Tag Archives: high protein diet

New Research Highlights Health Benefits of  High Protein Diets | The Paleo Diet

There’s no such thing as an inherently high protein diet. What we commonly call high protein diets are simply diets containing more protein than those recommended by the World Health Organization (WHO), the Institute of Medicine (IOM), and other institutions. But institutions, of course, can and have been wrong. We have seen this, for example, with respect to trans fats, dietary cholesterol, and other important areas of nutrition. So what if so-called high protein diets are actually an optimal-protein and what if the diets recommended by the aforementioned institutions are actually suboptimal? A new study, recently published in the American Journal of Clinical Nutrition, suggests this could be the case, particularly for those who are trying to lose weight.

The WHO and IOM recommend 0.8 grams of protein per kilogram of bodyweight for both men and women daily.1 For a 175 pound man, this equates to 64 grams of protein per day, and for a 125 pound woman, 45 grams of protein per day. The new study, however, published by researchers from the University of Missouri, suggests that 1.2 to 1.6 grams/day is the optimal range. Lead researcher Heather Leidy and her colleagues reviewed the scientific literature on protein consumption and concluded that moderately increased protein, consumed in a balanced way throughout the day, has significant benefits, including improvements in appetite, body weight management, and cardiometabolic risk factors.2

WHEN AND HOW?

According to this research, daily protein should be somewhat evenly distributed across breakfast, lunch and dinner. “Eating a protein-rich breakfast,” Leidy explained, “containing about 30 grams of protein leads to even greater satiety throughout the day and can reduce unhealthy snacking by improving appetite control.”3 Some people might struggle to consume this much protein at breakfast, but it’s much easier than you might think. Four to five eggs would get you there, but don’t assume that eggs are your only breakfast option. It’s only a matter of getting into the habit of treating breakfast just like any other meal. Beef, lamb, chicken, and fish, for example, are all suitable for breakfast.

Leidy also stresses that animal proteins, unlike most plant proteins, are high quality and “complete” because they contain all essential amino acids (EAA) and are easily digestible, whereas individual-source plant proteins lack certain EAAs and are harder to digest. Some people might worry about adverse side effects from consuming protein at the 1.6 gr per kg upper limit. These worries, however, are unfounded. For example, a 2004 review of the scientific literature found no adverse effects on liver or kidney function for protein consumption as high as 2.4 gr per kg, or 3 times the IOM’s benchmark level.4

With nearly two-thirds of Americans either overweight or obese, perhaps it’s time to start rethinking what’s “normal” and “optimal” with respect to protein consumption. Higher-protein diets are sometimes ridiculed or portrayed as dangerous, but the scientific literature says otherwise. By following the Paleo diet, which of course eliminates refined sugar and cereals, you’ll naturally be consuming increased quantities of protein in the 1.2 to 1.6 gr per kg range. You won’t need to make any calculations. If you’re trying to lose weight and just getting started with Paleo, focus on protein, particularly during breakfast and lunch.

Christopher James Clark, B.B.A.
@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

Christopher James Clark | The Paleo Diet TeamChristopher James Clark, B.B.A. is an award-winning writer, consultant, and chef with specialized knowledge in nutritional science and healing cuisine. He has a Business Administration degree from the University of Michigan and formerly worked as a revenue management analyst for a Fortune 100 company. For the past decade-plus, he has been designing menus, recipes, and food concepts for restaurants and spas, coaching private clients, teaching cooking workshops worldwide, and managing the kitchen for a renowned Greek yoga resort. Clark is the author of the critically acclaimed, award-winning book, Nutritional Grail.

 

REFERENCES

[1] Institute of Medicine of the National Academies. 2002. Dietary Reference Intakes. National Academies Press.

[2] Leidy, JH. (April 29, 2015). The role of protein in weight loss and maintenance. American Journal of Clinical Nutrition, [Epub ahead of print].

[3] University of Missouri-Columbia. (2015, April 30). Busy Americans can reap health benefits by balancing protein intake throughout the day. ScienceDaily.

[4] Manninen, A. (2004). High-Protein Weight Loss Diets and Purported Adverse Effects: Where is the Evidence? Journal of International Society of Sports Nutrition, 1(1).

Evolution and High Protein Diets Part 3 | The Paleo Diet

Did you miss Evolution and High Protein Diets Part 1? Click Here to Read It!

Did you miss Evolution and High Protein Diets Part 2? Click Here to Read It!

DIETARY PROTEIN: HEALTH AND WELL BEING

Establishing Cause and Effect between Diet and Disease

One of the challenges faced by nutritional scientists when they ultimately make recommendations regarding what we should and should not eat is to establish cause and effect between a dietary element and the subsequent development or prevention of disease. Some foods and some dietary habits promote good health whereas others promote disease.

No single procedure alone can establish cause and effect,65, 66 nor can any single study prove causality.67 Observational epidemiological studies can only show relationships among variables and are notorious for showing conflicting results68 and cannot provide decisive evidence by themselves either for or against specific hypotheses.69 For example increased animal protein has been associated with a decreased risk for coronary heart disease (CHD) in a large group of nurses (The Nurses Health Study),70 whereas exactly the opposite association was found for markers of CHD and meat consumption in people from rural China.71, 72 An analogy here may be appropriate to show you why observational epidemiological studies can only show relationships and not establish causality. In New York City, there is a strong association between the size of a structure fire and the number of fire trucks at the fire, but can we conclude that more fire trucks cause bigger fires?

In order to establish cause and effect between diet and disease, it takes more than just observational epidemiological evidence.69 There must also be what is referred to as “biological plausibility” in which evidence gathered from tissue, animal and short term human metabolic studies support causality.66 When observational epidemiological evidence is augmented by biological plausibility studies and confirmed by randomized controlled trials, the case for causality becomes ever more convincing. In regard to optimal amounts of dietary protein, the bulk of the evidence from tissue and animal studies and from human dietary interventions provides a compelling case for the therapeutic effects of high protein diets.

