and interregional correlational studies, dairy product consumption
has been consistently associated with prostate cancer mortality.[3-7]
The largest and most recent of these, based on World Health Organization
mortality figures for 1985-1989 from 59 countries and United Nations
food balance data for 1979-1981, reported a strong correlation between
per capita milk consumption and prostate cancer mortality (r = 0.78,
P<0.0001). A more geographically restricted study, conducted
in 20 Italian regions, found a similar correlation between prostate
cancer mortality and milk consumption (r = 0.75, P <0.01).
correlational studies typically rely on food "disappearance"
data, which may not accurately reflect intake, and are limited in
their ability to control for potential confounders. They are also
subject to variability in reporting practices, although this is
less likely to influence mortality data than incidence figures.
Some of the weaknesses of international correlational studies are
avoided in case-control and cohort studies. Case-control studies
compare the recalled diets of individuals with cancer to those of
individuals without cancer who are similar in other relevant respects.
Because cases and locally recruited controls are likely to have
similar dietary patterns, the sensitivity of such studies is often
limited. Cohort studies gather dietary information from healthy
volunteers who are then followed over time.
studies in geographically diverse areas have reported significantly
increased risk of prostate cancer (relative risk ranging from 1.5
to 2.5) for those in the highest categories of dairy product consumption,
compared to lower consumption levels (Table 1).[8-13] Four additional
studies reported nonsignificant positive associations, and two found
no association between dairy product consumption and prostate cancer
in northern Italy compared prostate cancer patients to hospital
controls, finding increased risk of prostate cancer among those
with the most frequent milk consumption.[8-10] Similarly, a study
at Roswell Park Memorial Institute in Buffalo, NY, found an increased
risk of prostate cancer with the daily consumption of three or more
glasses of whole milk, compared to never drinking milk. In Montevideo,
Uruguay, a comparison of prostate cancer patients to hospital controls,
most of whom had other forms of cancer, found an increased risk
of prostate cancer associated with drinking two or more milk servings
per day, compared to having less than one serving per day. In
Örebro county, Sweden, men with prostate cancer were compared to
controls selected from a population register. Higher dairy product
consumption was associated with increased relative risk of prostate
cancer. A preliminary study from a portion of this patient sample
found no associations between prostate cancer and any food recalled
as having been consumed during adolescence. A U.S. study compared
men newly diagnosed with prostate cancer and healthy population-based
controls in Georgia, New Jersey, and Michigan. Dairy product consumption
was associated with prostate cancer risk among whites, but not blacks.
have the methodologic strengths of statistical adjustment for age
and other factors and reasonably large sample sizes (Table 1). Of
those studies finding positive but nonsignificant associations between
dairy use and prostate cancer, several used smaller sample sizes
or failed to adjust for age or other variables (Table 1). In Los
Angeles and Chicago, prostate cancer patients were matched to hospital
controls, finding nonsignificant increases in dairy product consumption
among cancer patients. A Minnesota study comparing prostate
cancer patients with hospital and neighborhood controls reported
nonsignificant increases in dairy product consumption among cancer
patients. Similarly, a small study in Japan comparing prostate
cancer patients to healthy controls from a prostate cancer-screening
program found a nonsignificant increased risk associated with daily
milk consumption. In Athens, Greece, prostate cancer patients
were compared to hospital controls. Milk and dairy product consumption
was marginally positively associated with prostate cancer risk.
