The Western Diet and Chronic Kidney Disease

Abstract

Characteristics of the Western diet that fueled the obesity epidemic may also impact kidney disease incidence and progression. Enlarging portion sizes over the past half century has been accompanied by increased intake of protein, sodium, and processed foods while consumption of fruits and vegetables has declined. Overall dietary patterns play a strong role for chronic disease risk including chronic kidney disease. While dietary patterns high in fresh fruits and vegetables and low in red meats, such as the Mediterranean diet, decrease the risk of chronic diseases, the Western diet, characterized by high intake of red meat, animal fat, sweets, and desserts and low intake of fresh fruits and vegetables and low-fat dairy products, increases risk of chronic diseases. In this article, we review the potential mechanisms whereby several key characteristics of the typical Western diet may impact kidney disease incidence and progression. We also discuss a public health policy initiative to improve dietary choices. Reducing protein intake to the recommended daily allowance of 0.8 g/kg/day and increasing intake of fruit and vegetables and fiber may mitigate kidney disease progression and reduce risk of cardiovascular disease and mortality.

Full text

HYPERTENSION AND METABOLIC SYNDROME (JR SOWERS AND A WHALEY-CONNELL, SECTION EDITORS)
The Western Diet and Chronic Kidney Disease
Divya Hariharan &Kavitha Vellanki &Holly Kramer
#Springer Science+Business Media New York 2015
Abstract Characteristics of the Western diet that fueled the
obesity epidemic may also impact kidney disease incidence
and progression. Enlarging portion sizes over the past half
century has been accompanied by increased intake of protein,
sodium, and processed foods while consumption of fruits
and vegetables has declined. Overall dietary patterns play
a strong role for chronic disease risk including chronic
kidney disease. While dietary patterns high in fresh fruits
and vegetables and low in red meats, such as the Medi-
terranean diet, decrease the risk of chronic diseases, the
Western diet, characterized by high intake of red meat,
animal fat, sweets, and desserts and low intake of fresh
fruits and vegetables and low-fat dairy products, increases
risk of chronic diseases. In this article, we review the
potential mechanisms whereby several key characteristics
of the typical Western diet may impact kidney disease
incidence and progression. We also discuss a public health
policy initiative to improve dietary choices. Reducing protein
intake to the recommended daily allowance of 0.8 g/kg/day
and increasing intake of fruit and vegetables and fiber may
mitigate kidney disease progression and reduce risk of cardio-
vascular disease and mortality.
Keywords Nutrition .Chronic kidney disease .
Cardiovascular disease .Microbiome
Introduction
Westernization refers to the process of adopting certain prac-
tices associated with Western (European) culture [1]. The term
BWest e r n ^applies to cultures and practices in countries that
have been colonized by Europeans in the past such as Austra-
lia, New Zealand, or the USA and Canada. The term culture
refers to multiple aspects of population traditions including
diet, language, and religion along with other aspects of daily
life. Industrialization and Westernization are terms that are
frequently used interchangeably, but the terms are actually
distinct. Industrialization refers to the process of social evolve-
ment from a largely agrarian society into a largely urban so-
ciety [2]. Many non-Western countries have become industri-
alized or are becoming industrialized. However, given the
global business of fast food companies such as McDonalds
and processed foods and drinks such as Coca-Cola, the West-
ernization of diet is not limited to Western countries. In this
manuscript, we use the term Westernization to specifically
refer to the Western traditions of diet which have evolved over
time due to the cumulative result of industrialization within
the USA.
During the early part of the twentieth century, 1/3 of the US
population lived on a farm and approximately 40 % of the
workforce was found in agriculture [3]. The majority of the
US diet was vegetable based, and the meat consumed came
from animals raised on small farms. The industrialization of
farming led to sharp trends away from manual labor and over-
all decreases in the total costs required to produce food [3].
While the relative price of food compared with the costs of
purchasing other goods and services has decreased since the
mid-twentieth century, the decline has not been uniform
across different food groups. High-calorie foods have become
much relatively cheaper than healthier foods. For example,
since 1983, the price of fresh fruit has increased by almost
200 % while the cost of sugar increased by only 30 % [3].