Dietary Protein and Cardiovascular Disease

One of the reasons why observational epidemiological studies yield contradictory results is because of the influence of confounding variables which cause confusion in the interpretation of the results because of the mixing of effects from two or more variables.68 For example, although some observational studies have shown a positive association between animal protein and cardiovascular disease (CVD), it is entirely possible that this association is spurious because the measurement of animal protein is confounded by another variable that is also linked to CVD.  Meat is a major source of animal protein in the U.S. diet,20 but it is also a major source of saturated fat.73 Because meat comes as an inseparable package of (protein + saturated fat), animal protein ingestion will be highly correlated to saturated fat, thereby making it difficult to disengage the atherogenic effect of saturated fat from that of animal protein. Accordingly, experimental studies are more useful to determine the true effect animal protein may have upon cardiovascular risk factors because they can be designed to isolate the protein effects from the saturated fat effects.

Sinclair and colleagues74 performed an experiment in which they fed 10 adults a low fat, lean beef-based diet for five weeks. Energy intake was kept constant over the five week study. Total blood cholesterol concentrations fell significantly within one week of commencing the diet, but rose as beef fat drippings were added in a stepwise manner in weeks four and five.  The authors concluded, “. . . it is the beef fat, not lean beef itself, that is associated with elevations in cholesterol concentrations.

Numerous short term human dietary interventions have demonstrated the therapeutic effect of lean, animal based protein upon blood lipid parameters. Wolfe and colleagues have shown that the isocaloric substitution of protein (23% energy) for carbohydrate in moderately hypercholesterolemic subjects resulted in significant decreases in total, LDL and VLDL cholesterol, and triglycerides while HDL cholesterol increased.75 Similar blood lipid changes have been observed in normal healthy subjects76 and in type II diabetic patients in conjunction with improvements in glucose and insulin metabolism.77, 78

A litany of more recent studies has confirmed that elevations in dietary protein have a beneficial effect upon blood lipid profiles.79-85 The mechanism or mechanisms of action of high protein diets upon blood lipid chemistry are not clear; however animal studies suggest that the beneficial effects are caused by their powerful inhibition of hepatic VLDL synthesis, perhaps by altering apoprotein synthesis and assembly in the liver.86

The relationship between protein intake and blood pressure has been comprehensively examined in observational population studies, and support the notion that higher protein intake can lower blood pressure.87-89 A substantial number of randomized controlled trials have demonstrated that higher dietary protein either from soy,90-92 mixed dietary sources85 or from lean red meat93 significantly lower blood pressure.

Dietary Protein and Insulin/Glucose Metabolism and Weight Regulation

In addition to reducing CVD risk by improving the blood lipid profile and reducing blood pressure, higher protein diets have been shown to improve insulin sensitivity and glycemic control79, 81, 84, 94-96 while promoting greater weight loss80, 83, 84, 97, 98 and improved long term sustained weight maintenance99, 100 than low fat high carbohydrate calorie restricted diets. The weight loss superiority of higher protein, calorie restricted diets over either calorie restricted (low fat/ high carbohydrate) diets or calorie restricted (high fat/low carbohydrate) appears to be caused by the greater satiety value of protein compared to either fat or carbohydrate.macronutrients (protein, fat, carbohydrate), protein causes the greatest release of a gut hormone (PYY) that reduces hunger103 while simultaneously improving central nervous system sensitivity to leptin,97 another hormone that controls appetite and body weight regulation.

Dietary Protein and Bone Health

One of the crucial issues regulating bone mineral health and integrity is calcium balance which represents the difference between the amount of dietary calcium which is absorbed and the amount of calcium leaving the body through the urine and feces. Figure 5 demonstrates two key points: 1) most (~75%) of dietary calcium is not absorbed, and 2) calcium absorption increases with decreasing dietary intakes and decreases with increasing dietary intakes.104

Evolution and High Protein Diets | The Paleo Diet

Figure 5.  Relation between Calcium Intake and Absorption

Because dietary protein has been frequently, but not always,105-108 shown to increase urinary calcium excretion, it is possible that long term ingestion of high protein diets could lead to accelerated loss of calcium from the bones thereby impairing bone health and integrity.

Without the concurrent measurement of dietary calcium absorption along with urinary calcium losses the net calcium balance cannot be known. Hence, the simple observation that dietary protein ingestion may increase urinary calcium losses tells us little or nothing about calcium balance. In evaluating the effect of high protein diets upon bone mineral health, it is therefore crucial to measure both urinary calcium excretion and intestinal absorption of calcium. In this regard, Pannemans and colleagues109 compared a low protein (12% energy) to a high protein diet (21% energy) in young and elderly subjects.  Both a higher urinary calcium excretion and a higher intestinal absorption of calcium were induced by the high protein diet, thus no negative calcium balance occurred.

A similar experiment confirmed that elevated dietary protein enhances calcium absorption and thereby counters the increased urinary excretion of calcium.110

Furthermore, a series of recent dietary interventions in humans has shown that high protein, meat based diets do not cause loss of calcium from the skeleton, but actually have a favorable effect upon it by lowering bone resorption105, 107,  111, 112 and may actually increase bone formation by dietary protein induced increases in IFG-1.105

Dietary Protein and Kidney Function

One of the most common misperceptions about high protein diets is that they can damage the kidneys of healthy normal individuals. This concept is known as the “Brenner Hypothesis”113 and suggests that increased dietary protein elevates the kidney’s filtration rate (GFR) which in turn alters the kidney’s structure (glomerulosclerosis) which then causes albumin to appear in the urine (microalbuminuria).  Although these series of steps represent the hypothesis Brenner proffered,113 his experiments actually showed an entirely different series of events. In reality, Brenner demonstrated that patients with pre-existing kidney disease had an elevated GFR, glomerulosclerosis and microalbuminuria and that by reducing dietary protein the GFR and microalbuminuria could be lowered.113 He further suggested that because elevated dietary protein increased the GFR in short term studies (< 2 weeks) of healthy normal subjects, protein was responsible for kidney damage. The problem with this interpretation is that markers of functional kidney damage in the normal subjects (microalbuminuria) were not demonstrated along with the elevations in GFR, nor were any long term studies (3-6 months) carried out to determine if the kidneys adapted to a higher protein intake.

