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Feature Nutrition

The scientific report guiding the US dietary guidelines: is it scientific?

BMJ 2015; 351 doi: https://doi.org/10.1136/bmj.h4962 (Published 23 September 2015) Cite this as: BMJ 2015;351:h4962

Rapid Response:

USDA 2015 Dietary Guidelines ought to be withdrawn and replaced with better science

These are my opinions based on my research, 20+ years communications with USDA/HHS committees (like DGAC), attendance to professional conferences organized by USDA/HHS, lectures I gave to USDA/NIH entities, review of published articles.
Teicholz argues that “dietary guidelines not take account of all the relevant scientific evidence.” Comments (BMJ and elsewhere) criticize alleged conflicts of interests, results of experiments. In response, Millen, Chair, 2015 Dietary Guidelines Advisory Committee (DGAC) states: ”The procedures used to develop the DGAC Scientific report are expansive, transparent, and thoughtful, with multiple opportunities for public input through open commentary, public meetings, and hearings.”

In my experience with DGAC, “input” may end in intellectual black holes. DGAC overlooked fundamental issues.
The nutritional guidelines (previously USDA Food Pyramid), and critiques in BMJ.com, aicr.org, are misleading and counterproductive. DGAC procedures are expensive, not expansive or adequate. They omit material facts about FA metabolism that impair the guidelines; fail to consider critical research. See references.
Empirical data alone is misleading. Nutrition studies are unreliable because all relevant factors cannot be controlled. No participant in an experiment will eat and exercise identically for 20 years. Thus, nutrition studies rely on biomarkers. Feeding foods to people and measuring biomarkers can be meaningless. Differences in average biomarkers will occur; with over 100 subjects they will be statistically significant. So what? The studies I saw have low Rsquare. Individual data points are not available to researchers to review. Where are detailed graphs of individual data points (e.g., changes in Total/HDLC or BP or calprotectin) in response to different FA food intakes?

I consider it nonsense to argue to avoid or eat red meat or eggs or butter or vegetable oil without a biophysical model of their biochemistry in the body. Example: Does a 10% increased intake of SFA in butter or meat alter physical forces between cell molecules differently than corn oil leading to suboptimal immune response and 5% increase in Total/HDLC? How?
We need a theoretical model to explain data. Medicine and nutrition should use physical chemistry. What optimization or conservation principles regulate how the body utilizes nutrients? What mathematical equations make specific, measurable, predictions about relationships between Total/HDLC and FAs, how MUFA or TC change in response to dietary changes (is relationship linear? Exponential? Why?).

Physics has well established conservation (mass, energy) and optimization (least action) principles. Scientists should apply them to nutrition to make predictions of diet on CAD, cancer and recommend foods to eat. I did not find them in writings by DGAC or Teicholz. Instead, studies often look at data of a few nutrition factors over different ranges (without measuring body composition); relationships and models are either not explicit or with low predictive value.
DGAC, AICR.org, NIH, USDA. I challenge you to identify 3 best published articles with specific models, using physics, which provide a theoretical explanation how nutrition affects CAD and Cancer.

These are the issues DGAC should address.
What is the mathematical/biophysical model that explains the relationship between SFA, MUFAs, PUFAs, TFAs, Carbs calories, and CAD or cancer? What is the relative contribution of each factor to CAD or DNA mutations? How does each contribution change depending on body weight, genes, nutrient composition (relationships may be different for a person thin or overweight, in Alaska or Miami).
What is the biophysics/ biochemistry how eating/ avoiding butter, fish, milk, corn/ flax oil, change CAD?
Describe the biochemistry of FAs, the interconversion of SFAs to MUFAs. Evidence that some (many, most?) humans can or cannot convert/ make enough FA derivatives from linoleic and linolenic acid; eating too many omega6 interferes with conversion of linolenic to PUFAw3 (True?) (critical to eat vegetable or animal foods). Eating MUFAs is desirable or not; desirable ranges for daily intake of w3, w6 PUFA (absolute, by body weight, % calories, w3/w6 ratio). Explain theoretical (biophysical reasons). Role of different isomers (not just trans) of PUFAs.
How body biochemistry manage excess calories from fat v. carbs v protein. Biochemical consequences of replacing fats with carbs or vice-versa (hint: answer depends on specific factors DGAC should explain).
Different sources of PUFAs. What are the biochemical consequences (differences) of eating the same quantity (percent or grams) of w3 from flax, soy, fish, fish capsules, FA drugs ($1B+ market, a source of recent USDC decision on off label that may increase taxpayer expense). Is it better to eat soybean oil instead? Why?
Should we prohibit TFAs or the replacement with other fats (e.g., SFAs) is likely to encourage people to eat more calories and thus cause more harm?
How does location of PUFA in molecules (e.g., #1 or #2) affect biological function? With regard to the same FA, should we get it from oil or egg or meat or plants or fish? Should we get w3s from fish or plants (assuming fish and plants have no toxic chemicals)? What the biochemical reasons?
We need answers before DGAC recommends we eat more plants or red meat, chicken or whole grains, olive or flax or fish or tropical oils, butter or seeds, eggs or dairy, walnuts or almonds, avocados or peas, fish or green vegetables. What should we eat preferentially: bread with whole grains, lean steak, chicken, fish, spinach, potatoes, olives? Why? What changes in molecular forces they cause in cells? Can every person anywhere make the FAs we need from vegetable foods alone? Are geographic or genetic differences? Alaska, Miami?

