Chapter 5- LIPIDS- Supporting Document-based on Chapter 5: Section5.2&5.3 2e:pg 175 -183; 3e: pg 195-203
This supporting document discusses two topics:
1)The chemistry of dietary lipids
2) The digestion of lipids
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There are three major components of dietary lipids:
1) Triglycerides- the most common component of dietary lipids
2) Phospholipids
3) Sterols-cholesterol & plant sterols We will briefly discuss each.
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This concludes the discussion of lipid chemistry. Now we’ll continue with a brief discussion of lipid digestion.
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This concludes our discussion. Before closing the file try the practice questions below.
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1) Most fatty acids in food and in the body are covalently bonded to what molecule?
a) cholesterol b) triglycerides c) phosphate d) glycerol
2) Which statement most accurately describes alpha-linolenic acid?
a) a cis fatty acid with three double bonds, the first found on carbon-3, counting from the omega end.
b) a trans fatty acid with three double bonds, the first found on carbon-3, counting from the omega end. c) a cis and omega-3 fatty acid with three double bonds, the first found on carbon-6, counting from the omega end.
d) a cis fatty acid with two double bonds, the first found on carbon-3, counting from the omega end.
3) Which statement best describes a saturated fatty acid?
a) a fatty acid with one double bond
b) a fatty acid with no double bonds.
c) a linear fatty acid with hydrogen atoms on the opposite sides of a double bond. d) a fatty acid bonded to a sterol.
4) Which sterol is biosynthesized in the liver and is also consumed in the food we eat?
a) Plant-derived sterol
b) Cholesterol, which is only found in plant-based foods
c) Cholesterol, which is only found in animal-based foods
d) Phospholipids
5) Which enzyme plays an important role in lipid digestion?
a) Pancreatic lipase
c) Monoglyceride
d) Sucrase
6) Which of the following aid in the absorption of dietary lipids?
a) glucose and bile
b) micelles and bile
c) brush border enzymes and amylase d) triglycerides and cholesterol
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C05-Lipids-supporting documents
Questions Answers 1D 2A 3B 4C 5A 6B
Dietary fat and heart disease study is seriously misleading | The Nutrition Source | Harvard T.H. of Public Health 2021-10-08, 12:47
The Nutrition Source
Dietary fat and heart disease study is seriously misleading
The journal Annals of Internal Medicine recently published a paper suggesting there is no evidence supporting the longstanding recommendation to limit saturated fat consumption. Media reporting on the paper included headlines such as “No link found between saturated fat and heart disease” and articles saying “Saturated fat shouldn’t be demonized” springing up on social media.
However, , chair of the Department of Nutrition at Harvard School of Public Health, warns that the conclusions are seriously misleading, as the analysis contains major errors and omissions.
This paper is bound to cause confusion. A central issue is what replaces saturated fat if someone reduces the amount of saturated fat in their diet. If it is replaced with refined starch or sugar, which are the largest sources of calories in the U.S. diet, then the risk of heart disease remains the same. However, if saturated fat is replaced with polyunsaturated fat or monounsaturated fat in the form of olive oil, nuts and probably other plant oils, we have much evidence that risk will be reduced.
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Dietary fat and heart disease study is seriously misleading | The Nutrition Source | Harvard T.H. of Public Health 2021-10-08, 12:47
Dr. Willett emphasized that because this meta-analysis contains multiple serious errors and omissions, the study conclusions are misleading and should be disregarded.
The o!cial comment, as it appears on the Annals of Internal Medicine website, is as follows:
The meta-analysis of dietary fatty acids and risk of coronary heart disease by Chowdhury et al. (1) contains multiple errors and omissions, and the conclusions are seriously misleading, particularly the lack of association with N-6 polyunsaturated fat. For example, two of the six studies included in the analysis of N-6 polyunsaturated fat were wrong. The relative risks for Nurses’ Health Study (NHS) (2) and Kuopio Ischemic Heart Disease Study (KIHD) (3) were retrieved incorrectly and said to be above 1.0. However, in the 20-year follow-up of the NHS the relative risk for highest vs lowest quintile was 0.77 (95 percent CI: 0.62, 0.95); ptrend = 0.01 (the authors seem to have used the RR for N-3 alpha-linolenic acid from a paper on sudden cardiac death), and in the KIHD the relative risk was 0.39; 95% confidence interval [CI], 0.21-0.71) (the origin of the number used in the meta-analysis is unclear). Also, relevant data from other studies were not included (4 and 5).
Further, the authors did not mention a pooled analysis (6) of the primary data from prospective studies, in which a significant inverse association between intake of polyunsaturated fat (the large majority being the N-6 linoleic acid) and risk of CHD was found. Also, in this analysis, substitution of polyunsaturated fat for saturated fat was associated with lower risk of CHD. Chowdhury et al. also failed to point out that most of the monounsaturated fat consumed in their studies was from red meat and dairy sources, and the findings do not necessarily apply to consumption in the form of nuts, olive oil, and other plant sources. Thus, the conclusions of Chowdhury et al. regarding the type of fat being unimportant are seriously misleading and should be disregarded.
