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The Nutritional Characteristics
of a Contemporary Diet
Based Upon Paleolithic Food Groups
Loren Cordain, PhD1*
1Department of Health and Exercise Science, Colorado State University,
Fort Collins, Colorado
Loren Cordain, PhD
Department of Health and Exercise Science
Colorado State University
Fort Collins, CO 80526
Phone: 970-491-7436 Fax: 970-491-0445
The intent of the present study was to examine the
nutritional characteristics of a contemporary diet based
upon Paleolithic food groups and to determine how these
characteristics may impact the risk of chronic disease.
Nutritional software was employed to ascertain the
macro and trace nutrient characteristics of a diet composed
of commonly available modern foods, but devoid of
processed foods, dairy products and cereal grains. The rel-
ative contribution of plant and animal foods to the experi-
mental diet was based upon average values previously
determined in 229 hunter gatherer societies.
The analysis revealed that except for vitamin D, which
would have been supplied by endogenous synthesis in
hunter gatherers, it is entirely possible to consume a nutri-
tionally balanced diet from contemporary foods that mimic
the food groups and types available during the Paleolithic.
Despite the elimination of two major food groups, the trace
nutrient density of the experimental diet remained excep-
tionally high. The macronutrient content of the experimen-
tal diet (38 % protein, 39 % fat, 23 % carbohydrate by ener-
gy) varied considerably from current western values.
Contemporary diets based upon Paleolithic food
groups maintained both trace and macronutrient qualities
known to reduce the risk of a variety of chronic diseases in
There is a growing awareness among evolutionary biol-
ogists that humans like all species are genetically adapted to
the environment of their ancestors–that is, to the environ-
ment that their ancestors survived in and the environment
that consequently conditioned their genetic makeup.1-3 At
the same time, there is growing awareness that the pro-
found changes in the environment (e.g. in diet and other
lifestyle conditions) that began with the introduction of
agriculture and animal husbandry 10,000 years ago
occurred too recently on an evolutionary timescale for the
human genome to adjust.1-3 As a result of the mismatch
between the contemporary human diet and our genetically
determined physiology, many of the so-called diseases of
civilization have emerged.4-8 Previous studies have exam-
ined the dietary characteristics of humans living during the
Paleolithic,6,9,10 as well as of historically studied hunter-
gatherer societies,11,12 and their authors have suggested that
15 JANA Vol. 5, No. 3
Summer 2002 Vol.5, No. 3 JANA 16
the nutritional qualities of these diets may have therapeutic
value in the treatment of chronic disease. Although it is no
longer possible or practical for contemporary men and women
in western, industrialized countries to adopt and follow the
exact dietary patterns of humans living during the Paleolithic,
it is certainly possible to emulate the essential characteristics
of historically studied hunter-gatherer diets with common
foods and food groups available in all supermarkets.
The intent of this study was to examine the nutritional
qualities of a contemporary diet based upon Paleolithic
food groups and to characterize how these qualities may
impact health and well being.
Formulation of a Contemporary Diet Based Upon
Paleolithic Food Groups
In the United States and other western nations, foods
generally are organized into one of ﬁve food groups: 1)
bread, cereal, rice and pasta group, 2) fruit group, 3) veg-
etable group, 4) milk, yogurt and cheese group, and 5) meat,
poultry, ﬁsh, dry beans, eggs & nuts group.13 The formula-
tion of a contemporary diet based upon Paleolithic foods
groups necessarily excludes two of these major groups
(grains and dairy) because these foods were rarely or never
consumed by contemporary or Paleolithic hunter-gather-
ers.9,11,14-15 Additionally, within food group #5, dry beans
and legumes were not included in the analysis because, like
cereal grains, these foods did not become dietary staples
until Neolithic times.16 Finally, all modern processed foods
containing mixtures of grains, reﬁned sugars and oils, salt,
and food additives were likewise excluded from the model
because these food mixtures became part of the human
dietary repertoire only following the Agricultural and
Industrial Revolutions.9,11,14-15 Consequently, the present
model utilized only the following contemporary food types:
fruits, vegetables, meats, poultry, ﬁsh and nuts/seeds. For
each food type, only the most commonly consumed foods in
the U.S. diet were incorporated into the model. These were
then randomly arranged into three meals and snacks utiliz-
ing dishes that were not dissimilar from those normally
found in traditional western diets. The example diet was
then analyzed for macro and trace nutrients using nutrition-
al software (Nutritionist 5, First Data Bank, San Bruno, CA).
The 20 most commonly consumed fruits, vegetables,
and ﬁsh in the United States were employed in the random
meal selections (Table 1).17 For the 20 most commonly con-
sumed vegetable foods in the United States, two foods (pota-
toes and corn) were excluded from the model because corn
is a cereal grain, and potatoes maintain nutrient properties
(high glycemic and insulin responses)18 uncharacteristic of
traditional hunter-gatherer plant foods.19 Consequently, the
remaining 18 vegetable foods in Table 1 represent the food
choices available in the model.
For the meat food group, the four most commonly con-
sumed meats in the United States (beef, chicken, pork and
turkey)20 represented the meats of choice in the analysis.
