Tag Archives: Disease

Keep It Simple: Doctors Say Sound Nutrition Should Replace Calorie-Counting and Pharmacotherapy | The Paleo Diet

When we think about enormously complex problems, like the social and economic burdens of chronic degenerative diseases, we sometimes presume that the solutions must also be complex. Complex problems, however, often have simple, straightforward solutions.

Imagine you’re an astronaut living on a space station powered by enormous solar-powered generators. Your worst-case scenario would be for those generators to break down and for you to be missing the tools required to fix them. In 2012, astronauts aboard the International Space Station found themselves in precisely this situation. One of the station’s power distributors went down, but when the astronauts ventured outside to assess the situation, they discovered that metal shaving had accumulated around several critical bolts.

NASA had equipped them with highly technical tools, but none of their tools could remove the shavings, and if the shavings remained in place, the generator could not be repaired. After a thwarted 8-hour repair attempt, the astronauts went back inside to brainstorm solutions. Finally, they improvised a makeshift tool consisting of an allen wrench and a toothbrush. It worked – a $3 toothbrush saved a $100 billion space station.1

Could the same graceful simplicity be applied to the cardiovascular disease and diabetes crises? The American Heart Association estimates that in 2011 the annual cost of cardiovascular disease and stroke in the US was $320 billion.2 Similarly, the cost of diabetes increased over 40% from 2007 to 2012 and now costs at least $245 billion annually in the US.3

In a new editorial published in Open Heart, Doctors Aseem Malhotra, James DiNicolantonio, and Simon Capewell argue that complex, expensive, and ultimately ineffective “solutions” are exacerbating the heart disease and diabetes crises while simple, relatively inexpensive, effective solutions are being overlooked.

Specifically, they argue, “An exaggerated belief in the (modest) benefits of pharmacotherapy, aggressively reinforced by commercial vested interests, can often mislead patients and doctors, and promotes overtreatment in chronic disease management, and may even distract from and undermine the benefits of simple lifestyle interventions.4

In short, our approach to chronic diseases is one of treating symptoms rather than addressing underlying disease causes. Likewise, our approach to food is one focusing on calorie-counting and energy balance rather than sound nutrition. The diet industry generates $58 billion annually the US but long-term follow-up studies show the vast majority of dieters regain the weight they lost during diet regimens.5

So what is the solution? In their Open Heart editorial, the doctors point to numerous randomized controlled trials in which simple dietary interventions resulted in dramatic disease risk reductions. In the DART trial, for example, the consumption of fatty fish among survivors of myocardial infarction resulted in a significant 29% reduction in all-cause mortality compared to control patients. Moreover, in an Italian study, the consumption of 1 daily gram of omega-3 fatty acids led to clinically important and statistically significant reductions in all-cause and cardiovascular disease mortality.

Higher-fat diets inclusive of nuts, olive oil, oily fish, as well as plenty of vegetables, consistently outperform the antiquated low-fat, high-carbohydrate diet recommended by the American Heart Association with respect to attenuating inflammation, atherosclerosis, and thrombosis. In their editorial, the doctors specifically endorse “a high-fat Mediterranean-type diet and lifestyle.” A high-fat Mediterranean-type diet has remarkable overlaps with the Paleo diet, as both emphasize sound nutritional principles and a widely varied, yet balanced diet. Our modern health problems are complex, but the solutions can be as simple as respecting and embracing the dietary traditions and nutritional wisdom of our ancestors.

 

REFERENCES

[1] Garber, M. (September 6, 2012). “Behold, the Toothbrush That Just Saved the International Space Station,” The Atlantic.

[2] Mozaffarian, D., et al. (December 17, 2014). “Heart Disease and Stroke Statistics – 2015 Update,” Circulation 2015, 131.

[3] American Diabetes Association. (April 2013). “Economic costs of diabetes in the U.S. in 2012.” Diabetes Care, 36(4).

[4] Malhortra, A., et al. (August 26, 2015). “It is time to stop counting calories, and time instead to promote dietary changes that substantially and rapidly reduce cardiovascular morbidity and mortality,” Open Heart, 2(1).

[5] Strohacker, K., et al. (January 2010). “Influence of obesity, physical inactivity, and weight cycling on chronic inflammation,” Frontiers in Bioscience, 2.

Treating Malaria with Diet

Reductions in Blood Concentrations of p-aminobenzoic acid (PABA) and Folate are Therapeutic for Malaria Patients

Malaria is one of the most deadly diseases on the planet. It is a life-threatening infection caused by parasites that are transmitted to people through the bites of infected mosquitoes. The disease is responsible for more than 627, 000 deaths worldwide in 2012. Of the estimated deaths, most occur in sub-Saharan Africa (90%) and in children under 5 years of age (77%).

Strategies for the treatment, prevention and control of malaria typically involve pharmaceuticals, insecticides and nettings. Vaccines to prevent this disease have had little or no success to date. Rarely has diet been considered as an effective therapy to prevent or attenuate malarial morbidity (disease incidence) and mortality (disease death rate). Yet, virtually unknown to almost all malaria researchers is the notion that diets maintaining low concentrations of ρ-aminobenzoic acid (PABA) and folate represent an untapped tactic to thwart malarial infection.