A Swedish case-control
study including men with prostate cancer and unrelated controls
drawn from a twin registry found no relationship between cancer
risk and any dietary factor. An English study compared prostate
cancer patients to controls with benign prostatic hyperplasia (BPH)
and hospital controls with non-urological disease; data for both
groups of controls were combined. The study reported no association
between dairy product consumption and prostate cancer risk. The
use of BPH patients as controls in this study may have reduced its
sensitivity, as BPH may have antecedents similar to those of prostate
Five of eleven
cohort studies have found significant associations between milk
or dairy product consumption and prostate cancer incidence or mortality.[21-25]
Six studies found no association between milk or dairy product use
generally and prostate cancer incidence or mortality.[26-31]
A 20-year study
of prostate cancer mortality among California Seventh-day Adventists
reported a dose-related increased risk of age-adjusted prostate
cancer mortality with milk consumption (for >3 glasses
daily, RR = 2.4, 95% CI, 1.3-4.3; for 1-2 glasses daily, RR = 1.8,
95% CI, 1.0-3.0, compared to <1 glass per day.) In a multivariate
analysis adjusting for age, education, body weight, and consumption
of meat, milk, cheese, and eggs, the relative risk of fatal prostate
cancer associated with drinking >3 glasses of milk per
day was reduced to 1.5 and was no longer statistically significant
(p<0.10). However, adjustment for cheese consumption may
be inappropriate if the relevant dietary factor is dairy product
consumption generally. Similarly, adjustment for body weight may
be inappropriate if increased body weight is one of the mechanisms
by which dairy product consumption influences prostate cancer risk.
A separate study of California Adventists studied cancer incidence,
rather than mortality, finding no relationship with milk consumption.
relationship was also suggested by a cohort study including various
ethnicities in Hawaii. Relative risks of prostate cancer, adjusted
for age, ethnicity, and income, for men in the middle and highest
tertiles of milk consumption were 1.3 (CI, 1.01.9) and 1.4
(CI, 1.0-2.1), respectively, compared to the lowest tertile. Although
these 95% confidence intervals included 1.0, a statistically significant
trend was reported (Ptrend = 0.04).
In the Health
Professionals Follow-Up Study, a cohort of U.S. male dentists, optometrists,
osteopaths, pharmacists, and veterinarians, relative risk of advanced
prostate cancer associated with daily consumption of more than two
glasses of milk, compared to zero, was 1.6 (95% CI, 1.2-2.1,
Ptrend = 0.002). For metastatic disease, relative risk was 1.8 (95%
CI, 1.2-2.8, Ptrend = 0.01). Of the milk consumed, 83% was skim
Cohort Study reported a trend of increased prostate cancer risk
with increasing milk consumption after adjustment for age, family
history of prostate cancer, and socioeconomic status, although the
difference in risk, compared to the lowest (index) quintile of milk
consumption, was significant only for the 4th quintile (RR= 1.63,
95% CI, 1.20-2.20, Ptrend = 0.02).
In the Physicians'
Health Study cohort, consumption of two and one-half dairy servings
daily was associated with increased risk of prostate cancer,
compared to having less than one-half serving daily, after adjustment
for age, smoking, exercise level, and body mass index (BMI).
Among the studies
finding no association between dairy product use and prostate cancer,
one, conducted in Norway, found a significantly increased age-adjusted
risk of prostate cancer with consumption of skim milk, compared
to whole milk (incidence rate ratio 2.2, 95% CI, 1.3-3.7), although
milk consumption in general was not associated with risk. The authors
speculate that the relatively young age of their sample (mean age
43 years, range 16-56 years, at the outset of a 9- to15-year follow-up
period) may have reduced study sensitivity.
a protective effect of green and yellow vegetables, but no detectable
effect of milk consumption. Although the cohort was large (112,261
men), it identified only 63 cancer deaths during the follow-up period,
and did not limit the inclusion of the oldest participants. Milk
consumption was probably uncommon in this group, but the number
of men consuming milk with various frequencies was not reported.
In a cohort of men of Japanese ancestry living in Hawaii, there
was no association between milk consumption and age-adjusted prostate
cancer risk. Milk consumption was uncommon; only 34% of cases consumed
milk five times per week or more. In a Rancho Bernardo,
California, cohort (aged 50-84 at the study's outset), no relationship
was found between whole milk consumption and prostate cancer incidence
during 14-year follow-up, after adjustment for age, history of heart
disease or diabetes, BMI, systolic blood pressure, smoking, and
plasma cholesterol concentration. Milk consumption averaged 0.5
cups per day. In a cohort of white male policyholders of the
Lutheran Brotherhood Insurance Society, most of whom lived in Minnesota
and the northeastern U.S., no associations were identified between
prostate cancer mortality and any dietary factor. The authors cautioned
that the lack of an association between dietary factors and cancer
risk may be partially due to the limited number of items in the
food-frequency questionnaire and the homogeneous nature of the cohort,
heavily weighted toward individuals of Scandinavian descent.
