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Correcting four decades of the wrong dietary advice

Ritterman, Jeffrey MD

Journal of the American Academy of PAs: July 2016 - Volume 29 - Issue 7 - p 1–3
doi: 10.1097/01.JAA.0000484299.50943.55
Commentary
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Jeffrey Ritterman is an associate professor and assistant clinical coordinator of the joint master of physician assistant studies/master of public health program at Touro University in Vallejo, Calif. The author has disclosed no potential conflicts of interest, financial or otherwise.

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Every 5 years, following an expert panel's systematic review of the literature on diet, the US Department of Agriculture and the Department of Health and Human Services issue dietary guidelines. The 2015 Dietary Guidelines Advisory Committee (DGAC) report has two startling changes: The 30% upper limit on fat consumption has been eliminated and dietary cholesterol is no longer listed as a nutrient of concern.1 Lifting these restrictions on fat and cholesterol intake reverses 4 decades of dietary advice. This is nothing short of a scientific revolution.2

Research has shown no evidence that replacing fat with carbohydrates reduces cardiovascular disease. In fact, the opposite is true: researchers now know that dietary cholesterol is not a cause of clinical cardiovascular disease.3 With both dietary fat and dietary cholesterol exonerated as causes of cardiovascular disease and type 2 diabetes, much recent research has focused on the role of fructose as a cause of these modern-day epidemics.4

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HISTORY OF DIETARY GUIDELINES

The first US dietary guidelines were issued in 1977 by a commission chaired by Sen. George McGovern (D-S.D.).5 The commission recommended that Americans receive no more than 30% of their energy requirements from fat and no more than 10% of their calories as saturated fat.

At the time, Robert Olson, MD, PhD, professor of medicine and chairman of the biochemistry department at St. Louis University and an expert on nutrition science, argued that the recommendations were not supported by the available science, and asked for “more research on the problem before we make announcements to the American public.”5 Sen. McGovern, speaking for the commission, stated that “senators don't have the luxury the research scientist does of waiting until every last shred of evidence is in.”5

Sen. McGovern's comment concerning “every last shred of evidence” was widely off the mark. It was never a question of having supportive but incomplete evidence. There simply was no convincing scientific evidence in support of the commission's recommendations.

At the time the commission issued its dietary guidelines, only 2,500 people had been studied in randomized control trials that compared different macronutrient content. No study included women. No study showed that a low-fat diet was superior to a diet higher in fat content in any measure of health outcome. In fact, in the one study that compared a 10% saturated fat intake with a diet with unrestricted saturated fat, the patients in the low-fat group had a greater risk of glucose intolerance, insulin resistance, and inflammation. The patients on the low-fat diet also developed atherogenic dyslipidemia with an increase in small dense low-density lipoprotein (LDL) particles and a decrease in protective high-density lipoprotein (HDL) cholesterol.4 Yet, without any study recommending the dietary guidelines, and without any science to back up the guidelines, and with some evidence that the contrary was in fact true, 220 million Americans were advised to lower their saturated fat intake. And Americans have been following that advice for the last 40 years.

Unfortunately these recommendations were not only wrong, they were dangerously wrong. They have helped lead the way to the present epidemics in coronary heart disease and type 2 diabetes.

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SUGAR REPLACES FAT

When the food manufacturers started removing the fat from food, the taste went with the fat. The solution: Add sugar and lots of it. This worked well economically, as the introduction of high-fructose corn syrup made cheap sugar plentiful.6

It didn't work so well metabolically. The huge increases in sugar intake have exceeded patients' physiologic limits.7,8 The result is the pathophysiology that healthcare providers see all around us. Although added sugar seems to be the worst culprit, refined grains appear to share the blame. The 2015 DGAC report explains that more than 70% of the US population eats too much processed grain.

The medical community is beginning to acknowledge that the old paradigm is crumbling.

A recent review article titled “Added Fructose: A Principal Driver of Type 2 Diabetes Mellitus and Its Consequences” states that Americans on average consume 30 times more added sugar than they did when the Declaration of Independence was written.8 This added sugar, according to the article, is a major cause of today's diabetes epidemic.