My research describes the relative activities of enzymes in FA pathways (and consequences for eating vegetarian or animal fat); it provides the best predictor model for Total/HDLC given FAs; it explains how FAs affect CAD and IBD; it describes the relative roles of isomers and TFAs; the biochemical reasons (not just empirical data from difficult to design experiments) why replacing SFAs with carbs is likely to be counterproductive; and explains flaws in the USDA Food pyramid and dietary guidelines regarding fats (see my public exchange of letters with the USDA). As a minimum, DGAC should review my work, cite it appropriately.

References
Siguel E, Lerman, RH. Altered Fatty Acid Metabolism in Patients With Angiographically Documented Coronary Artery Disease. Metabolism 1994; 43:982-93.
Siguel E. Essential Fatty Acids in Health and Disease. 1994, P.O. Box 10187, Dept F, Gaithersburg, MD 20898 (book, out of print, new version being prepared)
Siguel E, Lerman RH. The Role of Essential Fatty Acids: Dangers in the USDA Dietary Recommendations ("Pyramid") and in Low Fat Diets. Am. J. Clin. Nutrition, 1994; 60:973-79 (let).
Siguel, E. A New Relationship between Total/HDL Cholesterol and Polyunsaturated Fatty Acids. Lipids, 1996; 31:S51-6.
Sinclair, HM. Prevention of coronary heart disease: the role of essential fatty acids. Postgrad Med J. 1980 Aug; 56(658): 579–584.
http://www.bmj.com/content/351/bmj.h4671/rapid-responses
http://www.bmj.com/content/351/bmj.h4583?etoc=
http://blog.aicr.org/2015/09/24/misleading-journal-article-attacks-us-di...
http://www.theverge.com/2015/9/23/9389391/us-dietary-guidelines-flawed-i...

Competing interests: I conduct many activities that influence my opinions (e.g., my research, write books or articles or patents, have websites, design foods, lecture about health and disease, health policies). I describe the types of fats to eat, exercise, stress management, diets, eating less, periodic fasting. I am developing a new theory of disease, including lipid metabolism and the cause of cardiovascular disease. I intend to profit from my intellectual property (IP) (e.g, write articles, web sites, books, patents, lectures, ads, biomarker tests, etc). I wrote a patent to measure fatty acids. I wrote one book on essential and trans fatty acids. I gave talks to corporations, conferences and trade shows, for which I was paid. I may receive compensation from food or other companies. This comment is an extract of books and articles either written or in progress (authorized by the author under the non-exclusive common license CC BY-NC 4.0 requested by BMJ). I criticized the value of the USDA nutrition guidelines, federal nutrition funding, and the National Cholesterol Education Program. I do not consider eggs harmful because they have cholesterol and fat, made my views public, received funding from egg industry. I tell my family to eat eggs and red meat, but avoid processed fat. I do not follow the USDA nutrition guidelines. I proposed a different Food pyramid and nutrition guidelines.

26 September 2015
Eduardo Siguel
Medical Research, MD, PhD
Retired researcher, Boston U Medical Center, USA
Gaithersburg, MD, USA