six of twelve case-control studies and five of eleven cohort studies
found significant associations between milk or dairy product consumption
and prostate cancer incidence and mortality. Particularly among
cohort studies, those reporting significant associations were generally
larger and more recent.
may influence the incidence or progression of prostate cancer by
several possible mechanisms. One for which evidence is particularly
compelling is the
effect of high-calcium
foods on vitamin D metabolism. In several prospective studies, calcium
intake has emerged as an independent predictor of prostate cancer
risk.[12,23,25] Vitamin D is derived either by conversion from 7-dehydrocholesterol
in a reaction catalyzed by ultraviolet light, or from dietary sources.
For conversion to the biologically active hormone, a hydroxyl group
is added in the liver to form 25(OH) vitamin D, and a second hydroxyl
group is added in the kidney, producing 1,25(OH)2 vitamin D.
Vitamin D receptors
are present on prostate epithelium. Among other functions, 1,25(OH)2
vitamin D reduces cell proliferation and enhances cell differentiation.
An oral calcium load suppresses parathyroid hormone secretion which,
in turn, reduces renal 1,25(OH)2 vitamin D production. Calcium itself
also downregulates this reaction. Although some dairy products are
supplemented with vitamin D, this inactive prehormone does not appreciably
increase 1,25(OH)2 vitamin D blood levels, and the net effect of
dairy consumption is a reduction in blood levels of this active
form of the hormone. Milk's high content phosphorus and animal protein
may aggravate this effect.
consumption has also been shown to increase serum concentrations
of insulin-like growth factor (IGF-I).[33,34] In in-vitro studies,
IGF-I has mitogenic and antiapoptotic properties on prostate epithelial
cells.[35,36] Case-control studies in diverse populations have shown
a strong and consistent association between serum IGF-I concentrations
and prostate cancer risk. In men and women aged 55 to 85 years,
the addition of 3 daily eight-ounce servings of nonfat or 1% milk
for 12 weeks was associated with a 10% increase in serum IGF-I concentration
(P<0.001). Mean serum IGF-I concentration among vegans was
shown to be 8 percent lower than among ovolactovegetarians (P=0.01)
and 9 percent lower than among meat-eaters (P=0.01). Changing
dietary protein sources from animal sources to plant sources has
been shown to reduce serum IGF-I concentrations.
Most dairy products
contain substantial amounts of fat and are devoid of fiber, a combination
that is likely to increase serum testosterone concentration and
activity, with a mitogenic effect on prostate tissue. However,
several studies have found an association of dairy product intake
with prostate cancer incidence and mortality that is independent
of total fat intake and other dietary variables.[25,40,41]
other than dairy products are also associated with risk. Generally
speaking, diets high in animal products are associated with higher
risk, while those rich in plant foods, particularly tomatoes, are
associated with reduced risk. Daily soymilk consumption was associated
with a significant reduction in prostate cancer risk in a cohort
of 13,855 Seventh-Day Adventist men (RR = 0.3, 95% CI, 0.1-1.0,
compared to those never drinking soymilk). Isoflavones in soymilk
inhibit growth of human prostate cancer cells and also inhibit 5a-reductase,
an enzyme that converts testosterone to 5a-dihydrotestosterone in
the prostate. A similar beneficial effect was demonstrated for
tofu consumption. Based on experience with a case-control study
in Athens, Greece, researchers calculated that the combined effect
of reducing dairy consumption, substituting olive oil for other
added fats, and increasing tomato intake to the levels consumed
by those in the lowest risk categories could reduce prostate cancer
risk in their population by 41 percent (95% CI, 23-59%).