Only very lean cuts of meat (turkey and chicken breasts
without skin, pork loin trimmed of fat, beef sirloin tip roast
trimmed of fat) that averaged 20 % fat by energy–a mean
value similar to that found in wild game meat21–were uti-
lized in the model. For the nuts/seeds group, 10 nuts and
seeds commonly consumed in the U.S. diet (almonds, wal-
nuts, pecans, ﬁlberts, brazil nuts, pistachio nuts, macadamia
nuts, coconut, sunﬂower seeds and pumpkin seeds) repre-
sented the available choices for this food type.
The primary consideration in the formulation of a “mod-
ern Paleolithic diet” is the relative contribution of each food
group to total energy intake. Compiled ethnographic studies
of 229 hunter-gatherer societies,11 as well as 13 quantitative
studies of hunter-gatherers12 have demonstrated that animal
foods contributed slightly more than half (55-65%) of the
daily energy, whereas plant foods would have made up the
remainder (35-45%) of the average daily caloric intake. Of
the energy obtained from animal foods, historically-studied
hunter-gatherers typically derived half of their energy from
aquatic animals and the other half from terrestrial animals.11
Animal food intake would have also been constrained by the
physiologic protein ceiling, which has been shown to occur
between 30 to 41% of total energy.11
In hunter-gatherer diets, the balance of total dietary ener-
gy (35-45%) derived from plant foods would have been quite
erratic in how it would have been apportioned among the var-
ious plant food groups due to varying environmental and eco-
logical considerations.11 Hence, in the formulation of a mod-
ern diet based upon Paleolithic food groups, the plant food
energy was arbitrarily divided equally among fruits, vegeta-
bles and nuts/seeds. Figure 1 displays the food type energy
weightings assigned to the example “Modern Paleolithic”
diet. Using these energy weightings for each of the ﬁve food
types, the diet outlined in Table 2 was formulated.
Figure 1. Apportionment of daily energy to the ﬁve food
types in a contemporary diet based upon Paleolithic food
17 JANA Vol. 5, No. 3 Summer 2002
Nutritional Characteristics of a Contemporary
Table 3 presents the macronutrient intake and other
qualities of the example diet analyzed from foods listed in
Table 2. The macronutrient characteristics of the example
diet, protein (38% energy), carbohydrate (23% energy), fat
(39% energy) are similar to values demonstrated in histori-
cally studied hunter-gatherer societies but different from
values (16% protein, 49% carbohydrate, 34% fat) in tradi-
tional western diets.11 Despite its relatively low carbohy-
drate content (23% energy), the contemporary Paleolithic
diet contained 42.5 g of plant ﬁber.
The contemporary Paleolithic diet contains more fat
(39% energy) than average values (34% energy) found in
western diets,11 however this extra fat occurs entirely as a
consequence of a greater intake of both polyunsaturated
(PUFA) and monounsaturated (MUFA) fats. Although more
than 50% of the energy in the contemporary Paleolithic diet
is derived from animal foods, the saturated fat content (7.0%
energy) falls within recommended healthful limits ( < 10%
energy).13 The contemporary Paleolithic diet is characterized
by a high intake of total omega 3 (n3) fatty acids (9.6 g) and
a relatively low intake of omega 6 (n6) fatty acids, which in
turn yield a total dietary n6/n3 of 1.5 to 1. The cholesterol
content of the contemporary Paleolithic diet is higher (461
mg) than recommended values (300 mg).13 The contempo-
Table 1. Top 20 most common fruits, vegetables and ﬁsh
sold in the United States.17
Table 3. Macronutrient and other dietary characteristics in
a contemporary diet based on Paleolithic food groups for
females (25 yrs, 2200 kcal daily energy intake).
Table 2. Sample 1-day menu for a modern diet based upon
Paleolithic food groups for females (25 yrs, 2200 kcal daily
Vol.5, No. 3 JANA 18Summer 2002
rary Paleolithic diet contains 12.5 times more potassium than
sodium. Except for calcium, all trace nutrients occur in con-
siderably greater quantities than the recommended daily
allowances (RDAs) (Table 4).
The results of this analysis demonstrate that it is entire-
ly possible to consume a nutritionally balanced diet from
commonly available contemporary foods that emulate the
food types available to Paleolithic hunter gatherers.
Despite the elimination of two major food groups (dairy and
cereals), the trace nutrient density of the diet remains
exceptionally high. Moreover, the diet maintains numerous
nutritional characteristics that have been demonstrated to
reduce the risk of a variety of chronic diseases.
