American Institute for Cancer Research 11th Annual
Research Conference on Diet, Nutrition and Cancer
The Macrobiotic Diet in Cancer1,2
Lawrence H. Kushi,*†3
Joan E. Cunningham,** James R. Hebert,** Robert H. Lerman,‡
Elisa V. Bandera††
and Jane Teas‡‡
*Program in Nutrition, Department of Health & Behavior Studies, Teachers College, Columbia University, New
York, NY; †
Herbert Irving Comprehensive Cancer Center, Columbia-Presbyterian Medical Center, New York,
NY; **Department of Epidemiology and Biostatistics, Norman J. Arnold School of Public Health, University of
South Carolina, Columbia, SC; ‡
The Institute for Functional Medicine and Functional Medicine Research
Center, Metagenics, Inc., Gig Harbor, WA; ††
Department of Nutritional Sciences, Rutgers University, New
Brunswick, NJ; and ‡‡
Department of Health Promotion, Research and Education, Norman J. Arnold School
of Public Health, University of South Carolina, Columbia, SC
ABSTRACT Macrobiotics is one of the most popular alternative or complementary comprehensive lifestyle
approaches to cancer. The centerpiece of macrobiotics is a predominantly vegetarian, whole-foods diet that has
gained popularity because of remarkable case reports of individuals who attributed recoveries from cancers with
poor prognoses to macrobiotics and the substantial evidence that the many dietary factors recommended by
macrobiotics are associated with decreased cancer risk. Women consuming macrobiotic diets have modestly
lower circulating estrogen levels, suggesting a lower risk of breast cancer. This may be due in part to the high
phytoestrogen content of the macrobiotic diet. As with most aspects of diet in cancer therapy, there has been
limited research evaluating the effectiveness of the macrobiotic diet in alleviating suffering or prolonging survival
of cancer patients. The few studies have compared the experience of cancer patients who tried macrobiotics with
expected survival rates or assembled series of cases that may justify more rigorous research. On the basis of
available evidence and its similarity to dietary recommendations for chronic disease prevention, the macrobiotic
diet probably carries a reduced cancer risk. However, at present, the empirical scientiﬁc basis for or against
recommendations for use of macrobiotics for cancer therapy is limited. Any such recommendations are likely to
reﬂect biases of the recommender. Because of its popularity and the compelling evidence that dietary factors are
important in cancer etiology and survival, further research to clarify whether the macrobiotic diet or similar dietary
patterns are effective in cancer prevention and treatment is warranted. J. Nutr. 131: 3056S–3064S, 2001.
KEY WORDS: ● macrobiotic diet ● neoplasms ● vegetarianism ● life change events ● yin-yang
● epidemiology
Published in 1982, Recalled by Life: The Story of My Recovery
from Cancer (1) recounted the autobiographical story of a
physician, Dr. Anthony Sattilaro, who was diagnosed at age
49 y with prostate cancer with multiple bone metastases.
Given a poor prognosis and feeling that he had nothing to
lose, Dr. Sattilaro adopted a macrobiotic, predominantly vegetarian,
whole-foods diet soon after diagnosis. Follow-up examinations
at 1 and 4 y after diagnosis revealed complete
resolution of metastatic bone lesions. Articles recounting his
story appeared in publications such as the Saturday Evening
Post (August, 1980) and Life magazine (August, 1982). Publication
of Dr. Sattilaro’s story was preceded in 1979 by another
autobiographical book, Healing Miracles from Macrobiotics (2),
which described the recovery of a music professor, Dr. Jean
Kohler, from pancreatic cancer, and was followed in 1983 with
the publication of Michio Kushi’s The Cancer Prevention Diet
[reissued in 1993 (3)], which detailed the macrobiotic approach
to cancer. Based on these and other stories of recovery
from cancer [see, for example (4–7)], macrobiotics has become
known popularly as a comprehensive dietary and lifestyle
approach to cancer.
The general notion that diet may inﬂuence carcinogenesis
is not new nor particularly out of the mainstream of biomed-
1
Presented as part of the 11th Annual Research Conference on Diet, Nutrition
and Cancer held in Washington, DC, July 16–17, 2001. This conference was
sponsored by the American Institute for Cancer Research and was supported by
the California Dried Plum Board, The Campbell Soup Company, General Mills,
Lipton, Mead Johnson Nutritionals, Roche Vitamins Inc. and Vitasoy USA. Guest
editors for this symposium publication were Ritva R. Butrum and Helen A.
Norman, American Institute for Cancer Research, Washington, DC.
2
Supported in part by grants RR09472 and AT00090 from the National
Institutes of Health and cooperative agreement U48/CCU409664 from the Centers
for Disease Control and Prevention. The contents of this paper are solely the
responsibility of the authors and do not necessarily represent the ofﬁcial views of
the National Institutes of Health or the Centers for Disease Control and Preven-
tion.
3
To whom correspondence should be addressed.
E-mail: lhk26@columbia.edu.
0022-3166/01 $3.00 © 2001 American Society for Nutritional Sciences.
3056S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019
ical thought. The roles that various dietary factors may play in
the process of carcinogenesis and the voluminous epidemiologic
literature that demonstrates associations of foods or nutrients
with the prevention of cancer were reviewed by the
American Institute for Cancer Research and the World Cancer
Research Fund in their 1997 report (8). Based on this
extensive review, a series of dietary recommendations for the
prevention of cancer was developed for the report. These
recommendations suggested that a plant-based diet that minimized
consumption of red meat and processed meat and
emphasized consumption of a variety of vegetables, fruits and
whole-grain cereals, would decrease the risk of a variety of
cancers.
The dietary pattern promoted by macrobiotics, although
derived largely from philosophical principles (9), is predominantly
vegetarian, emphasizing natural, minimally processed
foods. Thus, it is broadly compatible with many dietary recommendations,
not just for the prevention of cancer (8,10)
but also for the prevention of other chronic diseases (11,12)
and the promotion of health (13). Although it may thus be
reasonable to suggest that a macrobiotic diet may form the
foundation of a dietary approach for the prevention of these
diseases, it is unknown whether diet may prolong survival,
reduce unpleasant side-effects of chemotherapy or radiation or
prevent recurrence of cancer. The overall lack of empirical
evidence on this topic was noted recently by the American
Cancer Society (14). This paper is focused on the evidence
relating macrobiotic diets to cancer.
What is macrobiotics?
Broadly, macrobiotics is not just a therapeutic approach to
cancer. Rather, the word macrobiotics has been used to describe
a philosophy, a cultural movement and an eating pattern.
The word macrobiotic was used by the 18th century
German physician Christoph Hufeland to describe a program
for good health and prolonging life (15) and was used more
recently by British sinologist Joseph Needham (16) to describe
the philosophy underlying much of the Chinese view of science
and medicine. The speciﬁc context in which macrobiotics
has come to be thought of as an approach to cancer was
popularized initially by Japanese philosopher George Ohsawa
and his students, in particular, Michio Kushi (17).
Most people who would describe themselves as following a
macrobiotic lifestyle probably have not been diagnosed with
cancer or other serious illnesses; hence it is a misperception for
macrobiotics to be perceived strictly as a diet for treatment of
disease. Michio Kushi, the most well-known proponent of
macrobiotics in the world, has authored books describing the
philosophical bases of macrobiotics (9,18) as well as his own
motivations for devoting his life to macrobiotics (18). His
dedication to macrobiotics came out of his experiences as an
eyewitness to the devastation of World War II, his subsequent
studies in political science and a search for solutions for world
peace. He wrote, “I realized that it was essential to recover
genuine food, largely of natural, organic quality, and make it
available to every family at reasonable cost. Only then could
consciousness be transformed and world peace achieved” (18,
p. 30). Kushi described his use of the word macrobiotics:
“I adopted ‘macrobiotics’ in its original meaning, as the
universal way of health and longevity which encompasses the
largest possible view not only of diet but also of all dimensions
of human life, natural order, and cosmic evolution. Macrobiotics
embraces behavior, thought, breathing, exercise, relationships,
customs, cultures, ideas, and consciousness, as well
as individual and collective lifestyles found throughout the
world.