How Diet Impacts Malarial Infection

Shikimate Pathway | The Paleo DietAn Achilles heel in the lifecycle of Plasmodia species (the bacteria which causes malaria) is its reliance upon the availability of folate, an essential nutrient for these rapidly growing parasites. Pharmaceuticals such as pyrimethamine and sulfa drugs are somewhat effective anti-malarials because they interfere with the conversion of PABA to folate (depicted in the Shikimate pathway to the left). In vitro (test-tube) experiments indicate that Plasmodia species have the ability to synthesize limited amounts of folate endogenously, however further experiments show that these parasites cannot synthesize sufficient quantities of folate to survive in living animals (in vivo).1 Hence, without adequate supplemental stores of PABA and folate from their host’s tissues, Plasmodia species have no capacity to cause lethal malarial infections. In support of this scenario is an extensive, but older literature reviewed in references2, 3 showing that exclusive milk diets suppress malarial infections in birds, rodents, and primates. Milk contains very little PABA and yields low concentrations of folate (60-90 µg/1000 kcal; ~ 20 % of the DRI for a 3 yr old child). The suppression of malarial symptoms is abrogated when supplemental PABA is added to all milk diets of infected animals.2, 3 Further, rodent models of malaria demonstrate that dietary PABA and folate reduce the efficacy of sulfa drugs,4 and in humans, high blood concentrations of folate also impair the efficacy of pyrimethamine and sulfa drugs.5 An experimental study of 20 West African infants, up to 2 years of age who were naturally infected with Plasmodia falciparum demonstrated that exclusive milk diets reduced parasite density and decreased disease symptoms within a few days in a manner similar to those (n=12) serving as controls and treated with chloroquine therapy.2

The pastoralist Fulani of West and Central Africa exhibit a well established resistance to malaria compared to other non-milk drinking African sympatric ethnic groups that is unexplained by known genetic resistance factors,6 but rather by enhanced immunity.7 Displacement of PABA and folate rich foods by milk in this population may attenuate malaria infection while allowing immune exposure, serving to prevent serious disease sequelae and facilitate the establishment of protective immunity. In support of this concept are data showing a high prevalence of adult lactase persistence (~68 % of the population)8 in the Fulani which may represent a previously unrecognized genetic factor that indirectly reduces malarial mortality. Accordingly, in high malarial regions where adult lactase persistence is widespread, reduced dietary PABA and folate intake caused by high milk consumption may disrupt the life cycle of Plasmodia species by impairing folate metabolism, thereby reducing childhood malaria fatalities and overall morbidity within adults.

Except for a single modern study,1 research involving the efficacy of PABA deficient diets in preventing or attenuating malaria symptoms effectively stopped in the early 1970s with the widespread use of insecticides, nettings and pharmaceuticals.9 One of the major shortcomings in all of these early experiments was the failure to report milk PABA concentrations2, 3 which conceivably could have been quite variable – perhaps caused by various fodders fed to the cows or by different milk processing procedures. Additionally, because PABA is not an essential human nutrient, no tables of the PABA concentrations in common foods have ever been published. To my knowledge only a single study has reported the PABA concentrations in any food items (five vegetables: carrots, spinach, brussel sprouts, endive, and lettuce),10 whereas extensive USDA tables exist showing the folate concentrations in foods. Consequently, a crucial need exists to determine the PABA content of foods so that anti-malarial diets can be formulated and eventually tested.

The formulation of PABA deficient diets for humans will have no adverse health consequences as PABA is not required in human nutrition. Because about 80% of all deaths attributed to malaria occur in sub-Saharan Africa, mainly among children less than 5 years of age,2 the greatest risk to their lives comes not from inadequate folate intake, but rather from malaria.5 At a meeting hosted by the World Health Organization in 2006, five expert reports concluded that reducing folic acid supplementation in sub-Saharan African children may reduce fatal malarial infections.11

Conclusions

PABA deficient diets have virtually no adverse health effects in humans (both children and adults) because PABA is not required for human nutrition. Yet within the confines of the bacteria, Plasmodia species which cause malaria, deficiencies of this compound in their host’s bloodstream may have devastating effects upon the bacteria’s own metabolism and ability to reproduce and elicit lethal infections in humans. Unfortunately, no tables of PABA concentrations in everyday foodstuffs currently exist. Accordingly, we have no idea how to formulate PABA deficient diets in humans to thwart lethal malarial infections.

A good starting point would be descriptive in nature with the goal of characterizing the PABA content of a wide variety of foodstuffs, including sub-Saharan African ethnic foods. This PABA database along with pre-existing folate databases could be employed to formulate low PABA and folate diets that will be nutritionally adequate in all other respects. Further, it may be possible to formulate low PABA and folate diets without the use of milk which is contraindicated in many sub-Saharan African populations because of their inability to digest the milk sugar lactose without gastric upset.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

References

1. Kicska GA, Ting LM, Schramm VL, Kim K. Effect of dietary p-aminobenzoic acid on murine Plasmodium yoelii infection. J Infect Dis. 2003 Dec 1;188(11):1776-81

2. Kretschmar W, Voller A. Suppression of Plasmodium falciparum malaria in Aotus monkeys by milk diet. Z Tropenmed Parasitol. 1973 Mar;24(1):51-9.

3. Nowell F. The effect of a milk diet upon Plasmodium berghei, Nuttallia (=Babesia) rodhaini and Trypanosoma brucei infections in mice. Parasitology. 1970 Dec;61(3):425-33.

4. Jacobs RL Role of p-aminobenzoic acid in Plasmodium berghei infection in the mouse.
Exp Parasitol. 1964 Jun;15:213-25

5. Carter JY, Loolpapit MP, Lema OE, Tome JL, Nagelkerke NJ, Watkins WM Reduction of the efficacy of antifolate antimalarial therapy by folic acid supplementation. Am J Trop Med Hyg. 2005 Jul;73(1):166-70.