The incidence of diabetic end stage kidney disease has increased steadily over the past three decades.114, 115 If dietary protein were responsible for causing kidney damage, then one might expect that dietary protein would have steadily increased during this same time interval. In fact, dietary proten significand female subjects.118 The high protein diet did not cause urinary albumin to increase. Additionally, the specific GFR, which is an expression of the filtration rate per unit kidney volume, did not change during the high protein diet, indicating that renal (kidney) adaptation occurred to the higher protein load.  The authors summarized, “We therefore conclude that a high dietary protein intake does not appear to have adverse effects on renal function in individuals without renal impairment.”

Dietary Protein and Cancer

Observational epidemiological studies frequently,119 but not always120 show that high animal protein diets may increase the risk for a variety of cancers, particularly colorectal cancer.121 Consequently, it might be expected that non-meat eating vegetarians would have a lower risk for these cancers. Paradoxically, this effect has not been consistently demonstrated.119 A proposed mechanism of action for the carcinogenic effect of meat consumption is the formation of toxic N-nitroso compounds (NOC) in the gut from heme iron in meat.122, 123 Short term human studies are in agreement that increased meat consumption increases NOC formation both in the lower122 and upper123 gastrointestinal tract. However, whether this situation translates into increased cancer risk is not known because to date, no randomized controlled trials of increased meat consumption in humans, using cancer diagnosis as an end point, have been conducted.

The meats and fish consumed by pre-agricultural humans were almost always fresh, whereas current western diets contain significant quantities of processed, salted meats and fish preserved with nitrites and nitrates. Processed meats contains 10 times more NOC (5.5 µmol/kg) than fresh meat (0.5 µmol/kg).124 Pre-agricultural humans consumed their fresh meats along with high intakes s of fresh fruits and vegetables estimated to be between 35-45% of total energy14 compared to 8.1% of total energy in the current U.S. diet.125 Increased fruit and vegetable consumption increases the fecal transit time so that NOC have less contact time with the colonic mucosa and therefore may reduce the carcinogenic risk.126 Hence, the context under which high meat consumption occurred in hunter-gatherers varied significantly from what occurs in westernized populations.

Animal based foods were almost always consumed fresh in conjunction with copious quantities of fresh fruits and vegetables.  Even when vegetable intake was low or absent in these peoples, there is little evidence for an association of high protein, animal based diets with colorectal cancer. Prior to western acculturation, the Inuit may have consumed more than 95% of their daily energy from animal and seafood,15 yet a comprehensive review examining virtually all historical and ethnographic data of these people prior to westernization was unable to document a single case of colorectal cancer.126 Should a high protein meat based diet initiate or promote colorectal cancer, then one might expect obligate carnivores such as cats to demonstrate high incidences of these malignancies.  In, fact the opposite is true, and the rate of gastrointestinal tract cancers is quite low in domestic cats.128 In summary the case for animal based, high protein diets causing colorectal cancer, within the context of pre-agricultural diets, is weak.

Dietary Protein and Muscle Protein Synthesis and Fatigue

For athletes and individuals engaging in regular exercise, an animal based, high protein diet may be ergogenic and facilitate improved performance because of the stimulatory effect of dietary branch chain amino acids (BCCA) upon muscle protein synthesis,129-131 particularly when they are consumed in the post exercise window.132, 133 Table 2 demonstrates that lean meats and fish are much richer sources of the branch chain amino acids (valine, leucine and isoleucine) than are plant foods. In addition to facilitating muscle synthesis during the post exercise recovery period, BCCA may also improve endurance performance by reducing perceived exertion and mental fatigue by reducing the synthesis of brain 5-hydroxytryptamine, a substance that may promote central fatigue.134

DIETARY PROTEIN: SUMMARY AND CONCLUSIONS

The evolutionary evidence indicates that so called “high protein diets” (20-30% total energy) and “very high protein diets” (30-40% total energy) actually represent the norm which conditioned the present day the human genome over more than 2 million years of evolutionary experience. The evolutionary template would predict that human health and well being will suffer when dietary intakes fall outside this range. Hence the current U.S. consumption of protein (15% total energy) may not optimally promote health and well being. There is now a large body of experimental evidence increasingly demonstrating that a higher intake of lean animal protein reduces the risk for cardiovascular disease, hypertension, dyslipidemia, obesity, insulin resistance, and osteoporosis while not impairing kidney function.

 

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[82]Luscombe-Marsh ND, Noakes M, Wittert GA, Keogh JB, Foster P, Clifton PM. Carbohydrate-restricted diets high in either monounsaturated fat or protein are equally effective at promoting fat loss and improving blood lipids. Am J Clin Nutr. 2005 Apr;81(4):762-72

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[92]Washburn S, Burke GL, Morgan T, Anthony M. Effect of soy protein supplementation on serum lipoproteins, blood pressure, and menopausal symptoms in perimenopausal women. Menopause. 1999 Spring;6(1):7-13.

[93]He J, Gu D, Wu X, Chen J, Duan X, Chen J, Whelton PK. Effect of soybean protein on blood pressure: a randomized, controlled trial.Ann Intern Med. 2005 Jul 5;143(1):1-9.

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[95]Nuttall FQ, Gannon MC. The metabolic response to a high-protein, low-carbohydrate diet in men with type 2 diabetes mellitus. Metabolism. 2006 Feb;55(2):243-51.

[96]Nuttall FQ, Gannon MC. Metabolic response of people with type 2 diabetes to a high protein diet. Nutr Metab (Lond). 2004 Sep 13;1(1):6

[97]McAuley KA, Smith KJ, Taylor RW, McLay RT, Williams SM, Mann JI. Long-term effects of popular dietary approaches on weight loss and features of insulin resistance. Int J Obes (Lond). 2006 Feb;30(2):342-9.

[98]Weigle DS, Breen PA, Matthys CC, Callahan HS, Meeuws KE, Burden VR, Purnell JQ. A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. Am J Clin Nutr. 2005 Jul;82(1):41-8

[100]Due A, Toubro S, Skov AR, Astrup A. Effect of normal-fat diets, either medium or high in protein, on body weight in overweight subjects: a randomised 1-year trial. Int J Obes Relat Metab Disord. 2004 Oct;28(10):1283-90

[101]Westerterp-Plantenga MS, Lejeune MP, Nijs I, van Ooijen M, Kovacs EM. High protein intake sustains weight maintenance after body weight loss in humans. Int J Obes Relat Metab Disord. 2004 Jan;28(1):57-64.