international, case-control, and cohort studies suggests that men
who avoid dairy products are at lower risk for prostate cancer incidence
and mortality, compared to others. In case-control and cohort studies,
the relative risk of prostate cancer among subgroups with the most
frequent milk consumption, compared to those at the lowest consumption
levels, falls in the range of 1.3 to 2.5. These findings raise two
important questions: Does the observed relationship represent cause
and effect, and is available evidence sufficient to justify a recommendation
that milk-drinking men alter their dietary habits?
a cause-and-effect relationship include the relative consistency
of this association in diverse populations, evidence of a dose-response
relationship, plausible biological mechanisms that underlie the
observed associations, and no reasonable alternative explanation
for these findings. Perspective is lent to the second question by
a comparison with evidence linking alcohol use and breast cancer
risk. Although somewhat fewer studies have addressed the association
between milk and prostate cancer, their demonstrated effect strength
and consistency of evidence approach those relating alcohol to breast
cancer risk, an association that is now widely accepted and incorporated
into the Dietary Guidelines for Americans. A pooled analysis
of cohort studies showed that the adjusted relative risk of incident
breast cancer for women consuming 2-5 drinks (30-60 grams of alcohol)
per day was 1.41 (95% CI, 1.18-1.69). In a 1997 review by the
World Cancer Research Fund and the American Institute for Cancer
Research, six of eleven cohort studies and fifteen of thirty-six
case-control studies found such an association.
Men who choose
to avoid dairy products reap other nutritional benefits, such as
a reduction in total fat, saturated fat, and cholesterol intake.
Unless they replace dairy products with calcium-fortified products
or calcium supplements, they are likely to reduce their calcium
intake in the process. However, a reduction in calcium intake may
be an important mechanism by which reducing or avoiding dairy products
reduces prostate cancer risk. Moreover, there is no apparent risk
to moderate reductions in calcium intake. There is little evidence
to suggest that a high intake of calcium from dairy or other sources
reduces the risk of osteoporotic fractures among men. Few studies
have examined the effect of dietary calcium on osteoporosis risk
in adult men independently of vitamin D intake. There has been
some indication that a higher intake of calcium, including that
from dairy sources, in the context of an omnivorous American diet,
is associated with reduced recurrence of colonic adenomatous polyps.
However, in Africa, in the context of a low-calcium, low-dairy diet,
both adenomatous polyps and colon cancer are much rarer than in
Western countries. Some studies suggest that calcium, including
that in dairy products, may reduce blood pressure, but the effect,
if any, is small (on the order of <2 mm Hg systolic and <1
mm Hg diastolic), far smaller than the effect of adding vegetables
and fruits to the diet.[50-51]
several lines of evidence indicate that consumption of dairy products
is associated with increased risk of prostate cancer incidence and
mortality. Avoidance of these products may offer a means of reducing
risk of this common illness.
1. World Cancer Research Fund/American
Institute for Cancer Research. Food, Nutrition, and the Prevention
of Cancer: A Global Perspective. American Institute for Cancer Research,
Washington, D.C., 1997, p. 311.
2. Chan JM, Stampfer MJ, Giovannucci EL. What causes prostate
cancer? A brief summary of the epidemiology. Sem Canc Biol 1998a;8:263-73.
3. Howell MA. Factor analysis of international cancer mortality
data and per capita food consumption. Br J Cancer 1974;29:328-36.
4. Armstrong B, Doll R. Environmental factors and cancer
incidence and mortality in different countries, with special reference
to dietary practices. Int J Cancer 1975;15: 617-31.
5. Rose DP, Boyar AP, Wynder EL. International comparisons
of mortality rates for cancer of the breast, ovary, prostate, and
colon, and per capita food consumption. Cancer 1986;58:2363-71.
6. Decarli A, La Vecchia C. Environmental factors and cancer
mortality in Italy: correlational exercise. Oncology 1986;43:116-26.
7. Hebert JR, Hurley TG, Olendzki BC, Teas J, Ma Y, Hampl
JS. Nutritional and socioeconomic factors in relation to prostate
cancer mortality: a cross national study. J Natl Cancer Inst 1998;90(21):1637-47.