6. Modiano D, Petrarca V, Sirima BS, Nebié I, Diallo D, Esposito F, Coluzzi M. Different response to Plasmodium falciparum malaria in west African sympatric ethnic groups. Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13206-11

7. Bereczky S, Dolo A, Maiga B, Hayano M, Granath F, Montgomery SM, Daou M, Arama C, Troye-Blomberg M, Doumbo OK, Färnert A. Spleen enlargement and genetic diversity of Plasmodium falciparum infection in two ethnic groups with different malaria susceptibility in Mali, West Africa. Trans R Soc Trop Med Hyg. 2006 Mar;100(3):248-57

8. Swallow DM. Genetics of lactase persistence and lactose intolerance. Annu Rev Genet. 2003;37:197-219

9. Walther B, Walther M. What does it take to control malaria? Ann Trop Med Parasitol. 2007 Dec;101(8):657-72

10. Zhang GF, Mortier KA, Storozhenko S, Van De Steene J, Van Der Straeten D, Lambert WE. Free and total para-aminobenzoic acid analysis in plants with high-performance liquid chromatography/tandem mass spectrometry. Rapid Commun Mass Spectrom. 2005; 19(8): 963-9.

11. Oppenheimer S. Comments on background papers related to iron, folic acid, malaria and other infections. Food Nutr Bull. 2007 Dec;28(4 Suppl):S550-9

Sugar Is Killing Us

It’s no surprise a vast majority of the world recognizes sugar is destroying our health and ruining our lives.1, 2, 3, 4 Over the last 30 years, we’ve seen disease rates skyrocket, alongside our climbing intake of sugar.5, 6, 7, 8, 9 Our concern for this creeping information wavers and takes a backseat to social media, “selfies” and celebrities.10, 11

The growing concern around sugar deserves not only immediate attention, but immediate action.12, 13, 14 Unfortunately, the roadblocks are endless.15, 16 The least of which, is the food industry itself.17 Take, for example, the makers of orange juice, a product which contains a whopping 21g of sugar in a mere 8oz glass,18 and is traditionally the standard American breakfast beverage.

The addictive properties of sugar are well-documented, as are the risks of consuming too much.19, 20 And yet, we can’t seem to stop ourselves.21, 22 Sugar is often added to products surreptitiously, without our consent.23 It is also marketed – quite heavily – towards children.24, 25 We must put a stop to this. Our children are our future, and if they are obese, cognitively impaired, and sick – how much of a future do they really have?

So why sugar is so detrimental? The biochemistry says it all.20 As sugar enters the bloodstream, insulin is secreted.26 The more sugar you eat, the more insulin you secrete. High sugar diets can lead to insulin resistance.27 This condition is one of the hallmarks of obesity and overweight humans everywhere.28 If you consume too much sugar, you’re bound to experience hypoglycemia, commonly referred to as your “sugar crash.”29 This leaves your body craving more sugar – and the addictive process perpetuates.30

Sugar is Killing Us | The Paleo Diet

Sagittal, Coronal and Axial Representations of Glucose-related Regional Grey (A) and White (B) Matter Volumes.
doi:10.1371/journal.pone.0073697.g002

It’s a simple model, but one which we are all familiar with.36 Stress also leads us to overeat.31, 37 And we do not over-consume just any calories, but rather we eat neurologically-rewarding foods.38 This means foods that are either: high in sugar, or foods high in sugar and fat.39 In a study from 2010, researchers showed a disruption of sensitivity to brain-stimulation reward (BSR) from eating high fat and/or high carbohydrate food.40 So you become accustomed to the rewards of these foods, and crave them more.41

The rates of diabetes both nationally, and worldwide, have skyrocketed.42 This is not debatable. Guess what else has skyrocketed, in conjunction with diabetes rates? You guessed it: sugar consumption. There are now obese newborns.43, 44

All of these problems and conditions can be linked directly to sugar intake, and yet, you may be blindsided by how much sugar you’re consuming in the first place. A recent study showed food manufacturers not disclosing the actual values of fructose corn syrup on their product labels.45 Does this bother you? It should.

Sugar is Killing Us | The Paleo Diet

Besides the physiologic effects of too much sugar, there are vast and damning economic effects.32 Take, for example, that diabetes alone costs the United States $245 billion per year.46 This is a rise of 41% in a mere five years. That is an absolutely terrifying figure. Have I scared you yet?

How about the fact that higher glucose levels are associated with lower memory and reduced hippocampal microstructure?47 Or, how about the study from the New England Journal of Medicine, which showed that higher glucose levels may be a risk factor for dementia.48 What was interesting (and alarming) about this finding, was that this was the risk for those without diabetes. This means that you can be taking in “normal” amounts of sugar, not exhibit symptoms of diabetes, and still be risking dementia. Act and don’t turn a blind eye. Save your health.

Sugar is Killing Us | The Paleo Diet

N Engl J Med. Aug 8, 2013; 369(6): 540–548.

Other studies have shown, unsurprisingly, that sugar consumption promotes weight gain in children and adults.33 All behaviors have a biochemical basis. ADHD, ADD, et al, are all likely partially due to a poor diet.49, 50 A diet that, almost always, is high in sugar.51, 52 Since studies have shown that intense sweetness surpasses cocaine reward, it is not surprising that many Americans cannot stop consuming sugar.53 But, in order to help stop alarmingly rising healthcare costs, they must stop their gluttonous consumption, and re-focus their diet on whole, real foods, all part of a Paleo Diet.

Other studies have shown that most US adults consume more added sugar than is recommended,34 and that this overconsumption leads to increased risk for cardiovascular disease mortality.54 This is literally the smoking gun that shows that sugar is killing us. Other studies have shown that higher levels of sugar also lower fitness.55 And another interesting study showed that junk food alone made rats lazy.56 Does this give you food for thought? Perhaps you should prioritize a change to your diet?

Insulin, which is secreted in order to deal with sugar in the bloodstream, blocks leptin signaling.35 Leptin is the “satiety” hormone, which helps to tell our hypothalamus to stop eating.57 Since we are now secreting 2-3 times the amount of insulin than we used to, you can see, directly, how this has resulted in disastrous consequences for our world’s health.58 And why are we secreting more insulin? Quite simply, to deal with all the sugar we are over-consuming. It is not a complicated formula, but it is a formula that is bankrupting our nation, and making so many sick and overweight.