“In this sense, macrobiotics is not simply or mainly a diet.
Macrobiotics is the universal way of life with which humanity
has developed biologically, psychologically, and spiritually and
with which we will maintain our health, freedom, and happiness.
Macrobiotics includes a dietary approach but its purpose
is to ensure the survival of the human race and its further
evolution on this planet. In macrobiotics—the natural intuitive
wisdom of East and West, North and South—I found the
Medicine for Humanity that I had been seeking.”
Despite the broad view of macrobiotics presented by these
excerpts, in recent years, macrobiotics has come to be known
largely as a dietary approach to cancer. This is no doubt due in
part to the case histories noted above (1–7). This is also
evidenced in part by the Ofﬁce of Technology Assessment’s
publication, Unconventional Cancer Treatments, in which macrobiotic
diets are listed along with the Gerson Treatment and
Kelley Regimens as a common dietary approach to the treatment
of cancer (19). The well-regarded book on complementary
cancer therapies by Lerner, Choices in Healing: Integrating
the Best of Conventional and Complementary Approaches to Cancer
(20), devotes one chapter to macrobiotics. Indeed, the
macrobiotic diet is one of the most popular alternative approaches
used by people with cancer (19,21–23).
Aside from diet, other aspects of the application of macrobiotic
principles may also be beneﬁcial for cancer prevention,
including an emphasis on physical activity, avoidance of exposures
to pesticides and other chemicals as well as to electromagnetic
radiation, and stress reduction (3,9). Macrobiotic
philosophy promotes the concept that phenomena are universal
and interrelated, and thus the practice of macrobiotics
engenders a respect for the spiritual nature of life (9). In
addition, a lifestyle intervention such as macrobiotics presupposes
active participation of the individual. Eating macrobiotically
can restore a sense of power and agency as the patient
takes active steps to alter the course of treatment. Conventional
cancer treatments, on the other hand, are inherently
disempowering because the patient is the recipient of therapy
that can be overwhelmingly painful and debilitating and completely
out of the patient’s control. These factors may also be
important in cancer prevention and survival and in improving
the quality of life of people with cancer (24,25).
Macrobiotic dietary guidelines
The standard macrobiotic diet provides a framework that is
modiﬁed depending on one’s age, sex, level of activity, personal
needs and environment. It incorporates a respect for
traditional food and for climatic and seasonal inﬂuences on
food availability and personal and societal activity. It is also
based in large part on the application of Eastern philosophical
principles of yin and yang and related expressions of energetics
such as the theory of ﬁve transformations (9). Thus, the
macrobiotic diet is tailored to meet the needs of an individual
rather than reﬂect a rigid set of structures.
The standard macrobiotic diet can be described from a
macronutrient perspective as one that emphasizes a high complex
carbohydrate, low fat diet. One survey of 50 people
consuming a macrobiotic diet noted that total fat intake
averaged 23% of energy and total carbohydrate intake averaged
65% of energy (26). Saturated fat intake averaged an
extremely low 4.5% of energy, less than polyunsaturated fat
intake, which averaged 7.1% of energy. Dietary cholesterol
intake averaged 76 mg/d, demonstrating that although the
THE MACROBIOTIC DIET IN CANCER 3057S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019
macrobiotic diet is not a strict vegetarian diet, it is very low in
animal intake.
To the extent possible, foods are recommended to be organically
grown and minimally processed. The diet consists of
the following types of foods (3,9): 1) 40–60% by weight whole
cereal grains. This includes brown rice, barley, millet, oats,
wheat, corn, rye, buckwheat and other less common grains and
products made from them such as noodles, pasta and bread. 2)
20–30% vegetables, preferably locally grown, prepared in a
variety of ways. This may include smaller amounts of raw or
pickled vegetables. 3) 5–10% beans of various types, such as
azuki, chickpeas or lentils; bean products such as tofu, tempeh
or natto. 4) Regular consumption of sea vegetables, cooked
with the beans or as separate dishes. 5) Occasional foods to be
consumed a few times per week or less often, including fruits,
white meat ﬁsh, and seeds and nuts.
Foods that are generally avoided on a standard macrobiotic
diet include meat and poultry, animal fats including lard or
butter, eggs, dairy products, reﬁned sugars and foods containing
artiﬁcial sweeteners or other chemical additives. Consumption
of genetically modiﬁed foods is also discouraged. In
the context of cancer, these restrictions may be absolute for a
period of time until some recovery has occurred. The stories of
both Sattilaro (1) and Kohler (2) detail an initial period in
which all animal foods and fruit were to be avoided, followed
subsequently by periods in which these foods were reintroduced
into their diets.
More recently, Michio Kushi, the primary proponent of
macrobiotics, introduced the macrobiotic Great Life Pyramid.
This is presented in Figure 1. As can be seen, it differs from
other alternative food guide pyramids (such as the Mediterranean
food guide pyramid (27) or vegetarian food guide pyramid
(28) in its explicit inclusion of sea vegetables and a
deemphasis, but not exclusion, of fruit (but not vegetable)
intake. Like other alternative food guide pyramids and unlike
the USDA Food Guide Pyramid (29), red meat and dairy food
intakes are minimized.
Potential anticarcinogenic properties of the macrobiotic
diet. Many aspects of the dietary pattern promoted under
standard macrobiotic dietary recommendations have been suggested
to have anticancer effects. For example, whole grains
have been emphasized as a centerpiece of macrobiotic dietary
recommendations for many years. There is growing evidence
that whole grain consumption decreases the risk of cancers at
various sites (30,31). The effects of whole grains on cancer
prevention are probably not limited to dietary ﬁber effects but
may also involve effects on estrogen metabolism, glucose and
insulin metabolism, and oxidative processes (32). A wide
variety of vegetables are also recommended for regular consumption.
The evidence that vegetable intake is associated
with decreased risk of cancer is large and consistent and was
reviewed in the American Institute for Cancer Research and
World Cancer Research Fund report (8). This report noted
that increasing consumption of vegetables and fruits from
ϳ250 to 400 g/d may be associated with a 23% decreased risk
of cancer worldwide. It has been suggested that sea vegetables,
promoted in macrobiotics and an important part of traditional
East Asian cuisine, may decrease risk of breast cancer (33,34)
FIGURE 1 The Great Life Pyramid,
showing macrobiotic dietary
guidelines for a temperate climate.
Note that these are guidelines that may
be adjusted for climate and environment,
cultural or ethnic heritage, gender,
age, activity level, individual health
concerns and personal needs and
other considerations. Food consumed
should be of natural quality, organically
grown as much as possible and traditionally
or naturally processed.
SUPPLEMENT3058S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019
and endometrial cancer (35). These associations may be accounted
for in part by the antitumor activities of fucoidan, a
sulfated polysaccharide found almost exclusively in brown
seaweed (36), and fucoxanthin, the carotenoid responsible for
the brown color of brown seaweed (37,38).
The role of beans and bean products, particularly soyfoods,
in cancer prevention continues to garner substantial interest.
The interest in soy is based in part on the lower overall cancer
rates in the Far East, where soyfoods are a traditional part of
the diet, compared with the U.S. and other Western countries,
where soyfoods are consumed in much smaller quantities.