[102]Lejeune MP, Kovacs EM, Westerterp-Plantenga MS. Additional protein intake limits weight regain after weight loss in humans. Br J Nutr. 2005 Feb;93(2):281-9.

[103]Porrini M, Santangelo A, Crovetti R, Riso P, Testolin G, Blundell JE. Reid M, Hetherington M. Relative effects of carbohydrates and protein on satiety — a review of methodology. Neurosci Biobehav Rev 1997 May;21(3):295-308

[104]Poppitt SD, McCormack D, Buffenstein R. Short-term effects of macronutrient preloads on appetite and energy intake in lean women. Physiol Behav 1998 Jun 1;64(3):279-85

[105]Batterham RL, Heffron H, Kapoor S, Chivers JE, Chandarana K, Herzog H, Le Roux CW, Thomas EL, Bell JD, Withers DJ. Critical role for peptide YY in protein-mediated satiation and body-weight regulation. Cell Metab. 2006 Sep;4(3):223-33.

[106]O’Brien KO, Abrams SA, Liang LK, Ellis KJ, Gagel RF. Increased efficiency of calcium absorption during short periods of inadequate calcium intake in girls. Am J Clin Nutr. 1996 Apr;63(4):579-83

[107]Dawson-Hughes B, Harris SS, Rasmussen H, Song L, Dallal GE. Effect of dietary protein supplements on calcium excretion in healthy older men and women. J Clin Endocrinol Metab. 2004 Mar;89(3):1169-73

[108]Spencer H, Kramer L, Osis D, Norris C. Effect of a high protein (meat) intake on calcium metabolism in man. Am J Clin Nutr. 1978 Dec;31(12):2167-80

[109]Roughead ZK, Johnson LK, Lykken GI, Hunt JR. Controlled high meat diets do not affect calcium retention or indices of bone status in healthy postmenopausal women. J Nutr. 2003 Apr;133(4):1020-6

[110]Arjmandi BH, Khalil DA, Smith BJ, Lucas EA, Juma S, Payton ME, Wild RA. Soy protein has a greater effect on bone in postmenopausal women not on hormone replacement therapy, as evidenced by reducing bone resorption and urinary calcium excretion. J Clin Endocrinol Metab. 2003 Mar;88(3):1048-54

[111]Pannemans DL, Schaafsma G, Westerterp KR. Calcium excretion, apparent calcium absorption and calcium balance in young and elderly subjects: influence of protein intake. Br J Nutr. 1997 May;77(5):721-9.

[112]Kerstetter JE, O’Brien KO, Insogna KL. Dietary protein affects intestinal calcium absorption. Am J Clin Nutr. 1998 Oct;68(4):859-65.

[113]Kerstetter JE, O’Brien KO, Caseria DM, Wall DE, Insogna KL. The impact of dietary protein on calcium absorption and kinetic measures of bone turnover in women. J Clin Endocrinol Metab. 2005 Jan;90(1):26-31.

[114]Kerstetter JE, Wall DE, O’Brien KO, Caseria DM, Insogna KL. Meat and soy protein affect calcium homeostasis in healthy women. J Nutr. 2006 Jul;136(7):1890-5

[115]Brenner BM, Meyer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease.N Engl J Med. 1982 Sep 9;307(11):652-9.

[116]Lippert J, Ritz E, Schwarzbeck A, Schneider P. The rising tide of endstage renal failure from diabetic nephropathy type II–an epidemiological analysis. Nephrol Dial Transplant. 1995;10(4):462-7.

[117]Ritz E, Rychlik I, Locatelli F, Halimi S. End-stage renal failure in type 2 diabetes: A medical catastrophe of worldwide dimensions. Am J Kidney Dis. 1999 Nov;34(5):795-808.

[118]Wrone EM, Carnethon MR, Palaniappan L, Fortmann SP; Third National Health and Nutrition Examination Survey. Association of dietary protein intake and microalbuminuria in healthy adults: Third National Health and Nutrition Examination Survey. Am J Kidney Dis. 2003 Mar;41(3):580-7.

[119]Johnson DW. Dietary protein restriction as a treatment for slowing chronic kidney disease progression: the case against. Nephrology. 2006 Feb;11(1):58-62.

[120]Skov AR, Toubro S, Bulow J, Krabbe K, Parving HH, Astrup A. Changes in renal function during weight loss induced by high vs low-protein low-fat diets in overweight subjects. Int J Obes Relat Metab Disord. 1999 Nov;23(11):1170-7.

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Evolution and High Protein Diets Part 2 | The Paleo Diet

Did you miss Evolution and High Protein Diets Part 1? Click Here to Read It!

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THE EVOLUTIONARY EVIDENCE

The Fossil Evidence

A number of lines of evidence suggest that meat eating and high protein diets have been a component of human nutrition since the very origins of our genus Homo. Beginning approximately 2.6 million years ago (MYA), the hominin species that eventually led to Homo began to include more animal food in their diet. A number of lines of evidence support this viewpoint.

First, the very first stone tools (Oldowan lithic technology) appear in the fossil record 2.6 MYA, 28 and there is clear cut evidence to show that these tools were used to butcher and disarticulate animal carcasses. 29, 30 Stone tool cut marks on the bones of prey animals and evidence for marrow extraction appear concurrently in the fossil record with the development of Oldowan lithic technology by at least 2.5 MYA (Figure 2). 30 It is not entirely clear which specific early hominin species or group of species manufactured and used these earliest of stone tools; however, Australopithecus garhi may have been a likely candidate. 30, 31

The development of stone tools and the increased dietary reliance on animal foods allowed early African hominins to colonize northern latitudes outside of Africa where plant foods would have been seasonally restricted. Early Homo skeletal remains and Oldowan lithic technology appear at the Dmanisi site in the Republic of Georgia (40° N) by 1.75 MYA, 32 and more recently Oldowan tools dating to 1.66 MYA have been discovered at the Majuangou site in North China (40° N). 33 Both of these tool-producing hominins would likely have consumed considerably more animal food than pre-lithic hominins living in more temperate African climates, and it is likely the majority of their daily energy was obtained from animal foods during winter and early spring when plant food sources would have been scarce or unavailable.