Potential Nutritional Shortcomings of the
Contemporary Paleolithic Diet
Table 4 shows that the calcium intake (691 mg) would
be considerably lower than the RDA (1000 mg), while the
protein intake (217 g) would be more than 4 times recom-
mended values (50 g). Because increased dietary protein
increases obligatory loss of urinary calcium, it has been sug-
gested that a calcium (mg)/protein (g) ratio of >20:1 may
protect against bone loss.22 The calcium/protein ratio of the
contemporary Paleolithic diet (3.2 :1) is considerably lower
than that in the average U.S. diet (10.7:1)23 and therefore
might be expected to increase the risk for bone demineraliza-
tion, osteoporosis, and osteopenia. However, analyses of the
skeletons of ancestral humans living during the Paleolithic
24,25 as well as more recently studied hunter-gatherers26 have
shown these people maintained robust, fracture-resistant
bones, free from signs and symptoms of osteoporosis despite
consuming no dairy products. Their robust bones may be
due in part to greater activity levels (bone loading)24 and
greater sunlight exposure (increased vitamin D synthesis,
hence increased calcium absorption). However, more impor-
tantly it is likely that Paleolithic hunter gatherers would have
been in positive calcium balance despite a relatively low cal-
cium intake because the calciuretic effects of a high meat diet
were countered by high fruit and vegetable intake.11,12
Ingestion of meat protein induces calciuresis because
the oxidation of sulfur-containing amino acids presents a
net acid load to the kidney, which in turn must buffer the
acid load from base that ultimately is derived from calcium-
containing bone mineral salts.27 Previous studies have
demonstrated that ingestion of an alkalinizing agent pre-
vented the calciurea which normally accompanies high pro-
tein diets,28 and that when base is administered at a dose
sufficient to neutralize endogenous acid production, calci-
um balance is improved, bone resorption is reduced, and
bone formation is increased.29 In western diets, meats,
Table 4. Trace nutrients in a modern diet based on
Paleolithic food groups for females (25 yrs, 2200 kcal daily
Table 5. The potential renal acid load (PRAL) in the exam-
ple diet. Values for PRAL were adapted from Remer and
Manz’s database.30 (+) values are acid-producing,(-)values
Summer 200219 JANA Vol. 5, No. 3
cheeses, and cereal grains yield high potential renal acid
loads30 and hence may promote osteoporosis by producing
a net metabolic acidosis.27 In contrast, fruits and vegetables
yield a net alkaline renal load,30 and high fruit and veg-
etable diets have been shown to reduce urinary calcium
excretion rates.31 Accordingly, in hunter-gatherer popula-
tions consuming high protein diets, a concomitant con-
sumption of high levels of fruits and vegetables may have
countered the calciuretic effects of a high protein diet.
In the present model, the net renal ionic load was
slightly alkaline with base producing foods (-53.2) out-
weighing acid producing foods (51.4) (Table 5).
Consequently the high protein intake of the example diet
would not have caused an increased calciuresis, and sub-
jects consuming a similar diet likely would remain in calci-
um balance despite a calcium intake lower than the RDA.
The contemporary Paleolithic diet provides no dietary
vitamin D. Except for the livers of certain marine mammals
and ﬁsh, there are relatively few sources of vitamin D in the
normal food supply. In most hunter-gatherers, vitamin D
would have been obtained via the body’s synthesis of this
hormone from ultraviolet irradiation (sunlight exposure) of
cholesterol in the skin. Only with the fortiﬁcation of mar-
garine and milk, beginning in the mid 20th century, has vit-
amin D been widely available in the food supply.
Table 3 shows that the cholesterol intake (461 mg) for
the model diet is more than 50% higher than recommended
values (300 mg).13 However, it should be noted that dietary
cholesterol has a relatively minor impact on serum choles-
terol levels.32 The recently developed Howell et al. equa-
tion33 [∆serum cholesterol (mg/dL) = 1.918 x ∆SFA –
0.900 x ∆PUFA + 0.0222 x ∆cholesterol; where SFA = %
saturated fat energy, PUFA = % polyunsaturated fat energy,
and cholesterol = dietary cholesterol (mg)] reveals that a
reduction in dietary cholesterol from 461 mg (the value in
the example diet) to 300 mg (recommended value) would
only lower serum cholesterol levels by 3.5 mg/dL.
Additionally, in the example diet the ratio of polyunsaturat-
ed fatty acids to saturated fatty acids (P/S) is 1.5.
Schonfeld and colleagues34 have shown that when the
P/S was = 0.8, the addition of 750 mg of dietary cholesterol
did not elevate serum LDL cholesterol concentrations in
healthy, normal men. Consequently, the high P/S in the
contemporary Paleolithic diet likely would counter any ele-
vations in serum cholesterol that potentially could have
occurred from increased dietary cholesterol.
Potential Nutritional Beneﬁts of the Modern Paleolithic
Perhaps the most striking difference between the typi-
cal western diet and the current model diet lies in the much
higher protein intake. Although a high protein ingestion
can increase the rate of progression in renal dysfunction,35
a recent clinical trial has demonstrated that a high protein
diet (26% energy) had no adverse effects upon renal func-
tion in subjects with no pre-existing kidney disease.36
Because protein has more than three times the thermic
effect of either fat or carbohydrate37 and because it has a
greater satiety value than fat or carbohydrate,37,38 increased
dietary protein may represent an effective weight loss strat-
egy for the overweight or obese. Recent clinical trials have
demonstrated that calorie-restricted high protein diets are
more effective than calorie-restricted high carbohydrate
diets in eliciting weight loss in overweight subjects.39,40
There is an increasing body of evidence that suggests
high protein diets may improve blood lipid proﬁles41-45 and
thereby lessen the risk for cardiovascular disease (CVD).