Today, annual sugar consumption is tenfold higher compared
to the first part of the twentieth century, and the majority of
sugar consumed is high-fructose corn syrup [4]. Portion sizes
This article is part of the Topical Collection on Hypertension and
Metabolic Syndrome
D. Hariharan :H. Kramer (*)
Department of Public Health Sciences, Loyola University Chicago,
2160 First Avenue, Maywood, IL 60153, USA
e-mail: hkramer@luc.edu
K. Vellanki :H. Kramer
Department of Medicine, Division of Nephrology and Hypertension,
Loyola University Chicago, Maywood, IL, USA
Curr Hypertens Rep (2015) 17:16
DOI 10.1007/s11906-014-0529-6

have also changed dramatically over the last half century with
average caloric intake for a given meal increasing by over
20 % [3].
The aging of the population due to gains in life expectancy
combined with reduced physical activity and the Westerniza-
tion of diets has fueled the development of chronic diseases
including obesity, diabetes, hypertension, and chronic kidney
disease (CKD). During the early part of the twentieth century,
the lifetime risk of type 2 diabetes was 1 in 30. Today, the
lifetime risk of diabetes for individuals born during the early
part of the twenty-first century is 1 in 3 [5]. The rapid increase
in obesity prevalence has outpaced the development of health
policy strategies created to curb obesity trends. Within the
USA, approximately 1/3 of adults are overweight and 1/3
are now obese [6]. The number of adults with morbid obesity,
defined as a body mass index ≥40 kg/m
2
, continues to increase
with approximately 6 % of adults now extremely obese [6,7].
Given the strong link between obesity, especially morbid obe-
sity, and kidney failure [8–10], it is likely that the obesity
epidemic played a role in the epidemic of end-stage renal
disease that also occurred during this time period [11]. Al-
though obesity itself may impact kidney disease progression,
the characteristics of the Western diet that fueled the obesity
epidemic may also impact kidney disease incidence and pro-
gression. As portion sizes increased over the past century
(Fig. 1), so did the consumption of protein, sodium, and proc-
essed foods [12•]. In contrast, overall consumption of fruits
and vegetables did not increase. Currently, less than 20 % of
US adults consume the recommended servings of fruits and
vegetables [13]. The association between dietary macronutri-
ents, especially protein intake, and kidney disease incidence
and progression has been previously examined in multiple
clinical trials and summarized [14•]. However, it is likely that
overall dietary patterns play a greater role for chronic disease
risk given the strong consistency of dietary patterns within
individuals [15,16]. The Western diet, characterized by high
intake of red meat and animal fat, and low intakeof fresh fruits
and vegetables [17•], contains a high amount of highly proc-
essed foods and is high in saturated and trans fats [12•]. Strong
adherence to a Western dietary pattern correlates with in-
creased levels of inflammation [18] and heightened risk for
cardiovascular disease and mortality compared to non-
Western dietary patterns [19–21]. The Western diet has also
been associated with kidney disease. For example, individuals
with dietary patterns that reflect a typical Western diet are
more likely to have moderate to severely increased levels of
urine albumin excretion and are more likely to have a rapid
decline in GFR (≥3 ml/min/1.73 m
2
/year) compared to indi-
viduals whose dietary habits do not reflect a typical Western
dietary pattern [17•]. In this article, we review the potential
mechanisms whereby several key characteristics of the typical
Western diet may impact kidney disease incidence and pro-
gression. We also discuss a public health policy initiative to
improve dietary choices.
Protein
The typical US diet contains about twice the protein intake
recommended by the US dietary guidelines [22]. For patients
with CKD, managing proper protein intake remains one of the
most important modifiable factors for prevention of CKD pro-
gression. Several decades ago, multiple independent investi-
gators demonstrated that both renal blood flow and GFR in-
crease by at least 30 % when healthy persons transition from a
low animal protein diet to a high animal protein diet [23•,24].
These hemodynamic changes are limited to animal protein
because increasing vegetable protein intake does not lead to
Fig. 1 Illustration of the changes
in portion sizes in US diet
16 Page 2 of 9 Curr Hypertens Rep (2015) 17:16

heightened renal hemodynamics with vegetarians typically
having a lower GFR compared to nonvegetarians [25]. The
impact of excessive animal protein intake on kidney function
decline is multifactorial but largely a function of amino acids
triggering multiple humoral and local mediators to alter renal
hemodynamics [25–28].