Some evidence shows that soy intake is associated with decreased
risk of hormone-dependent cancers such as those of
the breast (39–41), endometrium (35) and prostate (42) and
may also decrease risk of other cancers such as those of the
stomach, although this may be limited to nonfermented soyfoods
(43). Soyfoods and other legumes may decrease risk of
cancer because of the presence of various compounds that may
have anticancer effects, including protease inhibitors and saponins
(44). There has been a particular interest in the role of
phytoestrogens such as genistein and daidzein, which are
found in high concentration in soybeans. These isoﬂavonoid
compounds may not only inﬂuence estrogen metabolism but
may also have antioxidant and antiangiogenesis effects and
may inﬂuence signal transduction and inhibit the action of
DNA topoisomerases (45). Phytoestrogen exposure through
the macrobiotic diet is discussed below.
Some foods that are linked to increased cancer risk are
minimized in standard macrobiotic dietary recommendations.
In contrast to the cancer-prevention effects of whole grains,
reﬁned grains, which are not recommended in macrobiotics,
may actually increase risk of cancer (46). With the exception
of ﬁsh, animal food intake is generally minimized in macrobiotics.
There is growing evidence that red meat intake increases
the risk of cancers of the colon and rectum (47) as well as
cancers of the prostate (48), pancreas (49) and perhaps other
sites (8). Eggs may be associated with increased risk of colorectal
(8) and ovarian cancer (50), and dairy food intake is
associated with increased risk of cancers of the prostate
(8,48,51), kidney (8) and ovary (50). A preference for natural,
organically grown foods would minimize exposure to pesticides,
herbicides and other such chemicals. Although the
association of dietary exposure to such chemicals and cancer
risk is controversial, some reports have suggested that exposure
to such compounds should be minimized (52).
Potential detrimental effects of a macrobiotic diet. Because
early macrobiotic books emphasized the use of a 10-d
grain-only “fast” as a cleansing regimen (53), a mistaken
perception arose that the goal of macrobiotics was to achieve
such a 100% grain-only diet. This led to early condemnation
of “Zen” macrobiotic diets by the American Medical Association
(54). Although this view of macrobiotics was clearly
mistaken, a vegetarian diet devoid of animal products can be
consistent with macrobiotic principles. Case reports of infants
with symptoms of malnutrition, including deﬁciencies of vitamin
B-12 and vitamin D, have been reported in the literature
(55–57). With systematic surveys of groups of infants and
families following a macrobiotic lifestyle, the possibility of the
occurrence of such nutritional deﬁciencies has been documented
(58–64). Although the direct relevance to cancer
prevention and therapy of such observations of nutrient deﬁciencies,
observed primarily in infants and growing children, is
questionable, such reports largely form the basis for warnings
against use of macrobiotic diets for cancer treatment (65). The
link that is made in such warnings is based on the problems of
cachexia and weight loss among cancer patients, thus the
supposition that risk of nutritional deﬁciencies should be minimized.
On the other hand, it has been suggested that these
same qualities may be responsible in part for the cancerostatic
and therapeutic potential of macrobiotics diets (66).
Biomedical literature related to macrobiotics and cancer
Macrobiotics and cancer prevention. Few studies have
looked speciﬁcally at the macrobiotic diet in the context of
cancer prevention. Studies by Goldin et al. (67,68) comparing
women eating a macrobiotic diet with women eating a typical
U.S. diet suggest differences in estrogen metabolism (Table 1).
Women eating a macrobiotic diet had substantially higher
fecal excretion and lower urinary excretion of estrogens, with
somewhat lower serum levels of estradiol. Goldin et al. (68)
suggested that these differences indicated a lower risk for
breast cancer for the women eating macrobiotically. Although
these conclusions were somewhat speculative, several prospective
cohort studies published since these observations have
reported a direct association between elevated blood estradiol
levels and subsequent risk of breast cancer (69). Differences in
urinary estrogen excretion along the lines of those observed
with macrobiotics have also been associated with decreased
breast cancer risk (70). If the cross-sectional observations of
Goldin et al. (67,68) are conﬁrmed in intervention studies in
which following a macrobiotic diet results in lower blood
estradiol levels, this would strengthen the inference that macrobiotic
diets may decrease risk of hormone-dependent cancers.
Such a study, funded by the National Institutes of
Health’s National Center for Complementary and Alternative
Medicine, is currently underway at Columbia University.
In subsequent studies by Adlercreutz et al. (71,72), it was
demonstrated that women consuming a macrobiotic diet had
dramatically higher urinary excretion levels of lignans such as
enterolactone or enterodiol and of isoﬂavonoids such as daidzein
and equol than did women consuming a lacto-ovo-vegetarian
diet or an omnivorous diet; women with breast cancer
had the lowest urinary excretion levels of these phytoestrogens.
This is shown in Table 2, which is taken from a paper by
TABLE 1
Fecal, urinary and plasma hormone levels among women
consuming macrobiotic or usual American diets1,2
Hormone
Omnivores
(n ϭ 10)
Macrobiotics
(n ϭ 10)
Fecal excretion, nmol/24 h
Estrone 0.83 (0.70–0.99) 1.96 (1.68–2.29)
Estradiol 0.61 (0.52–0.72) 1.52 (1.30–1.78)†
Estriol 0.72 (0.63–0.83) 1.72 (1.50–1.98)‡
Total estrogens 2.33 (2.01–2.70) 5.40 (4.70–6.21)†
Urinary excretion, nmol/24 h
Estrone 15.3 (13.8–17.0) 16.8 (15.0–18.8)
Estradiol 9.3 (8.6–10.0) 9.3 (8.5–10.2)
Estriol 21.0 (19.1–23.1) 13.2 (11.6–15.0)†
Estriol-3-glucuronide 38.5 (36.0–41.2) 28.0 (24.8–31.6)
Plasma levels, nmol/L
Estrone 0.40 (0.36–0.44) 0.34 (0.32–0.36)
Estradiol 0.32 (0.29–0.36) 0.26 (0.23–0.39)
Testosterone 1.13 (1.05–1.22) 1.15 (1.08–1.22)
Androstenedione 4.38 (4.17–4.60) 4.91 (4.68–5.16)
1 Adapted from Goldin et al. (68).
2 Values are geometric means and standard error ranges.
† Signiﬁcantly different from omnivores, P Ͻ 0.05.
‡ Signiﬁcantly different from omnivores, P Ͻ 0.01.
THE MACROBIOTIC DIET IN CANCER 3059S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019
Adlercreutz et al. (71). For example, omnivores in Boston
were observed to excrete ϳ2050 nmol enterolactone/24 h,
whereas lactovegetarians excreted ϳ4170 nmol/24 h and
women eating macrobiotically excreted 17,680 nmol/24 h
(71). For other urinary phytoestrogens, lactovegetarians excreted
between 1.4 and 3.9 times the amount excreted by
omnivores, whereas women eating macrobiotically excreted
from 11 to 22 times the levels seen in omnivores. Although
the evidence that phytoestrogens are important in breast or
other cancers is still controversial, at least one study reported
an inverse association of urinary excretion of phytoestrogens
with risk of breast cancer (73).
The markedly higher phytoestrogen excretion levels among
women consuming a macrobiotic diet are likely a result of the
foods eaten by these women. Concentrated sources of lignans
in the macrobiotic diet include whole grains, seeds and other
foods. Soyfoods and other legumes that are sources of phytoestrogenic
isoﬂavonoids are also consumed regularly. Indeed,
there was a strong correlation (r ϭ 0.99) between grain intake
and urinary enterolactone excretion on a group basis, comparing
women consuming various diets (71). Overall, the above
combined results suggest that a macrobiotic dietary pattern
may carry a lower risk of breast and other hormone-dependent
cancers such as those of the prostate or endometrium than
other vegetarian diets or typical omnivorous diets.