Wolfe and colleagues have shown that the isocaloric substi-
tution of protein (23% energy) for carbohydrate in moder-
ately hypercholesterolemic subjects resulted in signiﬁcant
decreases in total, LDL and VLDLcholesterol, and TG while
HDL cholesterol increased.43 Similar blood lipid changes
have been observed in type II diabetic patients in conjunc-
tion with improvements in glucose and insulin metabo-
lism.41,42 Further, high protein diets have been shown to
improve metabolic control in type II diabetes patients.41,42,46
In obese women, hypo-caloric high protein diets improved
insulin sensitivity and prevented muscle loss, whereas hypo-
caloric high carbohydrate diets worsened insulin sensitivity
and caused reductions in the fat free mass.47
Epidemiological evidence supports the clinical data
showing a cardiovascular protective effect of dietary pro-
tein. Increased protein intake has been shown to be inverse-
ly related to CVD in a cohort of 80,082 women.48 Dietary
protein is also inversely related to serum homocysteine
concentration,49 an independent risk factor for CVD. Meat
eating populations have been shown to maintain lower plas-
ma homocysteine concentrations than non-meat eaters.50,51
In numerous population studies, summarized by Obarzanek
et al.,52 higher blood pressure was associated with lower
intake of protein. Recently, a four-week dietary interven-
tion of hypertensive subjects demonstrated that a high pro-
tein diet (25% energy) was effective in signiﬁcantly lower-
ing blood pressure.53 Further, a number of population stud-
ies have established that stroke mortality is inversely relat-
ed to protein intake.54,55
Dietary Carbohydrate and Fiber
Table 3 reveals that the carbohydrate content (23%
energy) of the example diet is considerably lower than
average values (49% energy) in the U.S. diet,11 or suggest-
ed healthful ranges (55-60% energy).13,56 Although current
advice to reduce the risk of CVD is, in general, to replace
saturated fats with complex carbohydrate,13,56 there is
Vol.5, No. 3 JANA 20Summer 2002
mounting evidence to indicate that low fat, high carbohy-
drate diets may elicit undesirable blood lipid changes,
including reductions in HDL cholesterol and apolipoprotein
A-1, while concurrently elevating TG, VLDL cholesterol
and small dense LDL cholesterol.57-60 Collectively, these
blood lipid changes are associated with an increased risk for
CVD and other Syndrome X diseases.61
Table 6 shows both the glycemic index and glycemic
load (glycemic index x carbohydrate content in food por-
tion) in selected grain products, sugars/sweets, dairy foods,
fruits, and vegetables.62 High glycemic loads represent a
nearly universal characteristic of the typical western diet
because of a high reliance upon reﬁned sugars and cereal
grains. Added sugars represent 16.1% of the energy con-
sumed in the average U.S. diet, whereas reﬁned grain prod-
ucts comprise 85.3% of all the grains consumed in the
U.S.23 Table 6 reveals that dairy products maintain low
glycemic indices and loads, but paradoxically these foods
are highly insulinotrophic with insulin indices similar to
white bread.63 Consequently, the elimination of reﬁned sug-
ars, grains and dairy products in the example diet produces
a low-carbohydrate diet (23% energy) in which all of the
carbohydrates are derived from fruits, vegetables, and
seeds/nuts with their universally low glycemic loads. High
glycemic load diets have been implicated in the develop-
ment of obesity,64 and observational studies suggest that
foods with a high glycemic load increase the risk for type II
diabetes65,66 and CVD.67
The ﬁber content (42.5 g) of the example diet is con-
siderably higher than values in the U.S. diet (15.1 g) and
higher than recommended values (25-30 g).56 Soluble ﬁbers
modestly reduce LDL and total cholesterol concentrations
beyond those achieved by a diet low in saturated fat, and
ﬁber, by slowing gastric emptying, may reduce appetite and
help to control caloric intake.68
The total fat content (39% energy) of the example diet
is 30% higher than recommended intakes.13,56 However, it
should be noted that the overall dietary lipid proﬁle is
health-promoting and anti-atherogenic.
There is now substantial evidence to indicate that the
absolute amount of dietary fat is less important in lowering
blood lipid levels and reducing the risk for CVD than is the
relative concentrations of speciﬁc dietary fatty acids.69-72
Low (22% energy) and high (39% energy) fat diets which
had identical (polyunsaturated/saturated) (n3/n6) and
(monounsaturated/total fat) fatty acid ratios produced no
signiﬁcant differences in total or LDL cholesterol following
a 50 day trial.72 Hypercholesterolemic fatty acids include
12:0, 14:0, 16:0, and trans-9 18:1,73 whereas monounsatu-
rated (MUFA)70,74 and polyunsaturated (PUFA)73 fatty
acids are hypocholesterolemic, and 18:0 is neutral.74 Omega
3 PUFA have wide-ranging cardiovascular protective
capacities including lowering of plasma VLDL cholesterol
and triacylglycerol (TG) concentrations.69 Consequently, it
is entirely possible to consume relatively high fat diets that
do not necessarily produce a plasma lipid proﬁle that pro-
motes CVD72,75 given sufficient MUFA,70 PUFA,60 and an
appropriate n6/n3 PUFA ratio69 relative to the hypercho-
lesterolemic fatty acids.