Another article, with the provocative title “Carbohydrate Intake and Nonalcoholic Fatty Liver Disease: Fructose as a Weapon of Mass Destruction,” states that excessive fructose intake leads to fatty liver disease.9 This initiates a cascade of events resulting in metabolic syndrome and its related illnesses: coronary heart disease, type 2 diabetes, hypertension, and obesity.9

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EXCESS FRUCTOSE AND TYPE 2 DIABETES

The liver is the only organ in the human body capable of metabolizing fructose. When the liver is presented with a large fructose load, it converts some to energy through the Kreb cycle, and some to glycogen. The remaining fructose is shunted to the de novo lipogenesis pathway for conversion to fat. The greater the fructose load, the more fat produced. This fat is stored throughout the body, leading to obesity. Fat also is stored in the liver, causing nonalcoholic fatty liver disease.

A fatty liver is unable to perform normal hepatic functions and loses the ability to respond to insulin. This insulin resistance, in turn, provokes pancreatic beta-cell overactivity, as the pancreas attempts to meet the increased insulin requirements. Eventually the pancreatic beta cells wear out from the overwork, and type 2 diabetes results.

The fats produced by the liver in response to a high fructose load include triglycerides and small, dense LDL particles. A fatty liver also decreases production of protective HDL cholesterol. This combination of triglyceride and small, dense LDL particle elevation coupled with HDL reduction predisposes patients to coronary heart disease.10-12

One of the leaders in this field of nutrition science, James J. DiNicolantonio, PharmD, put it this way: “The global epidemic of atherosclerosis, heart disease, diabetes, obesity, and the metabolic syndrome is being driven by a diet high in carbohydrate/sugar as opposed to fat, a revelation that we are just starting to accept.”4

Now, the so-called French paradox makes sense. Frenchmen and women with their high intake of fatty foods do not have a correspondingly high incidence of coronary artery disease. Now we know why: Dietary fat isn't the cause of coronary artery disease.13,14

We also now understand how the Inuit could exist on caribou and seal meat, each with high saturated fat content, without developing coronary artery disease. They ate no sugar.15,16 Old paradigms die hard. Galileo spent the last 6 years of his life under house arrest for the heresy of believing that the earth was not the center of the universe. During Galileo's time, the Catholic Church was all powerful. The church found Galileo's ideas heretical.17

Today, we take for granted that the planets revolve around the sun and find it hard to imagine that this was once viewed as heretical. There will come a time when people will be surprised that we ever doubted that added sugars and refined carbohydrates were driving the coronary heart disease and type 2 diabetes epidemics. In order to reverse these epidemics, a new paradigm will need to be accepted by both the medical community and the lay public.

This will not be an easy task. A 2014 Gallup Poll shows that the erroneous dietary advice we have been giving has taken hold.18 Nearly twice as many Americans try to avoid fat in their diet as opposed to avoiding carbohydrates. Fewer Americans now avoid fat compared with our intake a decade ago. Removing the harmful sugars and refined carbohydrates from our diets is a major challenge for the healthcare industry. PAs are in a unique position to help facilitate this necessary shift.

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THE PA CAN PLAY A LEADING ROLE

Most physicians are undereducated on matters of nutrition. The paradigm implicating dietary fat as the cause of coronary heart disease has reigned supreme for so long that physicians are not aware that their scant dietary knowledge is out of date. PAs can disseminate the correct dietary information to the physicians with whom they are working.

Research shows that PAs are in an excellent position to provide health education to patients.19 Some physicians may find that they lack the skills, time, and interest to be effective health educators. These physicians may prefer to empower PAs on their teams to provide health education directly.

PAs are trained in general medical practice. Many PA programs train primary care providers who will work in underserved regions. These are the very same areas that suffer a high prevalence of metabolic syndrome and its tragic sequelae: coronary heart disease and type 2 diabetes. This appears to be due, at least in part, to food industry advertising campaigns, which preferentially target Hispanic and black youth.20 PAs can deliver a different message.