8. Talamini R, La Vecchia C, Decarli A, Negri E, Franceschi
S. Nutrition, social factors and prostatic cancer in a Northern
Italian population. Br J Cancer 1986;53:817-21.
9. Mettlin C, Selenskas S, Natarajan N, Huben R. Beta-carotene
and animal fats and their relationship to prostate cancer risk.
10. Talamini R, Franceschi S, La Vecchia C, Serraino D, Barra
S, Negri E. Diet and prostate cancer: a case-control study in Northern
Italy. Nutr Cancer 1992;118:277-86.
11. De Stefani E, Fierro L, Barrios E, Ronco A. Tobacco,
alcohol, diet and risk of prostate cancer. Tumori 1995;81:315-20.
12. Chan JM, Giovannucci EL, Andersson SO, Yuen J, Adami
HO, Wolk A. Dairy products, calcium, phosphorous, vitamin D, and
risk of prostate cancer (Sweden). Cancer Causes and Control 1998b;9:559-66.
13. Hayes RB, Ziegler RG, Gridley G, Swanson C, Greenberg
RS, Swanson GM, Schoenberg JB, Silverman DT, Brown LM, Pottern LM,
Liff J, Schwartz AG, Fraumeni JF Jr, Hoover RN. Dietary factors
and risks for prostate cancer among blacks and whites in the United
States. Cancer Epidemiol Biomar Prev 1999;8:25-34.
14. Rotkin ID. Studies in the epidemiology of prostatic cancer:
expanded sampling. Cancer Treatment Reports 1977;61:173-80.
15. Schuman LM, Mandel JS, Radke A, Seal U, Halberg F. Some
selected features of the epidemiology of prostatic cancer: Minneapolis-St.
Paul, Minnesota case-control study, 1976-1979. In Magnus K, Ed.
Trends in Cancer Incidence: Causes and Practical Implications, Hemisphere
Publishing, Washington, D.C.; 1982:345-54.
16. Mishina T, Watanabe H, Araki H, Nakao M. Epidemiological
study of prostatic cancer by matched-pair analysis. Prostate 1985;6:423-36.
17. Tzonou A, Signorello LB, Lagiou P, Wuu J, Trichopoulos
D, Trichopoulou A. Diet and cancer of the prostate: a case-control
study in Greece. Int J Cancer 1999;80:704-8.
18. Grönberg H, Damber L, Damber JE. Total food consumption
and body mass index in relation to prostate cancer risk: a case-control
study in Sweden with prospectively collected exposure data. J Urology
19. Ewings P, Bowie C. A case-control study of cancer of
the prostate in Somerset and east Devon. Br J Cancer 1996;74:661-6.
20. Andersson SO, Baron J, Wolk A, Lindgren C, Bergstrom
R, Adami HO. Early life risk factors for prostate cancer: a population-based
case-control study in Sweden. Cancer Epidemiol Biomar Prev 1995;4:187-92.
21. Snowdon DA, Phillips RL, Choi W. Diet, obesity,
and risk of fatal prostate cancer. Am J Epidemiology 1984;120:244-50.
22. LeMarchand L, Kolonel LN, Wilkens LR, Myers BC, Hirohata
T. Animal fat consumption and prostate cancer: a prospective
study in Hawaii. Epidemiology 1994;5:276-82.
23. Giovannucci E, Rimm EB, Wolk A, Ascherio A, Stampfer
MJ, Colditz GA, Willett WC. Calcium and fructose intake in relation
to risk of prostate cancer. Cancer Res 1998a;58:442-7.
24. Schuurman AG, van den Brandt PA, Dorant E, Goldbohm RA.
Animal products, calcium and protein and prostate cancer risk in
the Netherlands Cohort Study. Br J Cancer 1999;80:1107-1113.
25. Chan JM, Stampfer MJ, Ma J, Ajani U, Gaziano JM, Giovannucci
E. Dairy products, calcium, and prostate cancer risk in the Physicians'
Health Study. Presentation, American Association for Cancer Research,
San Francisco, April 2000.