Although more than 50 % of the energy in the contem-
porary Paleolithic diet is derived from animal foods, the
saturated fat content (7.0% energy) not only falls within
recommended healthful limits ( < 10 % energy),13,56 but
also within limits (<7 %) for individuals with elevated LDL
cholesterol concentrations or CVD.76 The dominant fats in
the example diet are cholesterol lowering MUFA (17.2 %
energy) and PUFA (10.4 % energy). MUFA may also con-
fer additional cardiovascular protective effects beyond low-
ering serum cholesterol by its ability to reduce LDL oxi-
dizability, a key step in the atherosclerotic process.77
Table 6. Glycemic indices and glycemic loads of various
food groups. Glycemic load = (glycemic index x carbohy-
drate content in 10g portions). The glycemic reference is
glucose with a glycemic index of 100. Data adapted from
Foster-Powell et al.62
Summer 200221 JANA Vol. 5, No. 3
The example diet is rich in omega 3 fatty acids (9.6 g)
compared to the average value (2.3 g) found in the U.S.
diet.78 Numerous studies have reported the beneficial
effects of an increased omega 3 fatty acid intake in CVD
patients.79-82 A 20% reduction in overall mortality and a
45% reduction in sudden death after 3.5 years were report-
ed in subjects with preexisting CVD when given 850 mg of
omega 3 fatty acids (20:5n3 and 22:6n3) either with or
without vitamin E.82 Omega 3 fatty acids may operate to
reduce CVD mortality via a number of mechanisms includ-
ing reductions in serum VLDL and triacylglycerol concen-
trations, thrombic tendencies, and the incidence of ventric-
Dietary Sodium and Potassium
Because no processed foods or added salt are included
in the example diet, the sodium intake (726 mg) is appre-
ciably lower than average U.S. values (3,271 mg)23 or rec-
ommended values (2,400 mg).56 Further, since potassium-
rich fruits and vegetables comprise 30% of the daily ener-
gy, the potassium content (9,062 mg) of the example diet is
nearly 3.5 times greater than average values (2,620 mg) in
the U.S. diet.23 Diets rich in potassium and low in sodium
have been repeatedly demonstrated to be therapeutic for a
variety of chronic conditions including: hypertension,
stroke, kidney stones, and osteoporosis.83,84
Table 4 demonstrates that, except for calcium, the
example diet is exceedingly rich in the 14 vitamins and
minerals most commonly deﬁcient in the U.S. diet.23 A
meta-analysis investigating the relationship between CVD
and serum homocysteine concentrations has demonstrated
that as much as 10% of CVD risk was attributable to hyper-
homocysteinemia.85 The normal metabolism of homocys-
teine requires an adequate supply of folate, vitamin B6, vit-
amin B12 and riboﬂavin. Lower serum folate concentra-
tions and vitamin B6have been associated with increased
CVD risk.86 Because the fruits (15% energy) and vegeta-
bles (15% energy) in the example diet are rich sources of
folate, the intake of this vitamin is quite high (891 µg or
223% RDA). Additionally, the ﬁsh (27.5% energy) and
lean meats (27.5% energy) contained in the example diet
are rich sources of vitamin B6, and along with the fruits,
vegetables and seeds/nuts, combine to yield a high intake
(6.7 mg or 515 % RDA) of this vitamin.
Despite a high reliance upon low fat animal foods
(55% energy), the experimental diet would not have neces-
sarily elicited unfavorable blood lipid proﬁles because of
the hypolipidemic effects of high dietary protein (38 %
energy) and the relatively low level of low glycemic index
dietary carbohydrates (23%). Although total fat intake (39%
energy) would have been higher than that found in western
diets, total saturated fat (7.0% energy) fell well within
healthful limits (10% energy). Important qualitative differ-
ences in fat intake, including relatively high levels of
MUFA and PUFA and a lower n6/n3 fatty acid ratio, also
would have served to reduce the risk for CVD. Other char-
acteristics of the example diet, including a high intake of
antioxidants, ﬁber, vitamins, and phytochemicals along
with a low salt intake would further deter the risk of CVD
and other chronic diseases.
1. Williams GC, Nesse RM. The dawn of Darwinian medicine.
Quart Rev Biol. 1991;66:1-22.
2. Wilson DR. Evolutionary epidemiology. Acta Biotheoretica.
3. Goldsmith MF. Ancestors may provide clinical answers, say
‘Darwinian’ medical evolutionists. JAMA. 1993;269:1477-
4. Cohen MN. Health and the Rise of Civilization. London: Yale
University Press; 1989.
5. Abrams HL. The relevance of Paleolithic diet in determining
contemporary nutritional needs. J Appl Nutr. 1979;31:43-59.
6. Eaton SB, Konner MJ. Paleolithic nutrition: a consideration of
its nature and current implications. N Engl J Med.
7. Truswell AS. Diet and nutrition of hunter-gatherers. In: Health
and Disease in Tribal Societies. New York: Elsevier; 1977.
8. Ridker PM. On evolutionary biology, inﬂammation, infection,
and the causes of atherosclerosis. Circulation. 2002;105:2-4.
9. Eaton SB. Humans, lipids and evolution. Lipids. 1992;27:814-
10. Eaton SB, Eaton SB III. Paleolithic vs. modern diets:selected
pathophysiological implications. Eur J Nutr. 2000;39:67-70.
11. 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
12. Cordain L, Eaton SB, Brand Miller J, Mann N, Hill K. The
paradoxical nature of hunter-gatherer diets: meat-based, yet
non-atherogenic. Eur J Clin Nutr. 2002;56 (suppl 1):S1-S11.
13. United States Department of Agriculture. The Food Guide
Pyramid. Center for Nutrition Policy and Promotion. Home
and Garden Bulletin 252. Washington, D.C., 2000.