Note that although studies of direct relevance to the role of
the macrobiotic diet in cancer prevention are few, several
studies investigated the macrobiotic diet in the context of
cardiovascular disease risk. As may be expected from the
dietary patterns and food recommendations of macrobiotics,
these studies demonstrate consistently that people consuming
a macrobiotic diet are at lower risk of cardiovascular disease
than is the general population because of substantially lower
blood cholesterol levels (26,74–78), lower blood pressure
(74,75) and higher plasma levels of antioxidants relative to
cholesterol (79). These studies also indicate that people consuming
a macrobiotic diet have low body weight (75,76),
which is also associated with decreased risk of several cancers
(8).
Macrobiotics and cancer therapy. In addition to the
accounts of individual recovery from cancer by Kohler and
Sattilaro cited earlier, a number of other reports of recovery
from cancer have been published in recent years. These include
complete books, such as accounts of recovery from
malignant melanoma by a nurse (4), from pancreatic cancer by
a physician (5) and from carcinosarcoma of the uterus with
multiple metastases (6), and compilations of case histories (7).
As noted by the Ofﬁce of Technology Assessment, however,
“although these various accounts reﬂect the authors’ beliefs
that they were helped by following a macrobiotic diet, they are
nevertheless inadequate to make an objective assessment of
the efﬁcacy of the diet in treating cancer” (19, p. 64).
At least four attempts have been made to obtain more
systematic information regarding the efﬁcacy of the macrobiotic
approach to cancer. All were hampered by a retrospective
design. The ﬁrst effort was conducted under the direction of
one of the coauthors (R.H.L.), then Director of the Clinical
Nutrition Unit at University Hospital in Boston. He and his
colleagues attempted to follow up individuals who had visited
the Ofﬁce of Michio Kushi for cancer during 1981–1984. An
unfunded proposal for this project was submitted to the American
Institute for Cancer Research in 1984 but was rejected
because the peer reviewers felt that macrobiotics was unworthy
of investigation. After securing a modest amount of independent
funding, in 1986, questionnaires were sent to 548 subjects
who sought counseling from Michio Kushi because of cancer
between 1981 and 1984. Subjects were limited to those with a
U.S. address in Kushi’s ﬁles. Ninety-eight responses were received,
for a response rate of 17.9%. Proﬁles of respondents
indicated that 68% were alive. Ninety-one percent of subjects
received at least one form of standard therapy such as chemotherapy,
and 56% used unconventional therapies other than
macrobiotics, such as vitamin and mineral supplementation
(20%), visualization (20%) and laetrile (7%). Sixty-one percent
reported close adherence to macrobiotic recommendations,
10% partial adherence and 1% none at all.
As noted in Table 3, subjective reports of beneﬁcial effects
of macrobiotics on cancer were reported by substantial proportions
of respondents. Subjective improvements were noted
in tolerance to chemotherapy or radiation, overall health,
emotional well-being and family-social relationships. A substantial
majority of respondents reported that spouses (90%)
and family members (82%) were generally supportive of the
use of macrobiotics, whereas only a minority of respondents
(25%) reported that their physicians were supportive. Indeed,
a similar proportion of respondents (19%) reported that their
physicians were opposed to their use of macrobiotics and 6%
did not inform their physician. The other 50% reported that
their physicians were indifferent to the use of macrobiotics.
Because diagnoses were not conﬁrmed by medical records or
other objective documentation and because of the low overall
TABLE 3
Proportion of respondents reporting subjective effects of
macrobiotics on topics related to living with cancer, among
98 cancer patients who sought macrobiotic counseling, 1986
Topic
Effect of macrobiotics
Beneﬁcial Detrimental No effect
%
Tolerance to chemotherapy
or radiation 59 2 39
Overall health 82 3 10
Emotional well-being 85 6 7
Family-social relationships 43 19 32
Overall effect of macrobiotics 68 4 24
TABLE 2
Urinary excretion of lignans and isoﬂavonic phytoestrogens
in young women on various habitual diets1,2
Omnivores Lactovegetarians Macrobiotics
nmol/24 h
Boston women
Enterolactone 2050 4170 17680
Enterodiol 280 740 6260
Daidzein 320 1260 3460
Equol 69 100 868
O-Desmethylangolensin 33 106 378
Helsinki women
Enterolactone 2460 3650
Enterodiol 203 368
Daidzein 219 275
Equol 102 64
O-Desmethylangolensin 25 43
1 Adlercreutz et al. (71), with permission from Elsevier Science.
2 Values are geometric means.
SUPPLEMENT3060S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019
response rate of 17.9%, it is difﬁcult to make much of the
results of this attempt to obtain more systematic information
about the effects of macrobiotics on cancer patients. Unfortunately,
because of a lack of ﬁnancial and other resources, it was
impossible at the time either to obtain medical records or to
attempt to increase response rates to provide better precision
of survey responses. However, the results of this survey do
suggest that most people with cancer who seek personal advice
about macrobiotics do so in addition to or after conventional
therapy. It also indicated that a substantial proportion of such
patients encountered opposition from their physicians or did
not inform their physician at all regarding their use of macrobiotics
for cancer.
A second attempt was conducted by Gordon Saxe while a
graduate student at Tulane University, and under the direction
of James Carter (19,80). This is the only effort to evaluate
macrobiotics for cancer that has been published in the peerreviewed
literature (80). This study involved two components,
one focused on primary pancreatic cancer, the other focused
on advanced prostate cancer. In both cases, study subjects were
individuals who had sought advice about macrobiotics from a
certiﬁed counselor. Through the use of records kept by macrobiotic
counselors, 109 people were identiﬁed who had seen a
counselor for pancreatic cancer in 1980–1984. Attempts were
made to recontact these individuals, and 36 of them (or their
next-of-kin) could be reached. Of these, 23 reported that they
had followed a macrobiotic diet for at least 3 mo. The median
survival of the 23 individuals who had followed macrobiotics
was 13 mo after diagnosis compared with a median survival for
pancreatic cancer patients from the National Cancer Institute’s
Surveillance, Epidemiology, and End Results (SEER)
program of 3 mo (81).
Unfortunately, this report was ﬂawed in that comparison of
survival times were biased in favor of macrobiotics. Most
importantly, the 23 individuals in the macrobiotic series had
to have survived at least 3 mo in order to be included. As
noted by the SEER data, 50% of all people diagnosed with
pancreatic cancer are dead at 3 mo after diagnosis. Lack of
information on other factors that may inﬂuence survival in
both the macrobiotic series of people with pancreatic cancer
and the people in the SEER program also limits the interpretability
of this study. The prostate cancer component of the
Tulane study was similarly ﬂawed. In this study, the 11 individuals
with prostate cancer had a median survival of 81 mo
compared with a median survival of 45 mo in matched control
subjects. It was unclear on what criteria control subjects were
matched or from where they were selected.
A third attempt at obtaining objective information about
the efﬁcacy of macrobiotics in cancer therapy was a compilation
of cases by Vivien Newbold, a physician in Pennsylvania.
Newbold collected information on six case histories of patients
who used macrobiotics for their cancer; all but one of these
were biopsy-proven (19). The Ofﬁce of Technology Assessment
requested an independent review of these cases by several
mainstream and unconventional physicians who were
consultants to their report on unconventional cancer therapies
(19). Although the cases appeared to be well-described, the
three mainstream physicians who were asked to review the
cases did not ﬁnd that they provided compelling evidence of
beneﬁt from macrobiotics. In most of the cases, the effects of
conventional therapy could not be ruled out adequately; one
case had no veriﬁcation of the continued presence of cancer at
the time macrobiotics was started. The unconventional physicians
found the cases to be more supportive of a role for
macrobiotics but disagreed on the extent of support in these
cases. The Ofﬁce of Technology Assessment did suggest, however,
that “If cases such as Newbold’s were presented in the
medical literature, it might help stimulate interest among
clinical investigators in conducting controlled, prospective
trials of macrobiotic regimens” (19, p. 66).
