Return of America’s Erratic Nutritional Guidelines

Last week, America’s nutrition advisory panel met in order to develop a new set of nutritional guidelines for the American public. This panel meets once every five years, and is composed of prominent doctors and nutrition experts, with the sole responsibility of determining a set of nutritional guidelines to recommend to the federal government.

Members of this committee have performed human clinical research and read thousands of studies in order to understand the cause-and-effect relationship between diet and human health. Just last week they set forth the following three recommendations:

Recommendation #1: Reduce Sugar Intake to Less Than 10% of Total Calories


For the past 10-15 years, Americans have been instructed to eat a low-fat diet in order to reduce the rate of heart disease. In response, food manufacturers loaded packaged products with excessive sugar and sweeteners like high fructose corn syrup, resulting in increased rates of obesity, diabetes and heart disease. Now the time has come to strongly reduce sugar intake, and to force food manufacturers to adopt a more sensible approach.

Few people will argue that eating less sugar will improve your overall health. Personally, I am glad to see that they have taken an aggressive stance at reducing the amount of added sugar in the diets of millions of Americans.

Recommendation #2: Eat Less Saturated Fat; Do Not Limit Total Fat Intake

Fit young woman fighting off fast foodWhile the government is aware that increased intake of saturated fat may accelerate the development of heart disease, instructing Americans to eat as much fat as they want is downright foolish.

This recommendation is a perfect example of the erratic nature of America’s nutritional guidelines:

When fat was the enemy, we turned a blind eye to sugar. Now that sugar is the enemy, we are turning a blind eye to fat.

Previously, Americans were advised to limit fat intake to 35% of total calories. Today, that recommendation is being rewritten, and Americans may soon be instructed to eat as much fat as they desire, while “opting” for unsaturated plant fats when possible. This stance strengthens the narrative of the Paleo community, a group of eaters who advocate behaving the way our Paleolithic ancestors did, by consuming large quantities of meat products containing copious amounts of saturated fat.

The problem with this all-you-can-eat-fat-buffet philosophy is simple: it completely negates the effect of excessive fat intake on the development of insulin resistance (1–19), IGF-1 imbalance (20,21), colon cancer (22,23) and all-cause mortality (24,25).

A substantial body of evidence supports the fact that even modest fat intake is associated with elevated rates of type 2 diabetes (1–19) and colon cancer (22,23).


Despite this compelling evidence, the government chooses to pay attention to only one condition: heart disease. And as long as dietary fat isn’t directly correlated with heart disease, then the recommendation to participate in the all-you-can-eat-fat-buffet will continue.

The question still remains: why have our nutritional guidelines become erratic?

Recommendation #3: Do Not Limit Cholesterol Intake

High-CholesterolIt turns out that cholesterol metabolism is more complicated than we once thought. While the amount of cholesterol in your blood is influenced both by what you eat and by how much your liver produces, recent evidence suggests that your liver is more in charge than we once thought.

What is the “normal” LDL (bad) cholesterol level?

Recent evidence suggests that “accumulating data from multiple lines of evidence consistently demonstrate that the physiologically normal LDL level and the thresholds for atherosclerosis development and CHD events are approximately 50-70 mg/dL (26).”

  • This amount of LDL cholesterol is what we are born with
  • This amount of LDL cholesterol is what our closest primate ancestors maintain
  • This amount of LDL cholesterol is found in populations free of heart disease

Given that atherosclerosis is endemic in our population, it is important to clearly define the threshold for increased risk.
The problem is that only a tiny fraction of people actually have LDL concentrations between 50-70 mg/dL.

In America especially, the average LDL concentration is 130 mg/dL, almost twice the normal physiological level, suggesting that a large proportion of the US population has abnormally high cholesterol levels (26).


It just so turns out that populations subsisting on plant-based diets naturally achieve LDL concentrations of about 70 mg/dL, without even trying (27–29). Therefore, recommending that Americans consume dietary cholesterol carte blanche negates the connection between elevated cholesterol and heart disease altogether.

If the previous recommendation to eat an unlimited amount of fat was foolish, the recommendation to eat an unlimited amount of cholesterol is simply irresponsible.

Recommendation #4: Plant Based Diets are Healthy Eating Patterns


Well how convenient.

Finally, prominent health care organizations such as the American Dietetic Association (30) are starting to espouse the health benefits of plant-based diets. As more research continues to demonstrate the efficacy of plant-based diets in reversing disease and in promoting optimal heart health (31–34), health care organizations may have no choice but to adopt plant-centric positions in the near future.

I remain optimistic that America can move towards plant-based diets in the near future, and strong stances like this can certainly help promote this message to the masses.