Prevention is paradigm. Avoid a high-sugar diet, become leaner, think faster, and feel better. There is not a single better thing you can do, diet-related, that will help you to improve your health. A Paleo Diet, which is intrinsically low in sugar, high in nutrient-dense foods, and filled with micronutrients, is the best path to wellness.

[/full_width]

References

1. Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature. 2012;482(7383):27-9.

2. Available at: http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html. Accessed September 13, 2014.

3. Available at: http://www.telegraph.co.uk/foodanddrink/healthyeating/9987825/Sweet-poison-why-sugar-is-ruining-our-health.html. Accessed September 13, 2014.

4. Moreira PI. High-sugar diets, type 2 diabetes and Alzheimer’s disease. Curr Opin Clin Nutr Metab Care. 2013;16(4):440-5.

5. Ford ES, Giles WH, Mokdad AH. Increasing prevalence of the metabolic syndrome among u.s. Adults. Diabetes Care. 2004;27(10):2444-9.

6. Seaquist ER. Addressing the burden of diabetes. JAMA. 2014;311(22):2267-8.

7. Available at: http://www.cdc.gov/nchs/data/databriefs/db122.htm. Accessed September 13, 2014.

8. Available at: http://wholehealthsource.blogspot.com/2012/02/by-2606-us-diet-will-be-100-percent.html. Accessed September 13, 2014.

9. Johnson RK, Appel LJ, Brands M, et al. Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation. 2009;120(11):1011-20.

10. Available at: http://www.newsherald.com/opinions/letters-to-the-editor/too-many-americans-are-selfish-and-self-absorbed-1.195653. Accessed September 13, 2014.

11. Available at: http://www.today.com/id/30312181/ns/today-today_books/t/me-me-me-americas-narcissism-epidemic/#.VBTMylbD_IU. Accessed September 13, 2014.

12. Available at: http://well.blogs.nytimes.com/2014/02/19/learning-to-cut-the-sugar/. Accessed September 13, 2014.

13. Available at: http://blogs.kqed.org/newsfix/2014/09/12/berkeley-is-talking-about-sugar-and-the-conversation-isnt-sweet/. Accessed September 13, 2014.

14. Available at: http://www.telegraph.co.uk/news/worldnews/europe/netherlands/10314705/Sugar-is-addictive-and-the-most-dangerous-drug-of-the-times.html. Accessed September 13, 2014.

15. Available at: http://www.nytimes.com/2010/07/03/nyregion/03sodatax.html. Accessed September 13, 2014.

16. Available at: http://www.publicintegrity.org/2009/11/04/2758/food-lobbys-war-soda-tax. Accessed September 13, 2014.

17. Available at: http://www.npr.org/blogs/thesalt/2013/02/26/172969363/how-the-food-industry-manipulates-taste-buds-with-salt-sugar-fat. Accessed September 13, 2014.

18. Available at: http://www.orangejuicefacts.com/nutrition.html. Accessed September 13, 2014.

19. Ahmed SH, Guillem K, Vandaele Y. Sugar addiction: pushing the drug-sugar analogy to the limit. Curr Opin Clin Nutr Metab Care. 2013;16(4):434-9.

20. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

21. Gearhardt A, Roberts M, Ashe M. If sugar is addictive…what does it mean for the law?. J Law Med Ethics. 2013;41 Suppl 1:46-9.

22. Available at: http://www.ars.usda.gov/is/AR/archive/jun00/sugar0600.htm. Accessed September 13, 2014.

23. Available at: http://www.webmd.com/food-recipes/features/sugar-shockers-foods-surprisingly-high-in-sugar. Accessed September 13, 2014.

24. Available at: http://www.cbsnews.com/news/cdc-kids-consume-too-much-sugar-mostly-from-processed-foods/. Accessed September 13, 2014.

25. Lythgoe A, Roberts C, Madden AM, Rennie KL. Marketing foods to children: a comparison of nutrient content between children’s and non-children’s products. Public Health Nutr. 2013;16(12):2221-30.

26. Daly M. Sugars, insulin sensitivity, and the postprandial state. Am J Clin Nutr. 2003;78(4):865S-872S.

27. Musselman LP, Fink JL, Narzinski K, et al. A high-sugar diet produces obesity and insulin resistance in wild-type Drosophila. Dis Model Mech. 2011;4(6):842-9.

28. Gallagher EJ, Leroith D, Karnieli E. Insulin resistance in obesity as the underlying cause for the metabolic syndrome. Mt Sinai J Med. 2010;77(5):511-23.

29. Hofeldt FD. Reactive hypoglycemia. Endocrinol Metab Clin North Am. 1989;18(1):185-201.

30. Yang Q. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010;83(2):101-8.

31. Oliver KG, Huon GF, Zadro L, Williams KD. The role of interpersonal stress in overeating among high and low disinhibitors. Eat Behav. 2001;2(1):19-26.

32. Available at: http://www.forbes.com/sites/aroy/2012/04/23/trustees-medicare-will-go-broke-in-2016-if-you-exclude-obamacares-double-counting/. Accessed September 13, 2014.

33. Malik, Vasanti S., Matthias B. Schulze, and Frank B. Hu. “Intake of sugar-sweetened beverages and weight gain: a systematic review.” The American journal of clinical nutrition 84.2 (2006): 274-288.

34. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med. 2014.

35. Kellerer M, Lammers R, Fritsche A, et al. Insulin inhibits leptin receptor signalling in HEK293 cells at the level of janus kinase-2: a potential mechanism for hyperinsulinaemia-associated leptin resistance. Diabetologia. 2001;44(9):1125-32.