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Dietary fat and heart disease study is seriously misleading | The Nutrition Source | Harvard T.H. of Public Health 2021-10-08, 12:47
Sincerely,
Harvard University
1. , Warnakula S, Kunutsor S, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk. Med 2014; 160(6):398-406.
2. Oh K, Hu FB, E, Stampfer MJ, C. Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the Nurses’ Health Study. Am J Epidemiol 2005;161:672-9.
3. Laaksonen DE, Nyyssonen K, Niskanen L, H, Salonen JT. Prediction of cardiovascular mortality in middle aged men by dietary and serum linoleic and polyunsaturated fatty acids. Arch Intern Med 2005;165:193-199.
4. de Goede J, Geleijnse JM, M, , Verschuren WM. Linoleic acid intake, plasma cholesterol and 10-year incidence of CHD in 20,000 middle-aged men and women in the Netherlands. Br J Nutr 2012;107:1070-6.
5. Dolecek TA. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the multiple risk factor intervention trial. Proc Soc Exp Biol Med 1992;200:177-82.
6. U, O’ J, Heitmann BL, A, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, , Pietinen P, , Stevens J, Virtamo J, C, Ascherio A. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J 2009:1425-32.
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HHS Public Access
Author manuscript
JAMA Intern Med. Author manuscript; available in PMC 2017 November 01.
Published in final edited form as:
JAMA Intern Med. 2016 November 1; 176(11): 1680–1685. doi:10.1001/jamainternmed.2016.5394.
Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents
Cristin E. Kearns, DDS, MBA, . Schmidt, PhD, MSW, MPH, and . Glantz, PhD
Philip R. for Health Policy Studies, San Francisco, California (Kearns, Schmidt, Glantz); Department of Orofacial Sciences, University of California, San Francisco, San Francisco (Kearns); Clinical and Translational Science Institute, San Francisco, California (Schmidt); Department of Anthropology, History, and Social Medicine, University of California, San Francisco (Schmidt); Department of Medicine, University of California, San Francisco, San Francisco (Glantz); Center for Tobacco Control Research and Education, San Francisco, California (Glantz); Cardiovascular Research Institute, San Francisco, California (Glantz); Family Comprehensive Cancer Center, San Francisco, California (Glantz)
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 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.
Corresponding Author: . Glantz, PhD, UCSF Center for Tobacco Control Research and Education, 530 Parnassus Ave, Ste 366, San Francisco, CA 94143-1390
Author Contributions: 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.
Study concept and design: All authors.
Acquisition, analysis, or interpretation of data: All authors.
Drafting of the manuscript: Kearns.
Critical revision of the manuscript for important intellectual content: All authors. Statistical analysis: Glantz.
Obtained funding: Glantz.
Administrative, technical, or material support: Kearns, Glantz.
Study supervision: Schmidt, Glantz.
Conflict of Interest Disclosures: None reported.
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Kearns et al.
In the 1950s, disproportionately high rates of coronary heart disease (CHD) mortality in American men led to studies of the role of dietary factors, including cholesterol, phytosterols, excessive calories, amino acids, fats, carbohydrates, vitamins, and minerals in influencing CHD risk.1 By the 1960s, 2 prominent physiologists were championing divergent causal hypotheses of CHD2,3: identified added sugars as the primary agent, while identified total fat, saturated fat, and dietary cholesterol. However, by the 1980s, few scientists believed that added sugars played a significant role in CHD, and the first 1980 Dietary Guidelines for Americans4 focused on reducing total fat, saturated fat, and dietary cholesterol for CHD prevention.
Although the contribution of dietary sugars to CHD is still debated, what is clear is that the sugar industry, led by the Sugar Association, the sucrose industry’s Washington, DC–based trade association,5 steadfastly denies that there is a relationship between added sugar consumption and CVD risk.6,7 This Special Communication uses internal sugar industry documents to describe how the industry sought to influence the scientific debate over the dietary causes of CHD in the 1950s and 1960s, a debate still reverberating in 2016.
The Sugar Association evolved from the Sugar Research Foundation (SRF), founded in 1943.8 We located correspondence between the SRF and , a professor who served on the SRF’s scientific advisory board (SAB) between 1959 and 1971, in the University of Illinois Archives9 (319 documents totaling 1551 pages). We located correspondence between the SRF and D. , professor of nutrition at the Harvard School of Public Health and codirector of the SRF’s first CHD research project from 1965 to 1966,10 in the Harvard Medical Library11 (27 documents totaling 31 pages).
We collected additional SRF materials through a World Cat search including annual reports, symposium proceedings, and internal reviews of research. We reviewed historical reports and statements contextualizing scientific debates in the 1950s and 1960s on dietary factors causally related to CHD published by the National Academy of Sciences–National Research Council (NAS-NRC), US Public Health Service, the American Heart Association (AHA), and American Medical Association (AMA). Findings were assembled chronologically into a narrative case study.