One of the largest clinical trials to examine the association
between protein intake and kidney disease progression was
the Modification of Diet in Renal Disease (MDRD) Study
[29•]. The MDRD study randomized 585 adults with
established CKD (predominantly nondiabetic) and GFR of
25–55 ml/min/1.73 m
2
to either a usual-protein diet or a
low-protein diet (1.3 or 0.58 g/kg/body weight per day). Dur-
ing the follow-up period, the low-protein group showed a
more rapid decline during the first 4 months compared to the
standard protein intake group, but thereafter, the decline in
GFR was slower. Multiple clinical trials of protein restriction
were completed subsequent to the MDRD Study, and results
from 13 randomized clinical trials with a total of 1, 919 pa-
tients with established CKD were pooled and summarized.
Overall, moderate protein restriction was associated with a
0.53 ml/min/year (95 % CI 0.08, 0.98) slower GFR decline
compared to a standard protein intake [14•]. Thus, although
moderate protein restriction reduces the rate of GFR decline,
the overall effects are modest. In addition, the impact of pro-
tein restriction may differ by diabetes status with stronger
effects noted in patients with diabetes [14•]. More severe pro-
tein restriction (<0.3 g/kg/day) does reduce GFR decline but
requires supplementation with essential amino acids and very
close monitoring to ensure adequate caloric and macronutrient
intake [29•].
Nonvolatile Acid Load
Nonvolatile acids, referred to as the endogenous acid load,
must be excreted by the kidneys in the form of ammonium
produced by the proximal tubule and via hydrogen ion excre-
tion by the distal tubule [30•]. Nonvolatile acids are produced
when organic sulfur from methionine and cysteine is oxidized
to inorganic sulfates. These acids are then balanced by alkali
obtained from the metabolizing of organic anions such as
citrate and malate found in fruits and vegetables. The net en-
dogenous acid production is thus equivalent to the total
amount of endogenous acids minus the alkali from foods
absorbed in the intestine [30•]. A diet that is high in animal
protein and cereal grains but low in fresh fruits and vegetables,
such as the Western diet, will lead to a high net endogenous
acid production and a high workload for each individual neph-
ron. This excess workload may lead to kidney disease progres-
sion among individuals who have a reduced working nephron
number such as persons with CKD or a solitary functioning
kidney. With decreasing nephron number, each individual
nephron must increase its production of ammonium produc-
tion and hydrogen ion excretion in order to maintain acid/base
balance given a particular endogenous acid load. The lower
the nephron number, the higher the tubular ammonium con-
centration in tubular cells heightening risk for tubular toxicity.
It is also postulated that higher net endogenous acid produc-
tion heightens the renin-angiotensin system, increases
endothelin-1, and activates the alternate complement cascade
culminating in kidney injury [31–37]. In contrast to the West-
ern diet, diets that are high in fruits and vegetables and lower
in animal protein are associated with lower endogenous acid
load, higher alkali levels, and overall lower net endogenous
acid production [30•]. The Dietary Approach to Stop Hyper-
tension (DASH) diet is high in fruits and vegetables and low-
fat dairy products and low in fats, oils, and animal protein.The
net endogenous acid production during consumption of a
DASH diet is approximately 50 % lower compared to the
typical Western diet [30•]. Modifying the diet of patients with
CKD to increase fruit and vegetable intake may lower net
endogenous acid excretion by over one third [38•]. Such re-
ductions in net endogenous acid production may minimize
kidney strain and ameliorate loss of GFR over time.
Dietary Fiber
Studies which focused on adults with CKD clinically attribut-
ed to hypertension have shown that the addition of either
sodium bicarbonate or fruits and vegetables is associated with
a slower decline in GFR [39–41]. Thus, the impact of in-
creased net endogenous acid excretion may be addressed with
providing sodium bicarbonate tablets rather than addressing
low intake of fruits and vegetables. However, increasing fruit
and vegetable intake has the added benefit of increasing the
fiber content of the diet.
Dietary fiber refers to carbohydrates or carbohydrate-
containing compounds that are not absorbed by the intestine.