The fourth attempt to examine macrobiotics in the context
of cancer therapy was initiated in 1994. As a ﬁrst step in
determining whether an alternative therapy is worthy of investigation,
the Division of Cancer Treatment, National Cancer
Institute, established criteria for identifying best cases that
may indicate a promising alternative therapy. This project was
an effort to assemble such a best-case series of individuals with
cancer who had followed a macrobiotic diet. The objective of
this study was to determine whether a basis sufﬁcient to justify
further rigorous studies of the macrobiotic approach to cancer
exists. Preliminary ﬁndings from this study were presented at
the 1996 Annual Meeting of the American Public Health
Association.
Potential best cases were identiﬁed by counselors afﬁliated
with the Kushi Institute (Becket, MA) and other macrobiotic
centers and through press releases in six macrobiotic or alternative
health magazines. From late 1994 through September
1995, 233 such people were identiﬁed. A questionnaire was
sent to these individuals to determine eligibility for consideration
as a best case. A total of 126 (54%) responded; of these,
37 were ineligible because of their use of chemotherapy or
radiation concurrent with macrobiotics, surgical removal of
tumor, nonmacrobiotic diets, inadequate diagnosis or noncancerous
condition or no clinical follow-up after initial medical
therapy. Detailed questionnaires and permission to obtain
medical records were sent to the remaining 89 individuals. A
total of 72 cases of individuals who had tried macrobiotics for
cancer, and for whom at least some medical records were
obtained, were thereby assembled. These 72 cases include
cancers of the prostate (26%), breast (16%), malignant melanoma
(10%), astrocytoma (7%) and other cancers. Although
review of these cases is incomplete, preliminary indications
suggested that several of these cases warrant inclusion in a
best-case series.
This study was supported initially by a grant from the
National Institutes of Health’s Ofﬁce of Alternative Medicine
(a predecessor to the National Center for Complementary and
Alternative Medicine). Hampered by various bureaucratic
hurdles and limited funds, the study was not completed at the
time of initial funding. However, funding from the Centers for
Disease Control and Prevention under the direction of one of
us (J.T.) has allowed this study to proceed.
In summary, none of the four attempts to establish a basis
for documenting a rationale for further investigation of macrobiotics
in the context of cancer therapy has been particularly
successful. Although they have documented a real interest in
the use of macrobiotics and indeed have also identiﬁed individuals
who attribute some beneﬁt to macrobiotics, none provides
a strong basis for determining whether macrobiotics is
effective for cancer.
Summary and future directions
Macrobiotic diets are among the most popular alternative
approaches to management of cancer in use in the United
States today (19,21–23). This interest in macrobiotics is fueled
by the lack of effective conventional therapies for many of the
major cancers and by case reports of dramatic recovery from
cancer in which macrobiotics was used (1–7). The recognition
that dietary factors play a prominent role in cancer prevention
(8) and that standard macrobiotic dietary recommendations
are one expression of public health recommendations to deTHE
MACROBIOTIC DIET IN CANCER 3061S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019
crease cancer risk (8,10) has also increased interest in the
macrobiotic approach to cancer. There is also increasing recognition
that dietary factors may play a role in the progression
of cancer after diagnosis despite the relatively few studies to
examine these relationships (14).
Although no studies have examined directly the effect of
macrobiotics on cancer prevention, studies have indicated
that women following a macrobiotic diet have somewhat lower
plasma estradiol levels (67,68) and higher urinary excretion
levels of phytoestrogen metabolites (71,72) and therefore may
be at lower risk of hormone-dependent cancers. In addition,
various foods or food groups recommended for consumption in
standard macrobiotic dietary recommendations are associated
with decreased risk of cancer, and other foods that are generally
minimized in macrobiotic diets are thought to increase the
risk of cancer. Thus, it is reasonable to suggest that the
macrobiotic diet may carry a substantially reduced risk of
cancer in comparison with standard U.S. dietary patterns.
The primary attempts to investigate macrobiotics in the
context of cancer treatment have been to assemble series of
cases of individuals who may have beneﬁted from their use of
macrobiotics for cancer. Such case series may provide a stronger
justiﬁcation for investigation of the role of the macrobiotic
diet in cancer, but they are only an incremental step above the
individual case histories recounted in popular books (1–7). To
determine whether the macrobiotic diet—or any diet—is effective
in preventing recurrence of cancer, enhancing quality
of life or prolonging survival from cancer, more systematic
studies using recognized study designs such as those of analytic
epidemiology will be required. For example, using the tools of
observational epidemiology, it may be possible to determine
whether people following a macrobiotic lifestyle are at reduced
risk of cancer or whether people with cancer who elect to
follow macrobiotics enhance their quality of life and improve
survival. Epidemiologic studies such as these prospective investigations
are, in general, underutilized in either the study of
alternative or complementary health practices or in the study
of cancer recurrence and survival.
In designing intervention studies of the efﬁcacy for cancer
prevention or treatment of an intervention such as macrobiotics,
it is clear that the fact that macrobiotics is not a single
agent must be taken into account. The macrobiotic diet is
individualized and multidimensional. In addition to the diet,
psychosocial aspects of the adoption of macrobiotics may also
play key roles in its effectiveness, as suggested by other studies
indicating the potential importance of such factors (24,25,82–
87). Although observational studies may attempt to measure
the joint effects of both biological and psychosocial effects of
macrobiotics, retrospective studies may be compromised by
methodological issues such as biases in recall of relevant exposures.
On the other hand, randomized, controlled trials of a
behaviorally oriented and complex intervention such as macrobiotics
may result in an underestimate of the magnitude of
potential beneﬁt. This is because the effects of the intervention
may be modiﬁed by the extent of the subject’s interest and
active participation. Although randomization is idealized as
the optimal method by which efﬁcacy of an intervention is
judged, it has several potential shortcomings, especially in
instances in which interventions are wholly behavioral or
have an important behavioral component (88–91). This
clearly would be the case with macrobiotics. Hybrid designs
that compare randomization with self-selection may allow the
study of the effect of crucially important motivational and
expectancy variables on participation and outcome (89,91–
93). Such designs also offer a model that permits exploration
of the effect of transition from pure efﬁcacy research toward
real-world clinical effectiveness. The explicit study of selfselection
also can be seen as promoting subjects’ roles as active
partners in the choice and management of their health care
(20,94). The study of macrobiotics represents an excellent
opportunity to put these principles of study design into play.
In the absence of such studies, the role of macrobiotics or
other dietary or lifestyle interventions in cancer therapy, remains
in the realm of speculation. Although such speculation
may be informed by direct experience or an understanding of
possible biological mechanisms, comments regarding the effectiveness
of diet in cancer therapy are likely to expose the
biases of the commentator as much as provide insight into the
possible role that diet may play in this area. Studies for
secondary prevention of breast cancer such as the ongoing
Women’s Intervention Nutrition Study (95) examining a low
fat diet and the Women’s Healthy Eating and Living Study
(96) examining a vegetarian diet, are necessary to determine
whether dietary factors, including the macrobiotic diet, may be
helpful in the context of cancer therapy.
In summary, the role of the macrobiotic diet in cancer
prevention and survival has not been investigated adequately
to justify scientiﬁcally the recommendation that macrobiotics
be used in the context of cancer. However, the lack of studies
that examine directly the effects of macrobiotics on cancer
prevention, survival or quality of life cannot be taken as
evidence against a beneﬁcial effect of macrobiotics. In particular,
there is extensive indirect evidence that macrobiotic
dietary patterns are associated with reduced cancer risk as well
as the potentially reassuring results of the few studies that
evaluated directly the effects of the macrobiotic diet on estrogen
metabolism and cardiovascular risk. Finally, the popularity
of macrobiotics among cancer patients underscores the importance
of evaluating the value of macrobiotics for cancer prevention
and survival.