36. Available at: http://www.huffingtonpost.co.uk/2013/07/26/why-is-sugar-so-addictive_n_3643965.html. Accessed October 2, 2014.

37. Greeno CG, Wing RR. Stress-induced eating. Psychol Bull. 1994;115(3):444-64.

38. Available at: http://www.cnn.com/2012/02/08/health/healthy-eating-tips-stress/. Accessed October 2, 2014.

39. Torres SJ, Nowson CA. Relationship between stress, eating behavior, and obesity. Nutrition. 2007;23(11-12):887-94.

40. Epstein DH, Shaham Y. Cheesecake-eating rats and the question of food addiction. Nat Neurosci. 2010;13(5):529-31.

41. Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010;13(5):635-41.

42. Weeratunga P, Jayasinghe S, Perera Y, Jayasena G, Jayasinghe S. Per capita sugar consumption and prevalence of diabetes mellitus–global and regional associations. BMC Public Health. 2014;14:186.

43. Soubry A, Murphy SK, Wang F, et al. Newborns of obese parents have altered DNA methylation patterns at imprinted genes. Int J Obes (Lond). 2013.

44. Available at: http://healthland.time.com/2012/11/29/predicting-obesity-at-birth/. Accessed October 2, 2014.

45. Walker RW, Dumke KA, Goran MI. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition. 2014;30(7-8):928-35.

46. Available at: http://www.diabetes.org/advocacy/news-events/cost-of-diabetes.html. Accessed September 29, 2014.

47. Kerti L, Witte AV, Winkler A, Grittner U, Rujescu D, Flöel A. Higher glucose levels associated with lower memory and reduced hippocampal microstructure. Neurology. 2013;81(20):1746-52.

48. Crane PK, Walker R, Hubbard RA, et al. Glucose levels and risk of dementia. N Engl J Med. 2013;369(6):540-8.

49. Millichap JG, Yee MM. The diet factor in attention-deficit/hyperactivity disorder. Pediatrics. 2012;129(2):330-7.

50. Johnson RJ, Gold MS, Johnson DR, et al. Attention-deficit/hyperactivity disorder: is it time to reappraise the role of sugar consumption?. Postgrad Med. 2011;123(5):39-49.

51. Kanoski SE, Davidson TL. Western diet consumption and cognitive impairment: links to hippocampal dysfunction and obesity. Physiol Behav. 2011;103(1):59-68.

52. Crescenzo R, Bianco F, Coppola P, et al. Fructose supplementation worsens the deleterious effects of short-term high-fat feeding on hepatic steatosis and lipid metabolism in adult rats. Exp Physiol. 2014;99(9):1203-13.

53. Lenoir M, Serre F, Cantin L, Ahmed SH. Intense sweetness surpasses cocaine reward. PLoS ONE. 2007;2(8):e698.

54. Schmidt LA. New unsweetened truths about sugar. JAMA Intern Med. 2014;174(4):525-6.

55. Ruff JS, Suchy AK, Hugentobler SA, et al. Human-relevant levels of added sugar consumption increase female mortality and lower male fitness in mice. Nat Commun. 2013;4:2245.

56. Blaisdell AP, Lau YL, Telminova E, et al. Food quality and motivation: a refined low-fat diet induces obesity and impairs performance on a progressive ratio schedule of instrumental lever pressing in rats. Physiol Behav. 2014;128:220-5.

57. Myers MG, Cowley MA, Münzberg H. Mechanisms of leptin action and leptin resistance. Annu Rev Physiol. 2008;70:537-56.

58. Larsson H, Ahrén B. Glucose intolerance is predicted by low insulin secretion and high glucagon secretion: outcome of a prospective study in postmenopausal Caucasian women. Diabetologia. 2000;43(2):194-202.

Rebuttal | The Paleo Diet

A series of three scientific papers were published this this month in the early edition of the Proceedings of the National Academy of Sciences1-3 evaluating the diet of numerous species of fossilized hominins, bipedal or upright walking apes, who lived in Africa from 4.1 to 1.4 million years ago. The diet of a grass eating baboon was examined as well.4 Many of the authors of these papers are friends and colleagues whose data contribute to our understanding of our remote African ancestors’ diets. Collectively, the papers examined the following hominin genus’s and the time frame they lived: Australopithecus (circa 4 million years ago [MYA]), Kenyanthropus (circa 3-3.6 MYA), Paranthropus (circa 2.5-1.4 MYA), and early Homo (circa 2.3-1.5 MYA).

Before I get into the details of these studies, let me first openly reprimand some of the popular press who have incorrectly interpreted these studies by suggesting that our distant ancestors were regular consumers of grass and grass seeds (cereal grains). For instance, popular blogger Carrie Arnold, titles her write-up5 of these three scientific studies as, “Even Our Ancestors Never Really Ate the “Paleo Diet,” and goes on to say, “Researchers are just beginning to understand what ancient humans ate, and these recent studies show that grasses and grains have been part of the human diet for millions of years.” As I will shortly show you, this statement represents sensationalistic journalism and is patently false, as nowhere in any of these three papers1-3 is this conclusion reached by any of the authors.

Another piece of inaccurate and hyped journalism6 by author Chris Joyce at NPR labels his piece, “Grass: It’s What’s For Dinner (3.5 Million Years Ago).” Chris then tells us, “What the tale of the teeth reveals is this: About 3.5 million years ago, our ancestors started switching from the ape diet – leaves and fruit – to grasses and grass-like sedges.” This statement is false and again nowhere in any of these three papers1-3 is this assumption made by the scientists who wrote these manuscripts. Chris finally gets it right in his following statement, “Now, one thing this carbon isotope technique can’t tell is whether Australopithecus just grazed like a bunch of antelope, or whether they ate the antelope that did the grazing.” However, in his final paragraph his conclusion again is erroneous: “So, what to make of this? Well, for one, those who favor a “Paleo diet” that resembles what our early ancestors lived on might consider investing in a lawn mower. After all, lawn grass is probably American’s largest un-harvested crop – there’s plenty to go around. Why not go back to our roots?”