The Genetic Evidence

In addition to the fossil evidence suggesting a trend for increased animal food consumption, hominins may have experienced a number of genetic adaptations to animal-based diets early in our genus’s evolution analogous to those of obligate carnivores such as felines. Carnivorous diets reduce evolutionary selective pressures that act to maintain certain anatomical and physiological characteristics needed to process and metabolize high amounts of plant foods. In this regard, hominins, like felines, have experienced a reduction in gut size and metabolic activity along with a concurrent expansion of brain size and metabolic activity as they included more energetically dense animal food into their diets. 16, 34, 35

Further, similar to obligate carnivores, 36 humans maintain an inefficient ability to chain elongate and desaturate 18 carbon fatty acids to their product 20 and 22 carbon fatty acids. 37 Since 20 and 22 carbon fatty acids are essential cellular lipids, then evolutionary reductions in desaturase and elongase activity in hominins indicate that preformed dietary 20 and 22 carbon fatty acids (found only in animal foods) were increasingly incorporated in lieu of their endogenously synthesized counterparts derived from 18 carbon plant fatty acids.

Finally, our species has a limited ability to synthesize the biologically important amino acid, taurine, from precursor amino acids, 38, 39 and vegetarian diets in humans result in lowered plasma and urinary concentrations of taurine. 40 Like felines 41, 42 the need to endogenously synthesize taurine may have been evolutionarily reduced in humans because exogenous dietary sources of preformed taurine (found only in animal food) had relaxed the selective pressure formerly requiring the need to synthesize this conditionally essential amino acid.

Another genetic adaptation to a high meat diet involves the metabolism of purines.  Purines are the nitrogenous base pairs which form the structural cross rung molecules of both DNA and RNA.  As DNA and RNA are broken down within cells, the purines then can be metabolized into uric acid by the liver and a few other tissues within the body.  The liver receives purines from two sources: 1) the diet, and 2) the daily breakdown of the body’s own tissues. About ⅔ of the daily purine load comes from the body’s turnover of cells, while ⅓ comes from the diet. 43 When the combined purine load (from both diet and turnover of the body’s own cells) exceeds the kidney’s ability to excrete it, blood concentrations of uric acid rise, thereby increasing the risk for gout, a painful disease caused by formation of uric acid crystals in the joints.

Although high protein, meat based diets contain high amounts of purines and would be expected to promote gout symptoms, protein ingestion actually decreases blood uric acid levels by increasing uric acid excretion. 44 This seemingly paradoxical effect occurs because the kidney increases its excretion of uric acid when faced with elevated dietary purines. 45 But more importantly, over the course of evolution, humans have evolved a genetic mutation which tends to prevent uric acid synthesis in the liver. Humans avoid the overproduction of uric acid in the face of increasing dietary purine intake from meats by decreasing the activity of an enzyme called xanthine oxidoreductase, 46 a key catalyst in the final synthesis of uric acid. Compared to other animals, xanthine oxidase activity is almost 100 times lower in humans. 47 This evolutionary adaptation has occurred because the gene coding for xanthine oxidoreductase has been repressed. 48 The final proof of the pudding has been borne out by dietary interventions showing that high protein, low glycemic load diets actually normalized serum uric acid concentrations in 7 of 12 gout patients and significantly decreased gout attacks. 49

The Isotopic Fossil Evidence

Since the evolutionary split between hominins and pongids (apes) approximately 7 million years ago, the available evidence shows that all species of hominins ate an omnivorous diet composed of minimally processed, wild-plant and animal foods. In support of this view is the omnivorous nature of chimpanzees, the closest living pongid link to hominins. Although chimpanzees (Pan paniscus and Pan troglodytes), our genetically closest nonhuman relatives, primarily consume a frugivorous diet, they still eat a substantial amount of meat obtained throughout the year from hunting and scavenging. 50-52 Observational studies of wild chimpanzees demonstrate that during the dry season meat intake is about 65g per day for adults. 51 Accordingly, it is likely that the very earliest hominins would have been capable of obtaining animal food through hunting and scavenging in a manner similar to chimpanzees.

Carbon isotope data also support the notion that early hominins were omnivorous. By about 3 million years ago MYA Australopithecus africanus obtained a significant portion of food from C4 sources (grasses, particularly seeds and rhizomes; sedges; invertebrates, including locusts and termites; grazing mammals; and perhaps even insectivores and carnivores). 53 Other fossils of early African hominins, including Australopithecus robustus and Homo ergaster, maintain carbon isotope signatures characteristic of omnivores. 54, 55 The finding of C4 in Australopithecus robustus fossils refutes the earlier view that this hominin was vegetarian. 54

There is little evidence to the contrary that animal foods have always played a significant role in the diets of all hominin species. Increased reliance on animal foods not only allowed for enhanced encephalization (brain expansion relative to body weight) and its concomitant behavioral sophistication, 16, 34, 35 but this dietary practice also permitted colonization of the world outside of Africa. An unresolved issue surrounding hominin diets is the relative amounts of plant and animal foods that were typically consumed.

Before the advent of Oldowan lithic technology about 2.6 MYA, quantitative estimates of hominin energy intake from animal food sources are unclear, other than they were likely similar to, or greater than, estimated values (4%–8.5% total energy) for chimpanzees. 51, 56 Although all available data point to increasing animal food consumption following the arrival of stone tool technology, the precise contribution of either animal or plant food energy to is unclear. Obviously, then as now, no single (animal/plant) subsistence ratio would have been necessarily representative of all populations or species of hominins. However, there are a number of lines of evidence which suggest more than half (>50%) of the average daily energy intake for most Paleolithic hominin species and populations of species was obtained from animal foods.

