to the question of how to modify the American diet to prevent CHD was RCTs that exclusively used serum cholesterol level as a CHD biomarker. Randomized clinical trials using serum cholesterol level as the CHD biomarker made the high sucrose content of the American diet seem less hazardous than if the entire body of evidence had been considered.

Following the NEJM review, the sugar industry continued to fund research on CHD and other chronic diseases “as a main prop of the industry’s defense.”51 For example, in 1971, it influenced the National Institute of Dental Research’s National Caries Program to shift its emphasis to dental caries interventions other than restricting sucrose.8 The industry commissioned a review, “Sugar in the Diet of Man,” which it credited with, among other industry tactics, favorably influencing the 1976 US Food and Drug Administration evaluation of the safety of sugar.51 These findings, our analysis, and current Sugar Association criticisms of evidence linking sucrose to cardiovascular disease6,7 suggest the industry may have a long history of influencing federal policy.

This historical account of industry efforts demonstrates the importance of having reviews written by people without conflicts of interest and the need for financial disclosure. Scientific reviews shape policy debates, subsequent investigations, and the funding priorities of federal agencies.52 The NEJM has required authors to disclose all conflicts of interest since 1984,53 and conflict of interest disclosure policies have been widely implemented since the sugar industry launched its CHD research program. Whether current conflict of interest policies are adequate to withstand the economic interests of industry remains unclear.54

Many industries sponsor research to influence assessments of the risks and benefits of their products.55– 57The influence of industry sponsorship on nutrition research is receiving increased scrutiny.58 Access to documents not meant for public consumption has provided the public health community unprecedented insight into industry motives, strategies, tactics, and data designed to protect companies from litigation and regulation.59 This insight has been a major factor behind successful global tobacco control policies.60 Our analysis suggests that research using sugar industry documents has the potential to inform the health community about how to counter this industry’s strategies and tactics to control information on the adverse health effects of sucrose.

Study Limitations

The Roger Adams papers and other documents used in this research provide a narrow window into the activities of 1 sugar industry trade association; therefore, it is difficult to validate that the documents gathered are representative of the entirety of SRF internal materials related to Project 226 from the 1950s and 1960s or that the proper weight was given to each data source. There is no direct evidence that the sugar industry wrote or changed the NEJM review manuscript; the evidence that the industry shaped the review’s conclusions is circumstantial. We did not analyze the role of other organizations, nutrition leaders, or food industries that advocated that saturated fat and dietary cholesterol were the main dietary cause of CHD. We could not interview key actors involved in this historical episode because they have died.

This study suggests that the sugar industry sponsored its first CHD research project in 1965 to downplay early warning signals that sucrose consumption was a risk factor in CHD. As of 2016, sugar control policies are being promulgated in international,61 federal,62,63 state, and local venues.64 Yet CHD risk is inconsistently cited as a health consequence of added sugars consumption. Because CHD is the leading cause of death globally, the health community should ensure that CHD risk is evaluated in future risk assessments of added sugars. Policymaking committees should consider giving less weight to food industry–funded studies, and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development.65

 

REFERENCES

Council on Foods and Nutrition (American Medical Association).  The regulation of dietary fat: a report of the council. JAMA. 1962;181(5):411-429.
Link to Article

Yudkin  J. Pure, White and Deadly: The Problem of Sugar. London, England: Davis-Poynter Ltd; 1972.

Yudkin  J.  Diet and coronary thrombosis hypothesis and fact. Lancet. 1957;273(6987):155-162.
PubMed   |  Link to Article

Yudkin  J.  Dietary fat and dietary sugar in relation to ischaemic heart-disease and diabetes. Lancet. 1964;2(7349):4-5.
PubMed   |  Link to Article

Technical Group of Committee on Lipoproteins and Atherosclerosis and Committee on Lipoproteins and Atherosclerosis of National Advisory Heart Council.  Evaluation of serum lipoprotein and cholesterol measurements as predictors of clinical complications of atherosclerosis: report of a cooperative study of lipoproteins and atherosclerosisCirculation. 1956;14(4, pt 2):691-742.
PubMed

Albrink  MJ.  Carbohydrate metabolism in cardiovascular disease. Ann Intern Med. 1965;62(6):1330-1333.
PubMed   |  Link to Article

Taubes  G, Couzens  CK. Big sugar’s sweet little lies: how the industry kept scientists from asking, does sugar kill? 2012. http://www.motherjones.com/environment/2012/10/sugar-industry-lies-campaign Accessed October 17, 2014.