ACKNOWLEDGMENT
This paper is dedicated to Ms. Aveline Tomoko Kushi (February
27, 1923–July 3, 2001).
LITERATURE CITED
1. Sattilaro, A. J. & Monte, T. (1982) Recalled by Life: The Story of My
Recovery from Cancer. Houghton Mifﬂin, Boston, MA.
2. Kohler, J. C. & Kohler, M. A. (1979) Healing Miracles from Macrobiotics:
A Diet for All Diseases. Parker Publishing, West Nyack, NY.
3. Kushi, M. & Jack, A. (1993) The Cancer Prevention Diet: Michio
Kushi’s Macrobiotic Blueprint for the Prevention and Relief of Disease. St. Martin’s
Press, New York, NY.
4. Brown, V. & Stayman, S. (1984) Macrobiotic Miracle: How a Vermont
Family Overcame Cancer. Japan Publications, New York, NY.
5. Faulkner, H. (1993) Physician, Heal Thyself. One Peaceful World
Press, Becket, MA.
6. Nussbaum, E. (1992) Recovery from Cancer. Avery Publishing Group,
Garden City Park, NY.
7. The East West Foundation with Fawcett, A. & Smith, C. (1991) CancerFree:
30 Who Triumphed Over Cancer Naturally. Japan Publications, New York,
NY.
8. World Cancer Research Fund & American Institute for Cancer Research.
(1997) Food, Nutrition and the Prevention of Cancer: A Global Perspective.
American Institute for Cancer Research, Washington, DC.
9. Kushi, M. & Jack, A. (1986) The Book of Macrobiotics: The Universal
Way of Health, Happiness, and Peace. Japan Publications, New York, NY.
10. The American Cancer Society 1996 Advisory Committee on Diet, Nutrition,
and Cancer Prevention (1996) Guidelines on diet, nutrition, and cancer
prevention: reducing the risk of cancer with healthy food choices and physical
activity. CA - Cancer J. Clin. 46: 325–341.
11. Krauss, R. M., Eckel, R. H., Howard, B., Appel, L. J., Daniels, S. R.,
Deckelbaum, R. J., Erdman, J. W. Jr, Kris-Etherton, P., Goldberg, I. J., Kotchen,
T. A., Lichtenstein, A. H., Mitch, W. E., Mullis, R., Robinson, K., Wylie-Rosett, J.,
St. Jeor, S., Suttie, J., Tribble, D. L. & Bazzarre, T. L. (2000) AHA Dietary
Guidelines: revision 2000: a statement for healthcare professionals from the
Nutrition Committee of the American Heart Association. Circulation 102: 2284–
2299.
SUPPLEMENT3062S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019
12. Committee on Diet and Health, National Research Council (1989) Diet
and Health: Implications for Reducing Chronic Disease Risk. National Academy
Press, Washington, DC.
13. U.S. Department of Agriculture & U.S. Department of Health and Human
Services (2000) Nutrition and Your Health: Dietary Guidelines for Americans,
5th ed., Home and Garden Bulletin no. 232. U.S. Government Printing Ofﬁce,
Washington, DC.
14. Brown, J., Byers, T., Thompson, K., Eldridge, B., Doyle, C. & Williams,
A. M. (2001) Nutrition during and after cancer treatment: a guide for informed
choices by cancer survivors. CA - Cancer J. Clin. 51: 153–187.
15. Wynder, E. L. (1974) A corner of history: Hufeland. Prev. Med. 3:
421–427.
16. Needham, J. (1981) Science in Traditional China. Harvard University
Press, Cambridge, MA.
17. Kotzsch, R.E. (1985) Macrobiotics Yesterday and Today. Japan Publications,
New York, NY.
18. Kushi, M. & Jack, A. (1987) One Peaceful World: Michio Kushi’s
Approach to Creating a Healthy and Harmonious Mind, Home, and World Community.
St. Martin’s Press, New York, NY.
19. U.S. Congress, Ofﬁce of Technology Assessment (1990) Unconventional
Cancer Treatments, OTA-H-405. U.S. Government Printing Ofﬁce, Washington,
DC.
20. Lerner, M. (1994) Choices in Healing: Integrating the Best of Conventional
and Complementary Approaches to Cancer. MIT Press, Cambridge, MA.
21. Cassileth, B. R., Lusk, E. J., Strouse, T. B. & Bodenheimer, B. J. (1984)
Contemporary unorthodox treatments in cancer medicine: a study of patients,
treatments, and practitioners. Ann. Intern. Med. 101: 105–112.
22. Schapira, D. V. & Wenzel, L. (1983) Florida CIS inquiries about unproven
methods of cancer treatment and immunotherapy. Oncology Times, June,
p. 12.
23. Clinical Oncology Group (1987) New Zealand cancer patients and
alternative medicine. N.Z. Med. J. 100: 110–113.
24. Fawzy, F. I., Fawzy, N. W., Hyun, C. S., Elashoff, R., Fahey, J. L. & Morton,
D. L. (1993) Malignant melanoma: effects of an early structured psychiatric
intervention, coping, and affective state on recurrence and survival 6 years later.
Arch. Gen. Psychiatry 50: 681–689.
25. Classen, C., Sephton, S. E., Diamond, S. & Spiegel, D. (1998) Studies
of life-extending psychosocial interventions. In: Psycho-Oncology (Holland, J. C.,
ed.), pp.730–742. Oxford University Press, New York, NY.
26. Kushi, L. H., Samonds, K. W., Lacey, J. M., Brown, P. T., Bergan, J. G. &
Sacks, F. M. (1988) The association of dietary fat with serum cholesterol in
vegetarians: the effect of dietary assessment on the correlation coefﬁcient. Am. J.
Epidemiol. 128: 1054–1064.
27. Willett, W. C., Sacks, F., Trichopoulou, A., Drescher, G., Ferro-Luzzi, A.,
Helsing, E. & Trichopoulos, D. (1995) Mediterranean diet pyramid: a cultural
model for healthy eating. Am. J. Clin. Nutr. 61: 1402S–1406S.
28. Haddad, E. H., Sabate, J. & Whitten, C. G. (1999) Vegetarian food
guide pyramid: a conceptual framework. Am. J. Clin. Nutr. 70: 615S–619S.
29. U.S. Department of Agriculture, Human Nutrition Information Service
(1992) The Food Guide Pyramid: Home and Garden Bulletin no. 252. Human
Nutrition Information Service, Hyattsville, MD.
30. Jacobs, D.R., Jr., Marquart, L., Slavin, J. & Kushi, L.H. (1998) Wholegrain
intake and cancer: an expanded review and meta-analysis. Nutr. Cancer 30:
85–96.
31. Jacobs, D. R., Jr., Meyer, K. A., Kushi, L. H. & Folsom, A. R. (1999) Is
whole grain intake associated with reduced total and cause-speciﬁc death rates
in older women? The Iowa Women’s Health Study. Am. J. Public Health 89:
322–329.
32. Slavin, J. L. (2000) Mechanisms for the impact of whole grain foods on
cancer risk. J. Am. Coll. Nutr. 19: 300S–307S.
33. Teas, J., Harbison, M. L. & Gelman, R. S. (1984) Dietary seaweed
[laminaria] and mammary carcinogenesis in rats. Cancer Res. 44: 2758–2761.
34. Yamamoto, I., Maruyama, H. & Moriguchi, M. (1987) The effect of
dietary seaweeds on 7,12-dimethylbenz[a]anthracene-induced mammary tumorigenesis
in rats. Cancer Lett. 35: 109–118.