Richards, Pettitt, and colleagues 57 have examined stable isotopes (δ13C and δ15N) in two Neanderthal specimens (~28,000—29,000 years ago) from Vindija Cave in northern Croatia and contrasted these isotopic signatures to those in fossils of herbivorous and carnivorous mammals from the same ecosystem. The analysis demonstrated that Neanderthals, similar to wolves and arctic foxes, behaved as top-level carnivores, obtaining all of their protein from animal sources. 57  More recent studies of corroborate this earlier work and points to Neanderthals “as top predators in an open environment, with little variation through time and space,58 and “the percentage of plants in the Neanderthal diet must have been close to zero.” 59 Because Neanderthals were not direct predecessors of modern humans, 60 it may be more relevant to examine the isotopic data from fully modern humans living during the Pleistocene. An analysis was made of five Upper Paleolithic Homo sapiens specimens dated to ~11,700–12,380 years ago from Gough’s and Sun Hole Caves in Britain. 61 The data indicated these hunter-gatherers were consuming animal protein year-round at a higher trophic level than the artic fox.

All of these studies 57-62 could be criticized as not being representative of typical hominin diets, as these two species lived in climates and ecosystems that fostered an abundance of large, huntable mammals, which were preyed upon preferentially. Additional clues to the typical plant-to-animal subsistence ratio in Paleolithic hominin diets can be found in the foraging practices of historically studied hunter-gatherers.

The Ethnographic Evidence

Our analysis (Figure 3) of the Ethnographic Atlas data 62 showed that the dominant foods in the majority of historically studied hunter-gatherer diets were derived from animal food sources. 14 Most (73%) of the world’s hunters-gatherers obtained >50% of their subsistence from hunted and fished animal foods, whereas only 14% of worldwide hunter-gatherers obtained >50% of their subsistence from gathered plant foods. For all 229 hunter-gatherer societies, the median subsistence dependence on animal foods was 56% to 65%. In contrast, the median subsistence dependence on gathered plant foods was 26% to 35%. 14

The major limitation of ethnographic data is that the preponderance of it is subjective in nature, and the assigned scores for the five basic subsistence economies in the Ethnographic Atlas are not precise, but rather are approximations. 63 Fortunately, more exact, quantitative dietary studies were carried out on a small percentage of the world’s hunter gatherer societies. 15, 64

Evolution and High Protein Diets Part 2 | The Paleo Diet

Figure 3. Frequency distribution of subsistence dependence upon animal foods in worldwide hunter gatherer societies (n = 229).

Table 1 lists these studies and shows the plant-to-animal subsistence ratios by energy. The average score for animal food subsistence is 65%, while that for plant-food subsistence is 35%. These values are similar to our analysis of the entire (n = 229) sample of hunter-gatherer societies listed in the Ethnographic Atlas in which the mean score for animal food subsistence was 68% and that for plant food was 32%. 14

Evolution and High Protein Diets Part 2 | The Paleo Diet

Table 1. Quantitatively determined proportions of plant and animal food in hunter-gatherer diets. 15, 64

When the two polar hunter-gatherer populations, who have no choice but to eat animal food because of the inaccessibility of plant foods, are excluded from Table 1 the mean score for animal subsistence is 59% and that for plant-food subsistence is 41%. These animal-to-plant subsistence values fall within the same respective class intervals (56%–65% for animal food; 26%–35% for plant food) as those we estimated from the ethnographic data when the confounding influence of latitude was eliminated. 14 Consequently, there is remarkably close agreement between the quantitative data in Table 1 and the ethnographic data 14 that animal food comprised more than half of the energy in historically studied hunter-gatherer diets.

Based upon hunter gatherer plant to animal subsistence ratios and the known macronutrient contents of wild plant and animal foods, it is possible to estimate the macronutrient content of these diets. 14 The typical hunter-gatherer protein intake would have fallen between 19 and 35% of total energy, 14 values which would be labeled either “high” or “very high” protein diets when compared to current U.S. values (15%).

Consequently, when framed in an evolutionary context, current western dietary protein intakes fall outside the range of diets that would have conditioned the human genome for nearly 2 million years. The evolutionary template would then suggest that when dietary protein intakes are restored to levels that our species is genetically accustomed, good health will prevail. Conversely, lower or higher values likely result in ill health.  Let’s see what the experimental evidence shows tomorrow in “Evolution and High Protein Diets Part 3” of The Evolutionary Basis for the Therapeutic Effects of High Protein Diets Series.

 

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[28]Semaw S, Rogers MJ, Quade J, Renne PR, Butler RF, Dominguez-Rodrigo M, Stout D, Hart WS, Pickering T, Simpson SW. 2.6-Million-year-old stone tools and associated bones from OGS-6 and OGS-7, Gona, Afar, Ethiopia. J Hum Evol. 2003 Aug;45(2):169-77.

[29]Bunn, HT, Kroll EM. Systematic butchery by Plio-Pleistocene hominids at Olduvai Gorge, Tanzania. Curr Anthropol 1986;20:365–398.

[30]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

[31]Asfaw B. White T, Lovejoy O, Latimer B, Simpson S, Suwa, G. Australopithecus garhi: A new species of early hominid from Ethiopia. Science 1999; 284, 629–635.

[32]Vekua A, Lordkipanidze D, Rightmire GP, Agusti J, Ferring R, Maisuradze G, Mouskhelishvili A, Nioradze M, De Leon MP, Tappen M, Tvalchrelidze M, Zollikofer C. A new skull of early Homo from Dmanisi, Georgia. Science. 2002 Jul 5;297(5578):85-9.

[32]Zhu RX, Potts R, Xie F. Hoffman KA, Deng CL, Shi CD, Pan YX, Wang HQ, Shi, RP, Wang YC, Shi GH, Wu NQ. New evidence on the earliest human presence at high northern latitudes in northeast Asia. Nature 2004; 431: 559–562.

[33]Aiello LC, Wheeler P. The expensive tissue hypothesis. Curr Anthropol 1995; 36:199–222.

[34]Leonard W.R, 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.

[35]Pawlosky R., Barnes A., Salem, N. Essential fatty acid metabolism in the feline: Relationship between liver and brain production of long-chain polyunsaturated fatty acids. J Lipid Res 1994;35: 2032–2040.