SRF’s Interest in Promoting a Low-Fat Diet to Prevent CHD
Sugar Research Foundation president ’s 1954 speech, “What’s New in Sugar Research,”12 to the American Society of Sugar Beet Technologists identified a strategic opportunity for the sugar industry: increase sugar’s market share by getting Americans to eat a lower-fat diet: “Leading nutritionists are pointing out the chemical connection between [American’s] high-fat diet and the formation of cholesterol which partly plugs our arteries and capillaries, restricts the flow of blood, and causes high blood pressure and heart trouble…if you put [the middle-aged man] on a low-fat diet, it takes just five days for the blood cholesterol to get down to where it should be… If the carbohydrate industries were to
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recapture this 20 percent of the calories in the US diet (the difference between the 40 percent which fat has and the 20 percent which it ought to have) and if sugar maintained its present share of the carbohydrate market, this change would mean an increase in the per capita consumption of sugar more than a third with a tremendous improvement in general health.”12
The industry would subsequently spend $600 000 ($5.3 million in 2016 dollars) to teach “people who had never had a course in biochemistry… that sugar is what keeps every human being alive and with energy to face our daily problems.”12
Growing Evidence That Sucrose Elevates Serum Cholesterol Level
In 1962, the SRF became concerned with evidence showing that a low-fat diet high in sugar could elevate serum cholesterol level. At its November 1962 SAB meeting,13 the SRF considered an AMA Council on Foods and Nutrition report, The Regulation of Dietary Fat,14 that, according to the SRF, “indicate[d] that, in low fat diets, the kind of carbohydrate ingested may have an influence on the formation of serum cholesterol.”13 The SAB concluded, “that research developments in the [CHD] field should be watched carefully.”13 The SRF’s vice president and director of research, , started closely monitoring the field.15
In December 1964, Hickson reported to an SRF subcommittee15 that new CHD research was a cause for concern: “From a number of laboratories of greater or lesser repute, there are flowing reports that sugar is a less desirable dietary source of calories than other carbohydrates, eg,—Yudkin.”15 Since 1957, British physiologist 16 had challenged population studies singling out saturated fat as the primary dietary cause of CHD and suggested that other factors, including sucrose, were at least equally important.17,18
Hickson proposed that the SRF “could embark on a major program” to counter Yudkin and other “negative attitudes toward sugar.”15He recommended an opinion poll “to learn what public concepts we should reinforce and what ones we need to combat through our research and information and legislative programs” and a symposium to “bring detractors before a board of their peers where their fallacies could be unveiled.”15 Finally, here commended that SRF fund CHD research: “There seems to be a question as to whether the [atherogenic] effects are due to the carbohydrate or to other nutrient imbalance. We should carefully review the reports, probably with a committee of nutrition specialists; see what weak points there are in the experimentation, and replicate the studies with appropriate corrections. Then we can publish the data and refute our detractors.”15
In 1965, the SRF asked , chair of the Harvard University School of Public Health Nutrition Department19 to join its SAB as an ad hoc member.20 Stare was an expert in dietary causes of CHD and had been consulted by the NAS,1 National Heart Institute,21 and AHA,22 as well as by food companies and trade groups.19 Stare’s industry-favorable positions and financial ties would not be widely questioned until the 1970s.23
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Link Between Sucrose and Elevated Serum Triglyceride Level
On July 1, 1965, the SRF’s Hickson visited D. , a faculty member of Stare’s department,24,25 after publication of articles in Annals of Internal Medicine in June 196526–29 linking sucrose to CHD. The first 2 articles26,27 reported results from an epidemiological study suggesting that blood glucose levels were a better predictor of atherosclerosis than serum cholesterol level or hypertension. The third28(p210) demonstrated that sucrose, more than starches, aggravated carbohydrate-induced hypertriglyceridemia and hypothesized that “perhaps fructose, a constituent of sucrose but not of starch, [was] the agent mainly responsible.” An accompanying editorial29(p1330) argued that these findings corroborated Yudkin’s research and that if elevated serum triglyceride levels were a CHD risk factor, then “sucrose must be atherogenic.”
On July 11, 1965, the ran a full-page article on the Annals articles stating that new research “threatened to tie the whole business [of diet and heart disease] in a knot.”30 It explained that, while sugar’s association with atherosclerosis was once thought to be theoretical and supported by limited studies, the new research strengthened the case that sugar increased the risk of heart attacks.
SRF Funds Project 226: A Literature Review on Sugars, Fats, and CHD
On July 13, 1965, 2 days after the Tribune article, the SRF’s executive committee approved Project 226,31 a literature review on “Carbohydrates and Cholesterol Metabolism” by Hegsted and Gandy, overseen by Stare.10 The SRF initially offered $500 ($3800 in 2016 dollars) to Hegsted and $1000 ($7500 in 2016 dollars) to McGandy, “half to be paid when you start work on the project, and the remainder when you inform me that the article has been accepted for publication.”31 Eventually, the SRF would pay them $650032 ($48 900 in 2016 dollars) for “a review article of the several papers which find some special metabolic peril in sucrose and, in particular, fructose.”31
On July 23, 1965, Hegsted asked Hickson to provide articles relevant to the review.33 Most of the articles Hicks
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