Take Home Message

The main problem with this finger-pointing approach is that every few years a new nutrition enemy is born. If you choose to operate under the assumption that poor health can be attributed to a single dietary component, then you will find limitless opportunities to assign blame.

However, common sense and volumes of scientific research suggest that America’s obesity, heart disease and diabetes epidemics do not stem from one single cause, and rather are the result of multiple lifestyle factors, including (but not limited to):

  • Physical activity
  • Stress
  • Dietary fat
  • Dietary cholesterol
  • Fiber consumption
  • Vitamin D production
  • Abdominal obesity
  • Blood pressure
  • Blood sugar control

When these new nutrition recommendations get put into play in the next few months, I have a strong suspicion that they will get rewritten in the next five years, once data becomes available to demonstrate that eating excessive quantities of dietary fat and excessive quantities of dietary cholesterol are only serving to feed America’s obesity, heart disease and diabetes epidemics.

As long as sugar is our new enemy, fat and cholesterol are being granted the opportunity to silently damage our health, only to resurface as enemies in the not-so-distant future.


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  1. Roden M, Price TB, Perseghin G, Petersen KF, Rothman DL, Cline GW, et al. Mechanism of free fatty acid-induced insulin resistance in humans. J Clin Invest. 1996 Jun 15;97(12):2859–65.
  2. Roden M. How free fatty acids inhibit glucose utilization in human skeletal muscle. News Physiol Sci Int J Physiol Prod Jointly Int Union Physiol Sci Am Physiol Soc. 2004 Jun;19:92–6.
  3. Brehm A, Krssak M, Schmid AI, Nowotny P, Waldhäusl W, Roden M. Increased lipid availability impairs insulin-stimulated ATP synthesis in human skeletal muscle. Diabetes. 2006 Jan;55(1):136–40.
  4. Hirabara SM, Silveira LR, Abdulkader F, Carvalho CRO, Procopio J, Curi R. Time-dependent effects of fatty acids on skeletal muscle metabolism. J Cell Physiol. 2007 Jan;210(1):7–15.
  5. Hirabara SM, Silveira LR, Alberici LC, Leandro CVG, Lambertucci RH, Polimeno GC, et al. Acute effect of fatty acids on metabolism and mitochondrial coupling in skeletal muscle. Biochim Biophys Acta. 2006 Jan;1757(1):57–66.
  6. Martins AR, Nachbar RT, Gorjao R, Vinolo MA, Festuccia WT, Lambertucci RH, et al. Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function. Lipids Health Dis. 2012;11:30.
  7. Hirabara SM, Curi R, Maechler P. Saturated fatty acid-induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells. J Cell Physiol. 2010 Jan;222(1):187–94.
  8. Yu C, Chen Y, Cline GW, Zhang D, Zong H, Wang Y, et al. Mechanism by which fatty acids inhibit insulin activation of insulin receptor substrate-1 (IRS-1)-associated phosphatidylinositol 3-kinase activity in muscle. J Biol Chem. 2002 Dec 27;277(52):50230–6.
  9. Griffin ME, Marcucci MJ, Cline GW, Bell K, Barucci N, Lee D, et al. Free fatty acid-induced insulin resistance is associated with activation of protein kinase C theta and alterations in the insulin signaling cascade. Diabetes. 1999 Jun;48(6):1270–4.
  10. Ley SH, Sun Q, Willett WC, Eliassen AH, Wu K, Pan A, et al. Associations between red meat intake and biomarkers of inflammation and glucose metabolism in women. Am J Clin Nutr. 2014 Feb;99(2):352–60.
  11. Lagiou P, Sandin S, Lof M, Trichopoulos D, Adami H-O, Weiderpass E. Low carbohydrate-high protein diet and incidence of cardiovascular diseases in Swedish women: prospective cohort study. BMJ. 2012;344:e4026.
  12. Smart CEM, Evans M, O’Connell SM, McElduff P, Lopez PE, Jones TW, et al. Both dietary protein and fat increase postprandial glucose excursions in children with type 1 diabetes, and the effect is additive. Diabetes Care. 2013 Dec;36(12):3897–902.
  13. Delarue J, Magnan C. Free fatty acids and insulin resistance. Curr Opin Clin Nutr Metab Care. 2007 Mar;10(2):142–8.
  14. Wang P-Y, Kaneko T, Wang Y, Tawata M, Sato A. Impairment of Glucose Tolerance in Normal Adults Following a Lowered Carbohydrate Intake. Tohoku J Exp Med. 1999;189(1):59–70.