35. Goodman, M. T., Wilkens, L. R., Hankin, J. H., Lyu, L.-C., Wu, A. H. &
Kolonel, L. N. (1997) Association of soy and ﬁber consumption with the risk of
endometrial cancer. Am. J. Epidemiol. 146: 294–306.
36. Itoh, H., Noda, H., Amano, H., Zhuaug, C., Mizuno, T. & Ito, H. (1993)
Antitumor activity and immunological properties of marine algal polysaccharides,
especially fucoidan, prepared from Sargassum thunbergii of Phaeophyceae. Anticancer
Res. 13: 2045–2052.
37. Nishino, H. (1998) Cancer prevention by carotenoids. Mutat. Res. 402:
159–163.
38. Okuzumi, J., Nishino, H., Murakoshi, M., Iwashima, A., Tanaka, Y., Yamane,
T., Fujita, Y. & Takahashi T. (1990) Inhibitory effects of fucoxanthin, a
natural carotenoid, on N-myc expression and cell cycle progression in human
malignant tumor cells. Cancer Lett. 55: 75–81.
39. Shu, X. O., Jin, F., Dai, Q., Wen, W., Potter, J. D., Kushi, L. H., Ruan, Z.,
Gao, Y. T. & Zheng, W. (2001) Soyfood intake during adolescence and subsequent
risk of breast cancer among Chinese women. Cancer Epidemiol. Biomark.
Prev. 10: 483–488.
40. Wu, A. H., Ziegler, R. G., Horn-Ross, P. L., Nomura, A. M., West, D. W.,
Kolonel, L. N., Rosenthal, J. F., Hoover, R. N. & Pike, M. C. (1996) Tofu and risk
of breast cancer in Asian-Americans. Cancer Epidemiol. Biomark. Prev. 5: 901–
906.
41. Wu, A. H., Ziegler, R. G., Nomura, A. M., West, D. W., Kolonel, L. N.,
Horn-Ross, P. L., Hoover, R. N. & Pike, M. C. (1998) Soy intake and risk of
breast cancer in Asians and Asian Americans. Am. J. Clin. Nutr. 68: 1437S–
1443S.
42. Kolonel, L. N., Hankin, J. H., Whittemore, A. S., Wu, A. H., Gallagher,
R. P., Wilkens, L. R., John, E. M., Howe, G. R., Dreon, D. M., West, D. W. &
Paffenbarger, R. S., Jr. (2000) Vegetables, fruits, legumes and prostate cancer:
a multiethnic case-control study. Cancer Epidemiol. Biomark. Prev. 9: 795–
804.
43. Wu, A. H., Yang, D. & Pike, M. C. (2000) A meta-analysis of soyfoods
and risk of stomach cancer: the problem of potential confounders. Cancer Epidemiol.
Biomark. Prev. 9: 1051–1058.
44. Steinmetz, K. A. & Potter, J. D. (1991) Vegetables, fruit, and cancer. II.
Mechanisms. Cancer Causes Control 2: 427–442.
45. Messina, M. J., Persky, V., Setchell, K. D. & Barnes, S. (1994) Soy
intake and cancer risk: a review of the in vitro and in vivo data. Nutr. Cancer 21:
113–131.
46. Kushi, L. H., Meyer, K. A. & Jacobs, D. R. Jr. (1999) Cereals, legumes,
and chronic disease risk reduction: evidence from epidemiologic studies. Am. J.
Clin. Nutr. 70: 451S–458S.
47. Sandhu, M. S., White, I. R. & McPherson, K. (2001) Systematic review
of the prospective cohort studies on meat consumption and colorectal cancer
risk: a meta-analytical approach. Cancer Epidemiol. Biomark. Prev. 10: 439–446.
48. Kolonel, L. N. (1996) Nutrition and prostate cancer. Cancer Causes
Control 7: 83–94.
49. Howe, G. R. & Burch, J. D. (1996) Nutrition and pancreatic cancer.
Cancer Causes Control 7: 69–82.
50. Kushi, L. H., Mink, P. J., Folsom, A. R., Anderson, K. E., Zheng, W.,
Lazovich, D. & Sellers, T. A. (1999) Prospective study of diet and ovarian
cancer. Am. J. Epidemiol. 149: 21–31.
51. Chan, J. M., Giovannucci, E., Andersson, S. O., Yuen, J., Adami, H. O. &
Wolk, A. (1998) Dairy products, calcium, phosphorous, vitamin D, and risk of
prostate cancer (Sweden). Cancer Causes Control 9: 559–566.
52. Committee on Pesticides in the Diets of Infants and Children, National
Research Council (1993) Pesticides in the Diets of Infants and Children.
National Academy Press, Washington, DC.
53. Ohsawa, G. (1995) Zen Macrobiotics: The Art of Rejuvenation and
Longevity. George Ohsawa Macrobiotic Foundation, Oroville, CA.
54. Council on Foods and Nutrition, American Medical Association (1971)
Zen macrobiotic diets. J. Am. Med. Assoc. 218: 397.
55. Robson, J.R.K. (1974) Zen macrobiotic problems in infancy. Pediatrics
53: 326–329.
56. Roberts, I. F., West, R. J., Ogilvie, D. & Dillon, M. J. (1979) Malnutrition
in infants receiving cult diets: a form of child abuse. Br. Med. J. 1: 296–298.
57. Salmon, P., Rees, J.R.P., Flanagan, M. & O’Moore, R. (1981) Hypocalcaemia
in a mother and rickets in an infant associated with a Zen macrobiotic diet.
Ir. J. Med. Sci. 150: 192–193.
58. Dwyer, J. T., Dietz, W. H., Hass, G. & Suskind, R. (1979) Risk of
nutritional rickets among vegetarian children. Am. J. Dis. Child. 133: 134–140.
59. Dwyer, J. T., Andrew, E. M., Berkey, C., Valadian, I. & Reed, R. B. (1983)
Growth in “new” vegetarian preschool children using the Jens-Bayley curve ﬁtting
technique. Am. J. Clin. Nutr. 37: 815–827.
60. Specker, B. L., Miller, D., Norman, E. J., Greene, H. & Hayes, K. C.
(1988) Increased urinary methylmalonic acid excretion in breast-fed infants of
vegetarian mothers and identiﬁcation of an acceptable dietary source of vitamin
B-12. Am. J. Clin. Nutr. 47: 89–92.
61. van Staveren, W. A. & Dagnelie, P. C. (1988) Food consumption,
growth, and development of Dutch children fed on alternative diets. Am. J. Clin.
Nutr. 48: 819–821.
62. Dagnelie, P. C., van Staveren, W. A., Vergote, F.J.V.R.A., Dingjan, P. G.,
van den Berg, H. & Hautvast, J.G.A.J. (1989) Increased risk of vitamin B-12
and iron deﬁciency in infants on macrobiotic diets. Am. J. Clin. Nutr. 50: 818–824.
63. Dagnelie, P. C., Vergote, F.J.V.R.A., van Staveren, W. A., van den Berg,
H., Dingjan, P. G. & Hautvast, J.G.A.J. (1990) High prevalence of rickets in
infants on macrobiotic diets. Am. J. Clin. Nutr. 51: 202–208.
64. Miller, D. R., Specker, B. L., Ho, M. L. & Norman, E. J. (1991) Vitamin
B-12 status in a macrobiotic community. Am. J. Clin. Nutr. 53: 524–529.
65. Bowman, B. B., Kushner, R. F., Dawson, S. C. & Levin, B. (1984)
Macrobiotic diets for cancer treatment and prevention. J. Clin. Oncol. 2: 702–711.
66. Weisburger, J. H. (1993) A new nutritional approach in cancer therapy
in light of mechanistic understanding of cancer causation and development.