These fibers are primarily the storage and cell wall polysac-
charides of plants that cannot be digested by enzymes in the
gastrointestinal tract [42•]. Fiber that is degraded by bacteria is
classified as fermentable, while fiber that is not degraded by
bacteria is considered non-fermentable [43•]. Low fiber intake
is associated with elevated levels of biomarkers of inflamma-
tion such as serum C-reactive protein, interleukin-6, and tu-
mor necrosis factor-alpha receptor-2 [44–47]. Elevated levels
of inflammatory markers are associated with increased risk of
cardiovascular disease and mortality in adults with and with-
out CKD [48–53]. High levels of inflammation are also asso-
ciated with CKD incidence and progression [54–57].
High fiber intake is associated with reduced cardiovascular
risk and mortality [58–61], and this association appears stron-
gerinadultswithCKD[62]. The American Dietetic Associ-
ation recommends that adults consume 14 g of dietary fiber
Curr Hypertens Rep (2015) 17:16 Page 3 of 9 16

per 1000 kcal per day [42•]. These reference intakes were
based on fiber intake thresholds associated with reduced car-
diovascular risk. High-fiber diets are more satiating and may
help reduce total caloric intake and avoid obesity and weight
gain [43•]. High-fiber foods include whole grains, legumes,
fruits, and vegetables. However, many people obtain their
fiber intake via fiber supplements. Given the lack of evi-
dence that fiber supplements reduce cardiovascular risk,
individuals should be encouraged to obtain their fiber from
whole foods and not supplements [42•]. Currently, there
are no specific recommendations for levels of dietary fiber
intake for adults with CKD but recommendations for the
general population are likely safe and may even be bene-
ficial as long as serum potassium and phosphate levels are
monitored.
Multiple mechanisms have been proposed whereby high
dietary fiber intake reduces cardiovascular risk. One of the
proposed mechanisms centers on the interaction between fiber
and the gut microbiome. The gut microbiome is defined as the
community of microbes that live in the intestinal tract and
interact with the host [43•]. The gut microbiome plays a role
in metabolizing certain fermentable carbohydrates [43•], syn-
thesizing vitamins K and B, and modulating the immune sys-
tem and the body’s response to environmental antigens [63].
The gut microbiome is also important for maintaining a
healthy intestinal epithelial barrier [43•]. The intestinal ep-
ithelium consists of epithelial cells that are linked by tight
junctions preventing translocation of intestinal contents. A
weakening of this barrier may permit excessive amounts of
endotoxins to leak into the circulation and incite an inflam-
matory response. It has been hypothesized that high fiber
intake reduces inflammation by prompting the growth of
commensal bacteria thereby increasing resistance to growth
of pathogenic bacteria [43•]. In patients with CKD, urease
bacterial end product formation is above normal and results
in urea accumulation [63,64]. Urea directly disrupts the
gut barrier function by reducing the presence of occludin
and zonula occludens proteins in the tight junctions and
thus increasing intestinal permeability [23•]. It is possible
that the reduced levels of inflammation associated with
high fiber intake are mediated by direct effects of fiber
on the gut microbiome.
Bifidobacterium is one of several endosymbiotic colonizers
of the gut. Increasing the growth of Bifidobacterium dis-
courages colonization with gram-negative pathogens and
may improve colonic health [43•,65] and other symbiotic
bacteria species depending on the fiber source [66–69].
The ability to degrade fermentable fibers is bacteria spe-
cies and strain dependent [43•]. For example, the genus
Bifidobacterium possesses a unique fructose-6-phosphate
phosphoketolase enabling it to ferment carbohydrates.
Thus, the type and amount of fiber consumed does appear
to shape the intestinal microbiome composition [43•].