Catherine Griffin, a writer for Science World Reports obviously did not carefully read any of these three papers1-3 because of incorrect statements she has made in her brief article,7 “Human Ancestors’ Ape-like Diet Changed 3.5 Million Years Ago to Grass”. Catherine informs us, “Feel like eating some grass? Didn’t think so – but our ancient ancestors did. About 3.5 million years ago, our human forebears added tropical grasses and sedges to an ape—like diet of leaves and fruits from trees and shrubs.” She goes on to make other statements like, “In the end, the scientists found a surprising increase in the consumption of grasses and sedges” and “The earliest ancestors that consumed substantial amounts of grass foods . . .” which were never made in the original scientific papers.

In science, the devil is almost always in the details. Accordingly, all three of these popular science writers have done their readers a disservice by inaccurately reporting the details of these three studies1-3 and making assumptions about ancient hominin diets that the scientists themselves did not make.

In all three papers the measurement of two stable isotopes of carbon (13C and 12C) were made from samples of enamel in teeth of extinct hominins. From the ratio 13C/12C a difference (delta) (δ13C) is calculated relative to a standard value (8). δ13C values can then be used to determine if the carbon isotopes in the enamel ultimately originated from plants using either the C3 or C4 photosynthesis pathways.

In Africa and elsewhere, C4 plants include grasses and sedges and little else, whereas C3 plants include trees, shrubs, herbs and bushes. C4 plants incorporate relatively more 13C into their tissues during photosynthesis than do C3 plants. Hence, δ13C values extracted from enamel can reveal the dietary source of the isotopic signature, be it: 1) grasses and sedges, 2) trees, bushes, shrubs, herbs or 3) a combination of both categories of plants.

Unfortunately, a number of fundamental limitations exist with δ13C analysis to evaluate diet. δ13C measurements cannot determine the exact species of either C3 or C4 plants that were consumed, but more importantly δ13C values cannot distinguish if the C3 or C4 signatures originated from the direct consumption of plants or from the indirect consumption of animals that consumed these plants. In all three studies,1-3 this crucial point was brought out again and again by the authors. Apparently, the popular science writers covering these papers missed it. The data from all three papers1-3 corroborates the increasing body of literature8 demonstrating an increased C4 signature in the enamel of African hominins starting about 3.5 MYA, but whether or not it resulted from increased consumption of animal or plant foods or both is unknown. The authors of one of these three scientific papers1 put it best, “The 13C-enriched resources that hominins ate remain unknown and must await additional integration of existing paleodietary proxy data and new research on the distribution, abundance, nutrition and mechanical properties of C4 (and CAM) plants.”

I would like to point out a number of logical shortcomings with any interpretation of the hominin C4 data suggesting that it originated primarily from increased consumption of either grass leaves, grass seeds (cereal grains) and sedges rather than from consumption of animals (grazers) that ate grasses and grains. The point in time (~3.5 MYA) at which the C4 signature begins to increase occurs simultaneously with the earliest known use (before 3.39 MYA) of stone tools to cut flesh from animal carcasses and to extract marrow from their bones.9 Such hominin dietary practices have also been documented by 2.5 MYA10 and appear to be widely employed by 2.0 MYA11 and by 1.5 MYA.12 Hence by triangulating these indisputable archaeological facts with stable carbon isotope data, it is virtually certain that δ13C values in hominin enamel were enriched partially or perhaps mainly from increasing consumption of animals that ate C4 plants.

Other lines of evidence indicate that early African hominins were increasingly consuming more animal foods during the same time interval (3.5 MYA to 1.5 MYA) that δ13C had become enriched. Aiello and Wheeler13 have shown that the mass of the human gastrointestinal tract is only about 60% of that expected for a similar-sized primate. Consequently, the increase in brain size that occurred in hominins starting ~2.5 MYA was balanced by an almost identical reduction in the size of the gastrointestinal tract.13 The selective pressures that simultaneously allowed for both a reduction in gut size and an increase in brain size are attributed to an improvement in dietary quality (DQ) that occurred largely as a result of increased consumption of animal foods by Australopithecine species prior to the emergence of the first members of Homo.13-15 Because a diet with an increased DQ contains less structural plant parts and more animal material,16 its nutrient and energy density is greater. Hence the greater DQ of animal foods permitted relaxation of the selective pressures in hominins that formerly selected for a large, metabolically active gut necessary to process low DQ foods, which in turn permitted the natural selection of a large metabolically active brain13, 14 Grass leaves and seeds maintain a low DQ,15 and are high in fiber and cellulose and are indigestible in their raw, unprocessed state in modern humans.17 Accordingly, the proposition that increased consumption of grass leaves and seeds were the C4 source in hominin enamel, is inconsistent with the evolutionary gut/brain metabolic tradeoff.13-15 Selective pressures that reduce the size and metabolic activity of the gut require more energetically dense foods like meat and marrow – not energy poor, high cellulose and high fiber foods like grasses and sedges.

In addition to their low DQ, grass leaves and seeds are devoid of long chain fatty acids of both the omega 6 family (arachidonic acid, 20:4n6) and omega 3 family (docosahexanoic acid, 22:6n3), as are all plant foods.15 These fatty acids are necessary structural elements required for the synthesis of brain and neural tissues and cannot be produced endogenously in sufficient quantities to relax the selective pressures normally constraining encephalization (brain volume expansion relative to body weight). Therefore, exogenous sources of these two fatty acids must be obtained through diet in hominins to permit the evolution of large metabolically active brains (15, 18-21). Likely candidate animal foods which simultaneously increased the DQ and provided arachidonic acid (AA) and docosahexanoic acid (DHA) were scavenged de-fleshed long bones (which contain marrow – a high fat food) and skulls (which contain brains – high in AA and DHA) from carnivore kills.15 These foods along with meats from grazing animals likely represent the dominant dietary source for the increasing C4 signature in our African ancestors.