J. Am. Coll. Nutr. 12: 205–208.
67. Goldin, B. R., Adlercreutz, H., Dwyer, J. T., Swenson, L., Warram, J. H. &
Gorbach, S. L. (1981) Effect of diet on excretion of estrogens in pre- and
postmenopausal incidence of breast cancer in vegetarian women. Cancer Res.
41: 3771–3773.
68. Goldin, B. R., Adlercreutz, H., Gorbach, S. L., Warram, J. H., Dwyer, J. T.,
Swenson, L. & Woods, M. N. (1982) Estrogen excretion patterns and plasma
levels in vegetarian and omnivorous women. N. Engl. J. Med. 307: 1542–1547.
69. Thomas, H. V., Reeves, G. K. & Key, T. J. (1997) Endogenous estrogen
and postmenopausal breast cancer: a quantitative review. Cancer Causes Control
8: 922–928.
70. Key, T. J., Wang, D. Y., Brown, J. B., Hermon, C., Allen, D. S., Moore,
J. W., Bulbrook, R. D., Fentiman, I. S. & Pike, M. C. (1996) A prospective study
of urinary oestrogen excretion and breast cancer risk. Br. J. Cancer. 73: 1615–
1619.
THE MACROBIOTIC DIET IN CANCER 3063S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019
71. Adlercreutz, H., Fotsis, T., Bannwart, C., Wa¨ ha¨ la¨ , K., Ma¨ kela¨ , T., Brunow,
G. & Hase, T. (1986) Determination of urinary lignans and phytoestrogen
metabolites, potential antiestrogens and anticarcinogens, in urine of women on
various habitual diets. J. Steroid Biochem. 25: 791–797.
72. Adlercreutz, H., Ho¨ ckerstedt, K., Bannwart, C., Bloigu, S., Ha¨ ma¨ la¨ inen,
E., Fotsis, T. & Ollus, A. (1987) Effect of dietary components, including lignans
and phytoestrogens, on enterohepatic circulation and liver metabolism of estrogens
and on sex hormone binding globulin (SHBG). J. Steroid Biochem. 27:
1135–1144.
73. Ingram, D., Sanders, K., Kolybaba, M. & Lopez, D. (1997) Case-control
study of phyto-oestrogens and breast cancer. Lancet. 350: 990–994.
74. Sacks, F. M., Rosner, B. & Kass, E. H. (1974) Blood pressure in
vegetarians. Am. J. Epidemiol. 100: 390–398.
75. Sacks, F. M., Castelli, W. P., Donner, A. & Kass, E. H. (1975) Plasma
lipids and lipoproteins in vegetarians and controls. N. Engl. J. Med. 292: 1148–
1151.
76. Bergan, J. G. & Brown, P. T. (1980) Nutritional status of “new” vegetarians.
J. Am. Diet. Assoc. 76: 151–155.
77. Knuiman, J. T. & West, C. E. (1982) The concentration of cholesterol
in serum and in various serum lipoproteins in macrobiotic, vegetarian and nonvegetarian
men and boys. Atherosclerosis 43: 71–82.
78. Sacks, F. M., Ornish, D., Rosner, B., McLanahan, S., Castelli, W. P. &
Kass, E. H. (1985) Plasma lipoprotein levels in vegetarians. The effect of
ingestion of fats from dairy products. J. Am. Med. Assoc. 254: 1337–1341.
79. Pronczuk, A., Kipervarg, Y. & Hayes, K. C. (1992) Vegetarians have
higher plasma alpha-tocopherol relative to cholesterol than do nonvegetarians.
J. Am. Coll. Nutr. 11: 50–55.
80. Carter, J. P., Saxe, G. P., Newbold, V., Peres, C. E., Campeau, R. J. &
Bernal-Green, L. (1993) Hypothesis: dietary management may improve survival
from nutritionally linked cancers based on analysis of representative cases.
J. Am. Coll. Nutr. 12: 209–226.
81. U.S. Department of Health and Human Services, U.S. Public Health
Service (1984) SEER Program:Cancer Incidence and Mortality in the United
States,1973–81: DHEW Publ. no. (NIH)85–1837. National Cancer Institute, Bethesda,
MD.
82. Spiegel, D., Bloom, J. R. & Yalom, I. (1981) Group support for patients
with metastatic cancer. Arch. Gen. Psychiatry. 38: 527–533.
83. Gruber, B. L., Hersh, S. P., Hall, N. R. S., Waletzky, L. R., Kunz, J. F.,
Carpenter, J. K., Kverno, K. S. & Weiss, S. M. (1993) Immunological responses
of breast cancer patients to behavioral interventions. Biofeedback Self Regul. 18:
1–22.
84. Spiegel, D. & Sands, S. H. (1989) Psychological inﬂuences on metastatic
disease progression. In: Metastasis/Dissemination (Gorelik, E., ed.), pp.
282–288. Kluwer Academic Publishers, Dordrecht, Netherlands.
85. Greer, S., Moorey, S., Baruch, J.D.R., Watson, M., Robertson, B. M.,
Mason, A., Rowden, L., Law, M. G. & Bliss, J. M. (1992) Adjuvant psychological
therapy for patients with cancer: a prospective randomized trial. Br. Med. J.
304: 675–680.
86. Greer, S., Morris, T., Pettingale, K. W. & Haybittle, J. L. (1990) Psychological
response to breast cancer and 15-year outcome. Lancet. 1: 49–50.
87. Fawzy, F. I. & Fawzy, N. W. (1998) Psychoeducational interventions.
In: Psycho-Oncology (Holland, J. C., ed.), pp. 676–693. Oxford University Press,
New York, NY.
88. Hebert, J. R., Hurley, T. G. & Ma, Y. (1998) The effect of dietary
exposures on recurrence and mortality in early stage breast cancer. Breast
Cancer Res. Treat. 51: 17–28.
89. Brewin, C. R. & Bradley, C. (1989) Patient preferences and randomized
clinical trials. Br. Med. J. 299: 313–315.
90. Hebert, J. R. (1997) An epidemiologist’s view of Block’s challenge: the
role of the self in cancer survival. Advances. 13: 39–43.
91. Marcus, S. M. (1997) Assessing non-consent bias with parallel randomized
and nonrandomized clinical trials. J. Clin. Epidemiol. 50: 823–828.
92. Schwartz, C. E., Chesney, M. A., Irvine, M. J. & Keefe, F. J. (1997) The
control group dilemma in clinical research: applications for psychosocial and
behavioral medicine trials. Psychosom. Med. 59: 362–371.
93. Rucker, G. (1989) A two-stage trial design for testing treatment, selfselection
and treatment preference effects. Stat. Med. 8: 477–485.
94. Eisenberg, D. M. (1997) Advising patients who seek alternative medical
therapies. Ann. Intern. Med. 127: 61–69.
95. Chlebowski, R. T., Nixon, D. W., Blackburn, G. L., Jochimson, P., Scanlon,
E. F., Insull, W. Jr, Buzzard, I. M., Elashoff, R., Butrum, R. & Wynder, E. R.
(1987) A breast cancer nutrition adjuvant study (NAS): protocol design and initial
patient adherence. Breast Cancer Res. Treat. 10: 21–29.
96. Pierce, J. P., Faerber, S., Wright, F. A., Newman, V., Flatt, S. W., Kealey,
S., Rock, C. L., Hryniuk, W. & Greenberg, E. R. (1997) Feasibility of a randomized
trial of a high-vegetable diet to prevent breast cancer recurrence. Nutr.
Cancer 28: 282–288.
SUPPLEMENT3064S
Downloadedfromhttps://academic.oup.com/jn/article-abstract/131/11/3056S/4686721byLekarskaFakulta-MasarykovaUniverzitauseron01April2019