Alternative Diets
Dietary patterns that reflect high intake of fruits and vegeta-
bles and low intake of red meat and saturated fats such as the
Dietary Approaches to Stop Hypertension (DASH) diet [70],
the Prudent diet [17•,19,20], the Japanese diet [71], and the
Mediterranean diet, contain higher amounts of fruits and veg-
etables and overall fiber and are lower in animal protein com-
pared to the Western diet. The Mediterranean diet is unique in
its incorporation of olive oil and nuts making the diet high in
monounsaturated fats [72–75]. The DASH and Mediterranean
diets have been shown to positively impact chronic disease
measures and outcomes including blood pressure [70,76,77]
and mortality [78,79•,80]. When combined with low sodium
consumption, the DASH diet reduces systolic blood pressure
levels by almost 12 mmHg among adults with hypertension
[70]. Given the fact that blood pressure reduction may be one
of the most important modifiable risk factors for slowing kid-
ney disease progression [81], the DASH diet combined with
salt restriction may be an effective intervention but fear of
high potassium and phosphorous levels and poor access to
fresh fruits and vegetables for many individuals with CKD
have likely precluded widespread acceptance of the DASH
diet for clinical use. Studies have demonstrated that individ-
uals with dietary patterns that reflect the DASH-type dietary
pattern have lower odds of moderate or severely increased
urine albumin excretion and lower odds of rapid kidney func-
tion decline, defined as a GFR decline ≥30 % of baseline
GFR, compared to individuals who have a more Western di-
etary pattern [17•]. A secondary analysis of the DASH study
also showed that a diet high in fruits and vegetables leads to
decreases in urine albumin excretion among individuals with
prehypertension or hypertension and a baseline urine albumin
excretion >7 mg/24. These findings were not explained by
reductions in blood pressure or total protein or sodium intake
[77].
Strong adherence to a Mediterranean diet, which is high in
fresh fruits, vegetables, fish, and unsaturated fats (mainly ol-
ive oil), is associated with lower prevalence of CKD and re-
duced mortality risk. Huang et al. examined the association
between levels of adherence to a Mediterranean diet and base-
line CKD prevalence and 10-year all-cause mortality among
men enrolled in the Uppsala Longitudinal Study of Adult
Men. These men were born between the years 1920 and
1924 and were living in Uppsala Sweden. Dietary patterns
were determined during years 1991–1995 using 7-day diet
records, and participants were followed for a 10-year period
for overall mortality. Men with high adherence to a Mediter-
ranean diet had 42 % lower odds of CKD at baseline, respec-
tively, after adjusting for presence of hypertension and diabe-
tes. Among men with kidney disease, medium or high adher-
ence to a Mediterranean diet was associated with an approxi-
mately 25 % lower risk of mortality compared to men with
16 Page 4 of 9 Curr Hypertens Rep (2015) 17:16

low adherence after adjusting for established cardiovascular
disease risk factors [78]. The results of this observational
study are supported by a large clinical trial (Prevención con
Dieta Mediterŕanea) that randomized 7447 adults aged
≥55 years to a standard low-fat diet, a Mediterranean diet
enhanced with extra virginal olive oil, or a Mediterranean diet
supplemented with walnuts, hazelnuts, and almonds. After a
median follow-up of 4.8 years, the trial was stopped due to a
30 % relative risk reduction of a combined cardiovascular
endpoint (heart attack, stroke, or cardiovascular death) in the
participants assigned to a Mediterranean diet enhanced with
either olive oil or nuts.
Nutritional Guidelines for CKD Stages 1–4
The National Kidney Foundation-Kidney Disease Outcomes
Quality Initiative Guidelines on Hypertension and Antihyper-
tensive Agents in CKD recommended a modified version of
the DASH diet for persons with CKD stages 3–4[82]. The
DASH diet includes higher protein intake than the recom-
mended daily allowance, but the majority of this protein is
from dairy products, vegetable sources, and non-red meat.
For persons with CKD, the DASH diet may be modified to
achieve a protein intake of 0.6–0.8 g/kg of ideal body weight
per day, as well as a lower phosphorus (0.8–1.0 g/day) and
Tabl e 1 Dietary interventions for persons with chronic kidney disease
not receiving dialysis
Goal Dietary intervention
Control blood pressure Limit sodium intake to <2300 mg per day.