Another nutritional point lends little support to the notion that the increasing C4 signature in hominins starting 3.5 MYA resulted from direct consumption of grass leaves or seeds. All great apes (chimps, gorillas, orangutans and gibbons) living in their native environment bear δ13C values indicative of near total reliance upon C3 plants. Only a single higher primate, a baboon species, Theropithecus gelada, consumes grass leaves and seeds as their primary dietary source. Accordingly, this baboon maintains a carbon isotopic signature that is nearly 100 % C4 derived.4

High reliance upon grass and grass seeds in Theropithecus gelada or in any hominin requires a number of evolutionary adaptations in the digestive tract to accommodate these low quality, high cellulose foods – none of which have been observed in contemporary humans. All vertebrates lack the enzyme cellulase which is required to breakdown cellulose and hemicellulose found in grass leaves and seeds into glucose. Mammals that rely heavily upon grass and grass seed consumption for their sustenance have evolved large hindguts (caecums) or a four compartment stomach (ruminants) containing enormous quantities of microflora which have the capacity to ferment and breakdown cellulose, hemicellulose, starches and proteins into simpler compounds which can then be assimilated and metabolized by the host animal. In the case of Theropithecus gelada (the grass eating baboon), it has evolved a large hindgut where microbial fermentation of grass takes place.22 In contemporary humans, and in the hominin line that led to Homo, there is no credible evidence that gut morphology became larger and more metabolically active to support fermentation of cellulose in the caecum, but rather the opposite.13, 14 Hence, without the evolution of hindgut fermentation, efficient consumption of grass and grass seeds would have been impossible in any hominin species.

Other comparative physiological data between modern humans and the grass eating baboon (Theropithecus gelada) support the notion that the increasing C4 signature in evolving African hominins was not a result of grass or sedge consumption. Dicots or C3 plants produce compounds called tannins which act as a chemical defense system that discourage animals from eating them. Monocots or C4 plants (such as grass and sedges) do not synthesize tannins.23 Over the course of evolution, mammals that consume tannin containing C3 plants have evolved measures to counter the adverse effects of tannins. The most important of these mechanisms are salivary proteins that act as a defense against dietary tannins.24 These proline rich salivary proteins (PRPs) bind tannins and form stable complexes which prevent tannins from producing adverse health effects.24-27

Species that usually ingest tannin containing foods as part of their natural diets produce high levels of PRPs, whereas species not exposed to tannins produce little or no PRPs.24 In this regard, the saliva of the grass (C4) eating baboon (Theropithecus gelada) produces a saliva devoid of PRPs23 In contrast, modern humans synthesize a saliva containing abundant concentrations of PRPs25-27 which have been suggested to result from the long evolutionary history of fruit and vegetable (C3 plants) consumption in human ancestors.25 If ancestral African hominins had intensely exploited C4 plants (grasses and sedges) for millions of years, then it might be expected that the line of hominins that led to Homo and modern humans would also maintain low concentrations of salivary PRPs similar to Theropithecus gelada. Data in contemporary Homo sapiens do not support this conclusion.

In summary, recent comprehensive analyses1-3 of δ13C values in the enamel of African hominins from 4.1 to 1.5 MYA support the conclusion that plants of C4 origin were ultimately responsible for this isotopic signature. Nevertheless, when the isotopic data is triangulated from archaeological, physiological and nutrition evidence, it is apparent that the C4 signature in ancestral African hominin enamel almost certainly is resultant from increased consumption of animals that consumed C4 plants.

I have written a formal letter to the Proceedings of the National Academy of Sciences to address shortcomings. I appreciate your willingness to help set the record straight by sharing this post and among others, Medical Meals’ Dr. Mark J. Smith’s Rebuttal to Christina Warinner’s TED talk “Debunking the Paleo Diet.”

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

References

1. Matt Sponheimer, Zeresenay Alemseged, Thure E. Cerling, Frederick E. Grine, William H. Kimbel, Meave G. Leakey, Julia A. Lee-Thorp, Fredrick Kyalo Manthi, Kaye E. Reed, Bernard A. Wood, and Jonathan G. Wynn. Isotopic evidence of early hominin diets. PNAS 2013 : 1222579110v1-201222579.

2. Jonathan G. Wynn, Matt Sponheimer, William H. Kimbel, Zeresenay Alemseged, Kaye Reed, Zelalem K. Bedaso, and Jessica N. Wilson. Diet of Australopithecus afarensis from the Pliocene Hadar Formation, Ethiopia. PNAS 2013 : 1222559110v1-201222559.
3. Thure E. Cerling, Fredrick Kyalo Manthi, Emma N. Mbua, Louise N. Leakey, Meave G. Leakey, Richard E. Leakey, Francis H. Brown, Frederick E. Grine, John A. Hart, Prince Kaleme, Hélène Roche, Kevin T. Uno, and Bernard A. Wood. Stable isotope-based diet reconstructions of Turkana Basin hominins. PNAS 2013 : 1222568110v1-201222568

4. Thure E. Cerling, Kendra L. Chritz, Nina G. Jablonski, Meave G. Leakey, and Fredrick Kyalo Manthi. Diet of Theropithecus from 4 to 1 Ma in Kenya. PNAS 2013 : 1222571110v1-201222571

5. Arnold, Carrie. “Even Our Ancestors Never Really Ate the “Paleo Diet” – The Crux | Discovermagazine.com.” DISCOVER Magazine: The Crux. Kalmbach Publishing Co., 3 June 2013.