  15. Wolpert HA, Atakov-Castillo A, Smith SA, Steil GM. Dietary Fat Acutely Increases Glucose Concentrations and Insulin Requirements in Patients With Type 1 Diabetes Implications for carbohydrate-based bolus dose calculation and intensive diabetes management. Diabetes Care. 2013 Apr 1;36(4):810–6.
  16. Savage DB, Petersen KF, Shulman GI. Disordered Lipid Metabolism and the Pathogenesis of Insulin Resistance. Physiol Rev. 2007 Apr 1;87(2):507–20.
  17. Pańkowska E, Błazik M, Groele L. Does the fat-protein meal increase postprandial glucose level in type 1 diabetes patients on insulin pump: the conclusion of a randomized study. Diabetes Technol Ther. 2012 Jan;14(1):16–22.
  18. Gormsen LC, Nielsen C, Jessen N, Jørgensen JOL, Møller N. Time-course effects of physiological free fatty acid surges on insulin sensitivity in humans. Acta Physiol Oxf Engl. 2011 Mar;201(3):349–56.
  19. Boden G. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes. 1997 Jan;46(1):3–10.
  20. Kaaks R, Lukanova A. Energy balance and cancer: the role of insulin and insulin-like growth factor-I. Proc Nutr Soc. 2001;60(01):91–106.
  21. Arcidiacono B, Iiritano S, Nocera A, Possidente K, Nevolo MT, Ventura V, et al. Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms. Exp Diabetes Res [Internet]. 2012 [cited 2014 May 21];2012. Available from:
  22. Russell WR, Gratz SW, Duncan SH, Holtrop G, Ince J, Scobbie L, et al. High-protein, reduced-carbohydrate weight-loss diets promote metabolite profiles likely to be detrimental to colonic health. Am J Clin Nutr. 2011 May 1;93(5):1062–72.
  23. Montonen J, Boeing H, Fritsche A, Schleicher E, Joost H-G, Schulze MB, et al. Consumption of red meat and whole-grain bread in relation to biomarkers of obesity, inflammation, glucose metabolism and oxidative stress. Eur J Nutr. 2013 Feb;52(1):337–45.
  24. Fung TT, van Dam RM, Hankinson SE, Stampfer M, Willett WC, Hu FB. Low-carbohydrate diets and all-cause and cause-specific mortality: Two cohort Studies. Ann Intern Med. 2010 Sep 7;153(5):289–98.
  25. Noto H, Goto A, Tsujimoto T, Noda M. Low-Carbohydrate Diets and All-Cause Mortality: A Systematic Review and Meta-Analysis of Observational Studies. PLoS ONE [Internet]. 2013 Jan 25 [cited 2014 May 9];8(1). Available from:
  26. O’Keefe JH, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142–6.
  27. Lu SC, Wu WH, Lee CA, Chou HF, Lee HR, Huang PC. LDL of Taiwanese vegetarians are less oxidizable than those of omnivores. J Nutr. 2000 Jun;130(6):1591–6.
  28. De Biase SG, Fernandes SFC, Gianini RJ, Duarte JLG. Vegetarian diet and cholesterol and triglycerides levels. Arq Bras Cardiol. 2007 Jan;88(1):35–9.
  29. Krajcovicová-Kudlácková M, Simoncic R, Béderová A, Klvanová J, Brtková A, Grancicová E. Lipid and antioxidant blood levels in vegetarians. Nahr. 1996 Feb;40(1):17–20.
  30. Craig WJ, Mangels AR, American Dietetic Association. Position of the American Dietetic Association: vegetarian diets. J Am Diet Assoc. 2009 Jul;109(7):1266–82.
  31. Mediterranean diet delivers a punch to LDL cholesterol. Mayo Clin Health Lett Engl Ed. 2011 May;29(5):4.
  32. Ornish D. Mostly plants. Am J Cardiol. 2009 Oct 1;104(7):957–8.
  33. Dunn-Emke SR, Weidner G, Pettengill EB, Marlin RO, Chi C, Ornish DM. Nutrient adequacy of a very low-fat vegan diet. J Am Diet Assoc. 2005 Sep;105(9):1442–6.
  34. Ferdowsian HR, Barnard ND. Effects of plant-based diets on plasma lipids. Am J Cardiol. 2009 Oct 1;104(7):947–56.


About The Author

Cyrus Khambatta

Diagnosed with type 1 diabetes at the age of 22, I have spent over a decade learning the fundamentals of nutrition at the doctorate level. My goal is to share my knowledge of practical nutrition and fitness with people with prediabetes, type 1 and type 2 diabetes. Diabetes is an OPPORTUNITY to attain excellent health. Reversing the effects of insulin resistance can be a fun and enjoyable process if the right system is in place. That's why I've spent over 10 years developing a rock solid system that can minimize blood glucose variability and insulin resistance.

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