14. Cordain L. Cereal grains: humanity’s double-edged sword.
World Rev Nutr Diet. 1999;84:19-73.
15. Eaton SB, Nelson DA. Calcium in evolutionary perspective.
Am J Clin Nutr. 1991;54(1 suppl):281S-287S.
16. Zohary D, Hopf M. Domestication of pulses in the Old World.
Vol.5, No. 3 JANA 22Summer 2002
17. Kurtzweil P. Nutritional info available for raw fruits, vegeta-
bles, ﬁsh. FDA Consumer Magazine. May, 1993. United
States Health and Human Services, Food and Drug
Administration, Rockville MD. http://www.fda.gov/fdac/spe-
cial/ foodlabel/ raw.html.
18. Holt SA, Brand Miller JC, Petocz P. An insulin index of foods:
the insulin demand generated by 1000-kJ portions of common
foods. Am J Clin Nutr. 1997;66:1264-1276.
19. Thorburn AW, Brand JC, Truswell AS. Slowly digested and
absorbed carbohydrate in traditional bushfoods: a protective
factor against disease. Am J Clin Nutr. 1987;45:98-106.
20. United States Department of Agriculture, Economic Research
Service. America’s Eating Habits: Changes and Consequences.
Agriculture Information Bulletin No. 750, Elizabeth Frazao,
ed.. Washington, D.C., 1999. http://www.ers.usda.gov/ publica-
21. Cordain L, Watkins BA, Florant GL, Kehler M, Rogers L, Li
Y. Fatty acid analysis of wild ruminant tissues: evolutionary
implications for reducing diet-related chronic disease. Eur J
Clin Nutr. 2002;56:1-11.
22. Heaney RP. Excess dietary protein may not adversely affect
bone. J Nutr. 1998;128:1054-1057.
23. U.S. Department of Agriculture, Agricultural Research
Service. 1997. Data tables: Results from USDA’s 1994-96
Continuing Survey of Food Intakes by Individuals and 1994-
96 Diet and Health Knowledge Survey, [Online]. ARS Food
Surveys Research Group. Available (under “Releases”):
http://www.barc.usda.gov/bhnrc/ foodsurrvey/ home.htm.
24. Bridges PS. Skeletal biology and behavior in ancient humans.
Ev Anthropol. 1995;4:112-120.
25. Ruff C, Trinklaus E, Walker A, Larsen CS. Postcranial robus-
ticity in Homo. I: Temporal trends and mechanical interpreta-
tion. Am J Phys Anthropology. 1993;91:21-53.
26. Kricun ME. Edward B D Neuhauser Lecture. Paleoradiology
of the prehistoric Australian aborigines. AJR Am J
27. Barzel US. The skeleton as an ion exchange system: implica-
tions for the role of acid-base imbalance in the genesis of
osteoporosis. J Bone Min Res. 1995;10:1431-1436.
28. Lutz J. Calcium balance and acid-base status of women as
affected by increased protein intake and by sodium bicarbon-
ate ingestion. Am J Clin Nutr. 1984; 39:281-288.
29. Sebastian A, Harris ST, Ottaway JH, Todd KM, Morris RC.
Improved mineral balance and skeletal metabolism in post-
menopausal women treated with potassium bicarbonate. N
Eng. J Med. 1994;33:1776-1781.
30. Remer T, Manz F. Potential renal acid load of foods and its
inﬂuence on urine ph. J Am Diet Assoc. 1995;95:791-797.
31. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM et al. A clin-
ical trial of the effects of dietary patterns on blood pressure. N
Engl J Med. 1997;336:1117-1124.
32. McNamara DJ, Kolb R, Parker TS, Batwin H, Samuel P,
Brown CD, Ahrens EH. Heterogeneity of cholesterol home-
ostasis in man. Response to changes in dietary fat quality and
cholesterol quantity. J Clin Invest. 1987;79:1729-1739.
33. Howell WH, McNamara DJ, Tosca MA, Smith BT, Gaines JA.
Plasma lipid and lipoprotein responses to dietary fat and cho-
lesterol: a meta-analysis. Am J Clin Nutr. 1997;65:1747-1764.
34. Schonfeld G, Patsch W, Rudel LL, Nelson C, Epstein M,
Olson RE. Effects of dietary cholesterol and fatty acids on
plasma lipoproteins. J Clin Invest. 1982;69:1072-1080.
35. Anonymous. Effects of dietary protein restriction on the pro-
gression of moderate renal disease in the Modiﬁcation of Diet
in Renal Disease Study. J Am Soc Nephrol. 1996;12:2616-
36. 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;23:1170-1177.
37. Crovetti R, Porrini M, Santangelo A, Testolin G. The inﬂu-
ence of thermic effect of food on satiety. Eur J Clin Nutr
38. Stubbs RJ. Nutrition Society Medal Lecture. Appetite, feed-
ing behaviour and energy balance in human subjects. Proc
Nutr Soc. 1998;57:341-356.
39. Skov AR, Toubro S, Ronn B, Holm L, Astrup A.
Randomized trial on protein vs carbohydrate in ad libitum
fat reduced diet for the treatment of obesity.
Int J Obes Relat Metab Disord. 1999;23:528-536.