Caloric reduction if overweight or obese
Reduce urine albumin
excretion and slow
loss of GFR
Limit dietary protein intake to 0.8 g/kg/day in
persons without diabetes and 0.8–1.0 g/kg/day
in persons with diabetes. Lowering protein
intake <0.6 g/kg/day may mitigate GFR loss
but patients must be followed closely and
adherence may be poor
Increase fruit and vegetable intake and/or utilize
sodium bicarbonate supplementation
Avoid metabolic
acidosis
Sodium bicarbonate supplementation or increase
fruit and vegetable intake while monitoring
serum potassium and phosphorous levels
Adapted from the National Institute of Diabetes and Digestive and
Kidney Diseases. National Kidney Disease Education Program. Chronic
kidney disease and diet: assessment, management and treatment.
Treating CKD patients who are not on dialysis. Revised June 2014,
www.nkdep.nih.gov
Fig. 2 Illustration of current
nutrition label (left) and proposed
new nutrition label (right)
Curr Hypertens Rep (2015) 17:16 Page 5 of 9 16

potassium (2–4 g/day) intake. These recommendations are
similar to the American Diabetes Association nutrition guide-
lines for persons with diabetes and CKD which state that
dietary protein intake should be consistent with the recom-
mended daily allowance of 0.8 g/kg of ideal body weight
per day for people with diabetes and CKD [83]. Protein intake
may be restricted to 0.6 g/kg of ideal body weight per day
when GFR decreases to <60 ml/min/1.73 m
2
. High-protein
diets should be avoided in persons with established CKD
who are not receiving dialysis [84]. Dietary fiber intake
is encouraged for persons with CKD, but no specific
levels of intake are suggested for person with CKD [84].
High dietary fiber intake may lead to higher phosphate
intake and require escalation of phosphate binder use. Table 1
summarizes some key nutritional recommendations for patients
with CKD stages 1–4.
Nutritional and Education Labeling Act
The day to day dietary choices of individuals strongly influ-
ences the future risk of chronic diseases including chronic
kidney disease [15,17•,85]. Helping people make better food
choices may greatly impact population health. Over the past
several years, there has been strong impetus to improve pop-
ulation nutrition given the rapid pace of the obesity epidemic
in the USA. Other countries, such as Finland and England,
have utilized population-based strategies to improve nutrition-
al choices and decrease sodium intake [86]. Such policies
include reducing the sodium content in processed foods such
as cereals and bread products and canned foods. Such strate-
gies have demonstrated success in reducing the incidence of
cardiovascular disease and lipid levels [87]. Since 1990, US
foods must include a nutrition label that provides information
on the total calories, calories from fat, total fats from saturated
fats and trans fats, and total carbohydrates and dietary fibers,
proteins, and sugars. The nutrition facts label has remained the
same for the last 20 years except for mandating the labeling of
trans fat content in 2006. Recently, there are several proposed
changes to the nutrition labels in order to better inform con-
sumers and to include additional information about food con-
tents. A few of the proposed changes for the nutrition labels
are the declaration of added sugars, updating the daily intake
values for nutrients, declaring the amount of potassium and
vitamin D, and modifying the serving size requirements to
reflect current eating and drinking habits. Figure 2illustrates
how the new labels would appear compared to existing
food labels. Comparing the American diet 20 years ago
to current-day eating habits reveals rapid changes in what
is considered a typical serving size (Fig. 1). To adapt to
these changes, serving size proportions on nutrition labels
need to also be modified. Proposed changes also involve
change of font size to have important nutritional information
more readable [88]. Unfortunately, the nutrition label proposal
does not include the addition of phosphate to the existing
nutrition label. Such information would be extremely useful
for patients with CKD [89].
Conclusion
In summary, Westernization of diet has led to increased intake
of animal protein and decreased intake of fruits, vegetables,
and overall fiber. Multiple other facets of the Western diet may
also affect kidney disease incidence and progression such as
phosphate- and sodium-based preservatives, fat content, and
high-fructose corn syrup. Clinicians should consider the indi-
vidual’s dietary patterns and traditions and culture when guid-
ing a patient toward healthier diets, but a simple message may
be applicable to all individuals regardless of background. That
message could be to eat whole foods, mostly plants and fruits,
and not eat too much [4].
Acknowledgments The authors wish to thank Tom Mattix for creating
Figs. 1and 2.
Compliance with Ethics Guidelines
Conflict of Interest Divya Hariharan, Kavitha Vellanki, and Holly
Kramer declare that they have no conflicts of interest.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
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