The desire and ability to educate and guide patients toward healthy lifestyle choices, coupled with an emphasis on providing primary care in underserved areas, place PAs in an ideal position. Training programs must prepare future PAs to understand the biochemistry, pathophysiology, and nutrition science related to excess fructose ingestion.

With this knowledge, PAs can lead the charge in reversing the devastating epidemics of coronary artery disease and type 2 diabetes.

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REFERENCES

1. Dietary Guidelines Advisory Committee. Scientific Report of the 2015 Dietary Guidelines Advisory Committee. 2015. www.health.gov/dietaryguidelines/2015-scientific-report/. Accessed March 25, 2016.
2. Schmidt LA. New unsweetened truths about sugar. JAMA Intern Med. 2014;174(4):525–526.
3. Kanter MM, Kris-Etherton PM, Fernandez ML, et al. Exploring the factors that affect blood cholesterol and heart disease risk: is dietary cholesterol as bad for you as history leads us to believe. Adv Nutr. 2012;3(5):711–717.
4. Volek JS, Fernandez ML, Feinman RD, Phinney SD. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res. 2008;47(5):307–318.
5. Harcombe Z, Baker JS, Cooper SM, et al. 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;2:1. http://openheart.bmj.com/content/2/1/e000196. Accessed March 25, 2016.
6. Lustig RH. Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease. New York, NY: Hudson Street Press; 2013:21,169.
7. Chanmugam P, Guthrie JF, Cecilio S, et al. Did fat intake in the United States really decline between 1989–1991 and 1994–1996. J Am Diet Assoc. 2003;103(7):867–872.
8. DiNicolantonio JJ, O'Keefe JH, Lucan SC. Added fructose: a principal driver of type 2 diabetes mellitus and its consequences. Mayo Clin Proc. 2015;90(3):372–381.
9. Basaranoglu M, Basaranoglu G, Bugianesi E. Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction. Hepatobiliary Surg Nutr. 2015;4(2):109–116.
10. Stanhope KL, Bremer AA, Medici V, et al. Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-Cholesterol, and apolipoprotein-B in young men and women. J Clin Endocrinol Metab. 2011;96(10):E1596–E1605.
11. Stanhope KL, Schwarz JM, Havel PJ. Adverse metabolic effects of dietary fructose: results from the recent epidemiological, clinical, and mechanistic studies. Curr Opin Lipidol. 2013;24(3):198–206.
12. Endocrine Society. Restricting Fructose in Obese Latino and African American Children May Reduce Fat Accumulation in Their Liver. www.endocrine.org/news-room/press-release-archives/2015/restricting-fructose-in-obese-latino-african-american-children. Accessed March 25, 2016.
13. Renaud S, de Lorgeril M. Wine, alcohol, platelets, and the French paradox for coronary heart disease. Lancet. 1992;339(8808):1523–1526.
14. Criqui MH, Ringel BL. Does diet or alcohol explain the French paradox. Lancet. 1994;344(8939–8940):1719–1723.
15. Draper HH. The Aboriginal Eskimo diet in modern perspective. Modern Anthropologist. 1977;79(2):309–316.
16. Dewailly E, Blanchet C, Lemieux S, et al. n-3 Fatty acids and cardiovascular disease risk factors among the Inuit of Nunavik. Am J Clin Nutr. 2001;74(4):464–473.
17. Stanford Encyclopedia of Philosophy. http://plato.stanford.edu/entries/galileo. Accessed March 25, 2016.
18. Dugan A. Americans still avoid fat more than carbs. www.gallup.com/poll/174176/americans-avoid-fat-carbs.aspx. Accessed March 25, 2016.
19. Ritsema TS, Bingenheimer JB, Scholting P, Cawley JF. Differences in the delivery of health education to patients with chronic disease by provider type, 2005-2009. Prev Chronic Dis. 2014;11:130175. www.cdc.gov/pcd/issues/2014/13_0175.htm. Accessed March 25, 2016.
20. Yale Rudd Center for Food Policy and Obesity. Fast Food FACTS. Food advertising to children and teens score. 2013. http://fastfoodmarketing.org/media/FastFoodFACTS_Report.pdf. Accessed March 25, 2016.
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