40. Baba NH, Sawaya S, Torbay N, Habbal Z, Azar S, Hashim
SA. High protein vs high carbohydrate hypoenergetic diet for
the treatment of obese hyperinsulinemic subjects. Int J Obes
Relat Metab Disord. 1999;23:1202-1206
41. O’Dea K. Marked improvement in carbohydrate and lipid
metabolism in diabetic Australian Aborigines after temporary
reversion to traditional lifestyle. Diabetes. 1984;33:596-603.
42. O’Dea K, Traianedes K, Ireland P, Niall M, Sadler J, Hopper
J, DeLuise M. The effects of diet differing in fat, carbohy-
drate, and ﬁber on carbohydrate and lipid metabolism in type
II diabetes. J Am Diet Assoc.1989; 89:1076-1086.
43. Wolfe BM, Giovannetti PM. Short term effects of substitut-
ing protein for carbohydrate in the diets of moderately hyper-
cholesterolemic human subjects. Metabolism. 1991;40:338-
44. Wolfe BM, Giovannetti PM. High protein diet complements
resin therapy of familial hypercholesterolemia. Clin Invest
45. Wolfe BM, Piche LA. Replacement of carbohydrate by pro-
tein in a conventional-fat diet reduces cholesterol and triglyc-
eride concentrations in healthy normolipidemic subjects. Clin
Inves. Med. 1999;22:140-148.
46. Seino Y, Seino S, Ikeda M, Matsukura S, Imura H. Beneﬁcial
effects of high protein diet in treatment of mild diabetes. Hum
Nutr Appl Nutr. 1983;37A(3):226-230.
47. Piatti PM, Monti F, Fermo I, Baruffaldi L, Nasser R,
Santambrogio G, Librenti MC, Galli-Kienle M, Pontiroli AE,
Summer 200223 JANA Vol. 5, No. 3
Pozza G. Hypocaloric high-protein diet improves glucose oxi-
dation and spares lean body mass: comparison to hypocaloric
high-carbohydrate diet. Metabolism. 1994;43:1481-1487
48. Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA,
Speizer FE, Hennekens CH, Willett WC. Dietary protein and
risk of ischemic heart disease in women. Am J Clin Nutr.
49. Stolzenberg-Solomon RZ, Miller ER III, Maguire MG, Selhub
J, Appel LJ. Association of dietary protein intake and coffee
consumption with serum homocysteine concentrations in an
older population. Am J Clin Nutr. 1999; 69:467-475.
50. Mann NJ, Li D, Sinclair AJ, Dudman NP, Guo XW, Elsworth
GR, Wilson AK, Kelly FD. The effect of diet on plasma
homocysteine concentrations in healthy male subjects. Eur J
Clin Nutr. 1999;53:895-899.
51. Mezzano D, Munoz X, Martinez C, Cuevas A, Panes O,
Aranda E, Guasch V, Strobel P, Munoz B, Rodriguez S,
Pereira J, Leighton F. Vegetarians and cardiovascular risk fac-
tors: hemostasis, inﬂammatory markers and plasma homocys-
teine. Thromb Haemost. 1999;81:913-917.
52. Obarzanek E, Velletri PA, Cutler JA. Dietary protein and
blood pressure. JAMA. 1996;275:1598-1603.
53. Burke V, Hodgson JM, Beilin LJ, Giangiulioi N, Rogers P,
Puddey IB. Dietary protein and soluble ﬁber reduce ambula-
tory blood pressure in treated hypertensives. Hypertension.
54. Klag MJ, Whelton PK. The decline in stroke mortality. An
epidemiologic perspective. Ann Epidemiol. 1993;3:571-575.
55. Kinjo Y, Beral V, Akiba S, Key T, Mizuno S, Appleby P,
Yamaguchi N, Watanabe S, Doll R. Possible protective effect
of milk, meat and ﬁsh for cerebrovascular disease mortality in
Japan. J Epidemiol. 1999;9:268-274.
56. Krauss RM, Deckelbaum RJ, Ernst N, et al. Dietary guide-
lines for healthy American adults. Circulation. 1996;94:1795-
57. Denke MA, Breslow JL. Effects of a low fat diet with water
and without intermittent saturated fat and cholesterol inges-
tion on plasma lipid, lipoprotein, and apolipoprotein levels in
normal volunteers. J Lipid Res. 1988;29: 963-969.
58. Dreon DM, Fernstrom HA, Miller B, Krauss RM.
Apolipoprotein E isoform phenotype and LDL subclass
response to a reduced-fat diet. Arterioscler Thromb Vasc Biol.
59. Jeppesen J, Schaaf P, Jones C, Zhou M-Y, Ida Chen Y-D,
Reaven GM. Effects of low-fat, high carbohydrate diets on
risk factors for ischemic heart disease in postmenopausal
women. Am J Clin Nutr. 1997;65:1027-1033.
60. Mensink RP, Katan MB. Effect of dietary fatty acids on serum
lipids and lipoproteins: a meta-analysis of 27 trials.
Arterioscler Thromb. 1992;12:911-919.
61. Grundy SM. Hypertriglyceridemia, insulin resistance, and the
metabolic syndrome. Am J Cardiol. 1999;83:25F-29F.
62. Foster-Powell K, Brand Miller J. International table of
glycemic index. Am J Clin Nutr. 1995;62:871S-893S.