[36]Hussein N, Ah-Sing E, Wilkinson P, Leach C, Griffin BA, Millward DJ. Long-chain conversion of [13C] linoleic acid and alpha-linolenic acid in response to marked changes in their dietary intake in men. J Lipid Res. 2005 Feb;46(2):269-80.

[37]Sturman JA, Hepner GW, Hofmann AF, Thomas PJ. Metabolism of [35S] taurine in man. J Nutr. 1975 Sep;105(9):1206-14.

[38]Chesney RW, Helms RA, Christensen M, Budreau AM, Han X, Sturman JA. The role of taurine in infant nutrition. Adv Exp Med Biol. 1998;442:463-76.

[39]Laidlaw SA, Shultz TD, Cecchino JT, Kopple JD. Plasma and urine taurine levels in vegans. Am J Clin Nutr. 1988 Apr;47(4):660-3.

[40]Knopf K, Sturman JA, Armstrong M, Hayes KC. 1978. Taurine: An essential nutrient for the cat. J Nutr 1978;108: 773–778.

[41]MacDonald ML, Rogers QR, Morris JG. Nutrition of the domestic cat, a mammalian carnivore. Annu Rev Nutr 1984; 4: 521–562.

[42]Fam AG. Gout: excess calories, purines, and alcohol intake and beyond. Response to a urate-lowering diet. J Rheumatol. 2005 May;32(5):773-7.

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[44]Loffler W. Grobner W, Medina R, Zollner N. Influence of dietary purines on pool size, turnover, and excretion of uric acid during balance conditions. Isotope studies using 15N-uric acid. Res Exp Med (Berl). 1982(2):113-123.

[45]Oda M, Satta Y, Takenaka O, Takahata N. Loss of urate oxidase activity in hominoids and its evolutionary implications. Mol Biol Evol. 2002 May; 19(5): 640-53.

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EVOLUTION AND HIGH PROTEIN DIETS PART 1

The Evolutionary Basis for the Therapeutic Effects of High Protein Diets Series

Did you miss Evolution and High Protein Diets Part 2? Click Here to Read It!

Did you miss Evolution and High Protein Diets Part 3? Click Here to Read It!

INTRODUCTION

Although humanity has been interested in diet and health for thousands of years, the organized, scientific study of nutrition has a relatively recent past.  For instance, the world’s first scientific journal devoted entirely to diet and nutrition, The Journal of Nutrition only began publication in 1928.  Other well known nutrition journals have a more recent history still: The British Journal of Nutrition (1947), The American Journal of Clinical Nutrition (1954), and The European Journal of Clinical Nutrition (1988).   The first vitamin was “discovered” in 1912 and the last vitamin (B12) was identified in 1948.1 The scientific notion that omega 3 fatty acids have beneficial health effects dates back only to the late 1970’s,2 and the characterization of the glycemic index of foods only began in 1981.3

Nutritional science is not only a newly established discipline, but it is also a highly fractionated, contentious field with constantly changing viewpoints on both major and minor issues that impact public health.  For example, in 1996 a task force of experts from the American Society for Clinical Nutrition (ASCN) and the American Institute of Nutrition (AIN) came out with an official position paper on trans fatty acids stating:

We cannot conclude that the intake of trans fatty acids is a risk factor for coronary heart disease.4

Fast forward six short years to 2002 and the National Academy of Sciences, Institute of Medicine’s report on trans fatty acids5 states:

Because there is a positive linear trend between trans fatty acid intake and total and LDL (“bad”) cholesterol concentration, and therefore increased risk of cardiovascular heart disease, the Food and Nutrition Board recommends that trans fatty acid consumption be as low as possible while consuming a nutritionally adequate diet.”

These kinds of complete turnabouts and divergence of opinion regarding diet and health are commonplace in the scientific, governmental and medical communities. The official U.S. governmental recommendations for healthy eating are outlined in the “My Pyramid” program6 which replaced the “Food Pyramid” – both of which have been loudly condemned for nutritional shortcomings by scientists from the Harvard School of Public Health.7 Dietary advice by the American Heart Association (AHA) to reduce the risk of coronary heart disease (CHD) is to limit total fat intake to 30% of total energy, to limit saturated fat to <10% of energy and cholesterol to <300 mg/day while eating at least 2 servings of fish per week.8

Although similar recommendations are proffered in the USDA “My Pyramid,” weekly fish consumption is not recommended because the authors of these guidelines feel there is only “limited” information regarding the role of omega 3 fatty acids in preventing cardiovascular disease.6 Surprisingly, the personnel makeup of both scientific advisory boards is almost identical. At least 30 million Americans have followed Dr. Atkins advice to eat more fat and meat to lose weight.9 In utter contrast, Dean Ornish tells us fat and meat cause cancer, heart disease and obesity, and that we would all would be a lot healthier if we were strict vegetarians.10 Who’s right and who’s wrong?  How in the world can anyone make any sense out of this apparent disarray of conflicting facts, opinions and ideas?

In mature and well-developed scientific disciplines there are universal paradigms that guide scientists to fruitful end points as they design their experiments and hypotheses.  For instance, in cosmology (the study of the universe) the guiding paradigm is the “Big Bang” concept showing that the universe began with an enormous explosion and has been expanding ever since. In geology, the “Continental Drift” model established that all of the current continents at one time formed a continuous landmass that eventually drifted apart to form the present-day continents. These central concepts are not theories for each discipline, but rather are indisputable facts that serve as orientation points for all other inquiry within each discipline. Scientists do not know everything about the nature of universe, but it absolutely unquestionable that it has been and is expanding. This central knowledge then serves as a guiding template which allows scientists to make much more accurate and informed hypotheses about factors yet to be discovered.

The study of human nutrition remains an immature science because it lacks a universally acknowledged unifying paradigm.11 Without an overarching and guiding template, it is not surprising that there is such seeming chaos, disagreement and confusion in the discipline. The renowned Ukrainian geneticist Theodosius Dobzhansky (1900-1975) said, “Nothing in biology makes sense except in the light of evolution.12 Indeed, nothing in nutrition seems to make sense because most nutritionists have little or no formal training in evolutionary theory, much less human evolution. Nutritionists face the same problem anyone who is not using an evolutionary model to evaluate biology: fragmented information and no coherent way to interpret the data.