6. Joyce, Chris. “Grass: It’s What’s For Dinner (3.5 Million Years Ago).” NPR the Salt. NPR, 3 June 2013.

7. Griffin, Catherine. “Human Ancestors’ Ape-like Diet Changed 3.5 Million Years Ago to Grass.” Science World Report: Nature & Environment. Science World Report, 4 June 2013.

8. Lee-Thorp JA, Sponheimer M, Passey BH, de Ruiter DJ, Cerling TE. Stable isotopes in fossil hominin tooth enamel suggest a fundamental dietary shift in the Pliocene. Phil. Trans. R. Soc. B (2010) 365, 3389–3396.

9. McPherron SP, Alemseged Z, Marean CW, Wynn JG, Reed D, Geraads D, Bobe R, Béarat HA. Evidence for stone-tool-assisted consumption of animal tissues before 3.39 million years ago at Dikika, Ethiopia. Nature. 2010 Aug 12;466(7308):857-60

10. de Heinzelin J, Clark JD, White T, Hart W, Renne P, WoldeGabriel G, Beyene Y, Vrba E. Environment and behavior of 2.5-million-year-old Bouri hominids. Science. 1999 Apr 23;284(5414):625-9.

11. Ferraro JV, Plummer TW, Pobiner BL, Oliver JS, Bishop LC, Braun DR, Ditchfield PW, Seaman JW 3rd, Binetti KM, Seaman JW Jr, Hertel F, Potts R. Earliest archaeological evidence of persistent hominin carnivory. PLoS One. 2013 Apr 25;8(4):e62174.

12. Pobiner BL, Rogers MJ, Monahan CM, Harris JW. New evidence for hominin carcass processing strategies at 1.5 Ma, Koobi Fora, Kenya. J Hum Evol. 2008 Jul;55(1):103-30.

13. Aiello L, Wheeler P. The expensive tissue hypothesis. Curr Anthropol 1995;36:199-221.

14. Leonard WR, Robertson ML: Evolutionary perspectives on human nutrition: the influence of brain and body size on diet and metabolism. Am J Hum Biol 1994;6:77–88.

15. Cordain L, Watkins BA, Mann NJ. Fatty acid composition and energy density of foods available to African hominids: evolutionary implications for human brain development. World Review of Nutrition and Dietetics, 2001, 90:144-161.
16. Sailer LD, Gaulin SC, Boster JS, Kurland JA: Measuring the relationship between dietary quality and body size in primates. Primates 1985;26:14–27.

17. Cordain L, (1999). Cereal grains: humanity’s double edged sword. World Review of Nutrition and Dietetics, 84: 19-73.

18. Broadhurst CL, Cunnane SC, Crawford MA: Rift valley lake fish and shellfish provided brainspecific nutrition for early Homo. B J Nutr 1998;79:3–21.

19. Crawford MA, Sinclair AJ: The long chain metabolites of linoleic and linolenic acids in liver and brains of herbivores and carnivores. Comp Biochem Physiol 1976;54B:395–401.

20. Crawford MA, Bloom M, Broadhurst CL, Schmidt WF, Cunnane SC, Galli C, Gehbremeskel K, Linseisen F, Lloyd-Smith J, Parkington J: Evidence for the unique function of docosahexaenoic acid during the evolution of the modern hominid brain. Lipids 1999;34:s39–s47.

21. Crawford MA: The role of dietary fatty acids in biology: Their place in the evolution of the human brain. Nutr Rev 1992;50:3–11.

22. Mau M, Johann A, Sliwa A, Hummel J, Südekum KH. Morphological and physiological aspects of digestive processes in the graminivorous primate Theropithecus gelada-a preliminary study. Am J Primatol. 2011 May;73(5):449-57

23. Mau M, Südekum KH, Johann A, Sliwa A, Kaiser TM. Saliva of the graminivorous Theropithecus gelada lacks proline-rich proteins and tannin-binding capacity.Am J Primatol. 2009 Aug;71(8):663-9

24. Shimada T. Salivary proteins as a defense against dietary tannins. J Chem Ecol. 2006 Jun;32(6):1149-63

25. Bennick A. Interaction of plant polyphenols with salivary proteins. Crit Rev Oral Biol Med. 2002;13(2):184-96

26. Bacon JR, Rhodes MJ. Binding affinity of hydrolyzable tannins to parotid saliva and to proline-rich proteins derived from it. J Agric Food Chem. 2000 Mar;48(3):838-43.

27. Yan Q, Bennick A. Identification of histatins as tannin-binding proteins in human saliva. Biochem J. 1995 Oct 1;311 ( Pt 1):341-7

ABSTRACT

This editorial outlines the data supporting aggressive lipid goals and options for treating low-density lipoprotein (LDL) cholesterol to a range of approximately 30 to 70 mg/dl. The physiologically normal cholesterol range is approximately 30 to 70 mg/dl for native hunter-gatherers, healthy human neonates, free-living primates, and virtually all wild mammals. Randomized statin trials in patients with recent acute coronary syndromes and stable coronary artery disease have demonstrated that cardiovascular events are reduced and cardiovascular survival optimized when LDL cholesterol is reduced to <70 mg/dl. Secondary prevention trials have shown a decrease in all-cause mortality in proportion to the magnitude of LDL cholesterol reduction. An original analysis of available data shows that the ability of a lipid-lowering therapy to reduce the C-reactive protein level is closely correlated with its efficacy in LDL cholesterol reduction. Randomized trial data have shown no relation between either percentage LDL cholesterol decrease or final LDL cholesterol level achieved and the risk for myopathy or hepatic transaminase elevations associated with statins. Therefore, intensive LDL cholesterol reduction to levels of 30 to 70 mg/dl should be pursued in subjects with or at high risk for coronary artery disease.

[download id=61]