63. Bjorck I, Liljeberg H, Ostman E. Low glycaemic-index foods.
B J Nutr. 2000;83(suppl 1):S149-S155.
64. Ebbeling CB, Ludwig DS. Treating obesity in youth: should
dietary glycemic load be a consideration? Adv Pediatr.
65. Salmeron J, Ascherio A, Rimm EB, Colditz GA, et al. Dietary
ﬁber, glycemic load, and risk of NIDDM in men. Diabetes
66. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL,
Willett WC. Dietary ﬁber, glycemic load, and risk of non-
insulin-dependent diabetes mellitus in women. JAMA.
67. Liu S, Willett WC, Stampfer MJ, Hu FB, Franz M, Sampson
L, Hennekens CH, Manson JE. Aprospective study of dietary
glycemic load, carbohydrate intake, and risk of coronary
heart disease in US women. Am J Clin Nutr. 2000;71: 1455-
68. Anderson JW, Smith BM, Gustafson NJ. Health beneﬁts and
practical aspects of high-fiber diets. Am J Clin Nutr
69. Connor SL, Connor WE. Are ﬁsh oils beneﬁcial in the pre-
vention and treatment of coronary artery disease? Am J Clin
70. Gardner CD, Kraemer HC. Monounsaturated versus polyun-
saturated dietary fat and serum lipids: a meta-analysis.
Arterioscler Thromb Vasc Biol. 1995;15:1917-1927.
71. Oliver MF. It is more important to increase the intake of
unsaturated fats than to decrease the intake of saturated fats:
evidence from clinical trials relating to ischemic heart dis-
ease. Am J Clin Nutr. 1997; 66:980S-986S.
72. Nelson GJ, Schmidt PC, Kelley DS. Low-fat diets do not
lower plasma cholesterol levels in healthy men compared to
high-fat diets with similar fatty acid composition at constant
caloric intake. Lipids. 1995;30: 969-976.
73. Grundy SM. What is the desirable ratio of saturated, polyun-
saturated, and monounsaturated fatty acids in the diet? Am J
Clin Nutr. 1997;66:988S-990S.
74. Yu S, Deer J, Etherton T, Kris-Etherton P. Plasma cholesterol-
predictive equations demonstrated that stearic acid is neutral
and monounsaturated fatty acids are hypocholesterolemic.
Am J Clin Nutr. 1995;61:1129-1139.
75. Garg A, Bonanome A, Grundy SM, Zhang Z-J, Unger RH.
Comparison of a high- carbohydrate diet with a high-
monounsaturated fat diet in patients with non-insulin depen-
dent diabetes mellitus. N Eng J Med. 1988;319:829-834.
76. National Cholesterol Education Program. Second Report of
the Expert panel on Detection, Evaluation and Treatment of
High Blood Cholesterol in Adults (Adult Treatment Panel II).
77. O’Byrne DJ, O’Keefe SF, Shireman RB. Low-fat, monoun-
saturated-rich diets reduce susceptibility of low density
lipoproteins to peroxidation ex vivo. Lipids. 1998;33:149-157.
Vol.5, No. 3 JANA 24Summer 2002
78. U.S. Department of Agriculture, Agricultural Research
Service. 1997. Data tables: Intakes of 19 Individual Fatty
Acids: Results from USDA’s 1994-96 Continuing Survey of
Food Intakes by Individuals, [Online]. ARS Food Surveys
Research Group. Available (under “Releases”):
http://www.barc.usda.gov/bhnrc/ foodsurvey/ home.htm.
79. de Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J,
Mamelle N. Mediterranean diet, traditional risk factors, and
the rate of cardiovascular complications after myocardial
infarction: final report of the Lyon Diet Heart Study.
80. Singh RB, Niaz MA, Sharma JP, Kumar R, Rastogi V, Moshiri
M. Randomized, double-blind, placebo-controlled trial of ﬁsh
oil and mustard oil in patients with suspected acute myocar-
dial infarction: the Indian experiment of infarct survival-4.
Cardiovasc Drugs Ther. 1997;11:485-491.
81. von Schacky C, Angerer P, Kothny W, Theisen K, Mudra H.
The effect of dietary omega-3 fatty acids on coronary athero-
sclerosis: a randomized, double-blind, placebo-controlled
trial. Ann Intern Med. 1999;130:554-562.
82. GISSI-Prevention Investigators. Dietary supplementation with
n-3 polyunsaturated fatty acids and vitamin E after myocar-
dial infarction: results of the GISSI-Prevenzione trial. Gruppo
Italiano per lo Studio della Sopravvivenza nell’Infarto mio-
cardico. Lancet. 1999;354:447-455.
83. Antonios TF, MacGregor GA. Salt–more adverse effects.
84. Massey LK, Whiting SJ. Dietary salt, urinary calcium, and
kidney stone risk. Nutr Rev. 1995;53:131-139.
85. Boushey CJ, Beresford SA, Omenn GS, et al. A quantitative
assessment of plasma homocysteine as a risk factor for vas-
cular disease: probable beneﬁts of increasing folic acid
intakes. JAMA. 1995;274:1049-1057.
86. Robinson K, Arheart K, Refsum H, et al. Low circulating
folate and vitamin B6 concentrations: risk factors for stroke,
peripheral vascular disease, and coronary artery disease:
European COMAC Group. Circulation. 1998;97:437-443.