All human nutritional requirements like those of all living organisms are ultimately genetically determined.  Most nutritionists are aware of this basic concept; what they have little appreciation for is the process (natural selection) which uniquely shaped our species nutritional requirements. By carefully examining the ancient environment under which our genome arose, it is possible to gain insight into our present day nutritional requirements and the range of foods and diets to which we are genetically adapted via natural selection.13-16 This insight can then be employed as a template to organize and make sense out of experimental and epidemiological studies of human biology and nutrition.11

THE DIETARY PROTEIN CONUNDRUM: HOW MUCH IS ENOUGH?

An important dietary issue that has come under debate in recent years is the safety of high protein diets and their long term influence upon health and well being.17, 18 In the current U.S. diet the average protein intake is 98.6 g/day (15.5% of total energy) for men and 67.5 g/day (15.1% of total energy) for women.19 Animal products provide approximately 75% of the protein in the U.S. food supply followed by dairy, cereals, eggs, legumes, fruits and vegetables.20 Diets containing  20% or more of their total energy as protein have been labeled “high protein diets” and those containing 30% or more energy as protein have been dubbed “very high protein diets.”18 Accordingly, a “high protein diet” for the average U.S. male daily energy intake (2,618 kcal)19 would contain between 125 to 186 grams of protein per day and for the average female (1,877 kcal)19 between 89 to 133 grams of protein per day.

At this point, it should be noted that there is a physiological limit to the amount of protein that can be ingested before it becomes toxic.14, 21 A byproduct of dietary protein metabolism is nitrogen, which in turn is converted into urea by the liver and then excreted by the kidneys into the urine. The upper limit of protein ingestion is determined by the liver’s ability to synthesize urea. When nitrogen intake from dietary protein exceeds the ability of the liver to synthesize urea, excessive nitrogen (as ammonia) spills into the bloodstream causing hyperammonemia and toxicity.14, 21 Additionally excess amino acids from the metabolism of high amounts of dietary protein may become toxic by entering the circulation causing hyperaminoacidemia.14, 21

The avoidance of the physiological effects of protein excess has been an important factor in shaping the subsistence strategies of hunter-gatherers.22- 24 Multiple historical and ethnographic accounts have documented the deleterious health effects that have occurred when humans were forced to rely solely upon the fat depleted, lean meat of wild animals.22  Excess consumption of dietary protein from the lean meats of wild animals leads to a condition referred to by early American explorers as “rabbit starvation” which initially results in nausea, then diarrhea and eventual death.22 Clinical documentation of this syndrome is virtually non-existent, except for a single case study.25

Using known maximal rates of urea synthesis (MRUS) in normal subjects [65 mg N/h ×  kg (body weight )0.75] (range 55-76), it is possible to calculate the maximal protein intake, beyond which will exceed MRUS and result in hyperammonemia and hyperaminoacidemia.21 The mean maximal protein intake for the average weight U.S. male (189.4 lbs)26 is then 270 g/day (range 233-322 g/day), and for an average weight female (162.8 lbs),26 246 g/day (range 208-288 g/day).  Consequently, “very high protein diets” for the average U.S. male could range from 187 to 270 g/day and for females, 134 to 246 g/day.

So let’s summarize a few key points. The average protein intake in the U.S. is about 15% of the normal daily caloric intake.  Diets labeled as “high protein” contain 20-29% protein of the normal daily caloric intake, and diets with 30-40% protein are branded “very high protein.” It should be pointed out that this categorization is completely arbitrary and based almost entirely upon comparisons to the U.S. norm.

A salient question from an evolutionary perspective would be, “Is the average U.S. protein intake necessarily average or normal for our species?”  For example, blood pressure in the U.S. and most other westernized countries is considered “normal” when systolic pressure is 120 mm Hg and diastolic pressure is 80 mm Hg. However, in many non-westernized people these values would be higher than normal. Consider the data in Figure 1 below showing blood pressure in the Yanomamo Indians of Brazil, a non-salt consuming society. Not only is blood pressure lower than normal western values, but it stays uniform throughout life and does not rise with age.27

Figure 1. Blood pressure in a group of 506 Brazilian Indians.26

The Evolutionary Basis for the Therapeutic Effects of High Protein Diets Series | The Paleo Diet
The Evolutionary Basis for the Therapeutic Effects of High Protein Diets Series | The Paleo Diet

In order to objectively answer the question whether or not high protein diets have detrimental or therapeutic health effects compared to the U.S. norm (15% total energy), we will frame this question from an evolutionary perspective before examining the experimental and epidemiological evidence tomorrow in “Evolution and High Protein Diets Part 2” of The Evolutionary Basis for the Therapeutic Effects of High Protein Diets Series.

REFERENCES

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[4] No authors listed. Position paper on trans fatty acids. ASCN/AIN Task Force on Trans Fatty Acids. American Society for Clinical Nutrition and American Institute of Nutrition. Am J Clin Nutr. 1996 May;63(5):663-70.

[5] National Academy of Sciences, Institute of Medicine. Letter Report on Dietary Reference Intakes for Trans Fatty Acids, 2002. //www.iom.edu/CMS/5410.aspx.

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[10] Ornish D. Dr. Dean Ornish’s Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery. New York : Random House, 1990.

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[4] Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr. 2000 Mar;71(3):682-92.

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[16] 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 Rev Nutr Diet 2001, 90:144-161.

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[18] St Jeor ST, Howard BV, Prewitt TE, Bovee V, Bazzarre T, Eckel RH et al.. Dietary protein and weight reduction: a statement for healthcare professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2001 Oct 9;104(15):1869-74.

[19] Wright JD, J Kennedy-Stephenson J, Wang CY, McDowell MA, Johnson CL, National Center for Health Statistics, CDC. Trends in intake of energy and macronutrients—United States, 1971-2000. JAMA. 2004;291:1193-1194.

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[27] Oliver WJ, Cohen EL, Neel JV. Blood pressure, sodium intake, and sodium related hormones in the Yanomamo Indians, a “no-salt” culture. Circulation. 1975 Jul;52(1):146-51.

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