Bero  L.  Implications of the tobacco industry documents for public health and policy. Annu Rev Public Health. 2003;24:267-288.
PubMed   |  Link to Article

US Department of Health and Human Services and US Department of Agriculture. 2015-2020 Dietary Guidelines for Americans. 8th ed. Washington, DC: U.S. Government Printing Office; 2016.

US Food and Drug Administration. Changes to the nutrition facts label. 2016.http://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/LabelingNutrition/ucm385663.htm. Accessed June 7, 2016.

Miller  M, Stone  NJ, Ballantyne  C,  et al; American Heart Association Clinical Lipidology, Thrombosis, and Prevention Committee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Nursing; Council on the Kidney in Cardiovascular Disease.  Triglycerides and cardiovascular disease: a scientific statement from the American Heart AssociationCirculation. 2011;123(20):2292-2333.
PubMed   |  Link to Article

Teicholz  N. The Big Fat Surprise: Why Butter, Meat, and Cheese Belong in a Healthy Diet. New York, NY: Simon and Schuster; 2014.

 

Other related articles published in this Open Access Online Scientific Journal include the following:  

 

Metabolomics, Metabonomics and Functional Nutrition: The Next Step in Nutritional Metabolism and Biotherapeutics

Larry H. Bernstein, MD, FCAP  and Aviva Lev-Ari, PhD, RN

Reference Genes in the Human Gut Microbiome: The BGI Catalogue

Aviva Lev-Ari, PhD, RN

Two Mutations, in the PCSK9 Gene: Eliminates a Protein involved in Controlling LDL Cholesterol

Aviva Lev-Ari, PhD, RN

HDL-C: Target of Therapy – Steven E. Nissen, MD, MACC, Cleveland Clinic vs Peter Libby, MD, BWH

Aviva Lev-Ari, PhD, RN

 

The following articles in


Series A: e-Books on Cardiovascular Diseases

Series A Content Consultant: Justin D Pearlman, MD, PhD, FACC

VOLUME THREE

Etiologies of Cardiovascular Diseases:

Epigenetics, Genetics and Genomics

http://www.amazon.com/dp/B018PNHJ84

 

by  

Larry H Bernstein, MD, FCAP, Senior Editor, Author and Curator

and

Aviva Lev-Ari, PhD, RN, Editor and Curator

 

2.2.2: Endothelium, Angiogenesis, and Disordered Coagulation

 

2.2.2.1 What is the Role of Plasma Viscosity in Hemostasis and Vascular Disease Risk? 

Larry H Bernstein, MD, FACP and Aviva Lev-Ari, PhD, RN

 

2.2.2.2 Special Considerations in Blood Lipoproteins, Viscosity, Assessment and Treatment 

Larry H Bernstein, MD, FACP  and Aviva Lev-Ari, PhD, RN

 

2.2.2.3 Biomarkers and risk factors for cardiovascular events, endothelial dysfunction, and thromboembolic complication

Larry H Bernstein, MD, FCAP

 

2.2.2.4 A future for plasma metabolomics in cardiovascular disease assessment  

Larry H Bernstein, MD, FCAP
2.2.2.5 Nitric Oxide Function in Coagulation – Part II

Larry H Bernstein, MD, FACP

 

2.2.2.6 Nitric Oxide, Platelets, Endothelium and Hemostasis (Coagulation Part II)

Larry H Bernstein, MD, FACP

 

2.2.2.7 Peroxisome Proliferator-Activated Receptor (PPAR-gamma) Receptors Activation: PPARγ Transrepression for Angiogenesis in Cardiovascular Disease and PPARγ Transactivation for Treatment of Diabetes 

Aviva Lev-Ari, PhD, RN

Endothelium Inflammatory Biomarkers

 

2.2.2.8 Cardiovascular Risk: C-Reactive Protein BioMarker and Plasma Fibrinogen

Aviva Lev-Ari, PhD, RN

 

2.2.2.9 Cardiovascular Risk Inflammatory Marker: Risk Assessment for Coronary Heart Disease and Ischemic Stroke ­ – Atherosclerosis

Aviva Lev-Ari, PhD, RN

 

2.2.2.10 Importance of high sensitivity C-reactive protein (hs-CRP)

Larry H Bernstein, MD, FCAP

 

See also our Series A: Cardiovascular Diseases

 

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