26. Hirayama T. Epidemiology of prostate cancer with special
reference to the role of diet. Natl Cancer Inst Monogr 1979;53:149-55.
27. Mills PK, Beeson WL, Phillips RL, Fraser GE. Cohort study
of diet, lifestyle, and prostate cancer in Adventist men. Cancer
28. Severson RK, Nomura AMY, Grove JS, Stemmermann GN. A
prospective study of demographics, diet, and prostate cancer among
men of Japanese ancestry in Hawaii. Cancer Res 1989;49:1857-60.
29. Thompson MM, Garland C, Barrett-Connor E, Khaw KT, Friedlander
NJ, Wingard DL. Heart disease risk factors, diabetes, and prostatic
cancer in an adult community. Am J Epidemiol 1989;129:511-7.
30. Hsing AW, McLaughlin JK, Schuman LM, Bjelke E, Gridley
G, Wacholder S, Co Chien HT, Blot WJ. Diet, tobacco use, and fatal
prostate cancer: results from the Lutheran brotherhood cohort study.
Cancer Res 1990;50:6836-40.
31. Veierřd MB, Laake P, Thelle DS. Dietary fat intake and
risk of prostate cancer: a prospective study of 25,708 Norwegian
men. Int J Cancer 1997;73:634-8.
32. Giovannucci E. Dietary influences of 1,25(OH)2
vitamin D in relation to prostate cancer: a hypothesis. Cancer Causes
and Control 1998b;9:567-82.
33. Cadogan J, Eastell R, Jones N, Barker ME. Milk intake
and bone mineral acquisition in adolescent girls: randomised, controlled
intervention trial. BMJ 1997;315:1255-60.
34. Heaney RP, McCarron DA, Dawson-Hughes B, Oparil S, Berga
SL, Stern JS, Barr SI, Rosen CJ. Dietary changes favorably affect
bone remodeling in older adults. J Am Dietetic Asso 1999;99:1228-33.
35. Iwamura M, Sluss PM, Casamento JB, Cockett ATK. Insulin-like
growth factor I: action and receptor characterization in human prostate
cancer cell lines. Prostate 1993;22:243-52.
36. Culig Z, Hobisch A, Cronauer MV, Radmayr C, Trapman J,
Hittmair A, Bartsch G, Klocker H. Androgen receptor activation in
prostatic tumor cell lines by insulin-like growth factor-I, keratinocyte
growth factor, and epidermal growth factor. Eur Urol 1995;27(suppl
37. Cohen P. Serum insulin-like growth factor-I levels and
prostate cancer riskinterpreting the evidence. J Natl Cancer
38. Allen NE, Appleby PN, Davey GK, Key TJ. Hormones and
diet: low insulin-like growth factor-I but normal bioavailable androgens
in vegan men. Br J Cancer 2000;83:95-7.
39. Kontessis PA, Bossinakou I, Sarika L, Iliopoulou E, Papantoniou
A, Trevisan R, Roussi D, Stipsanelli K, Grigorakis S, Souvatzoglou
A. Renal, metabolic, and hormonal responses to proteins of different
origin in normotensive, nonproteinuric type I diabetic patients.
Diabetes Care 1995;18:1233-40.
40. Ross RK, Henderson BE. Do diet and androgens alter prostate
cancer risk via a common etiologic pathway? J Natl Cancer Inst 1994:86:252-4.
41. Giovannucci E, Rimm EB, Colditz GA, Stampfer MJ, Ascherio
A, Chute CC, Willett WC. A prospective study of dietary fat
and risk of prostate cancer. J Natl Cancer Inst 1993;85:1571-9.
42. Jacobsen BK, Knutsen SF, Fraser GE. Does high soy milk
intake reduce prostate cancer incidence? The Adventist Health Study
(United States). Cancer Causes and Control 1998;9:553-7.
43. Bosetti C, Tzonou A, Lagiou P, Negri E, Trichopoulos
D, Hsieh C-C. Fraction of prostate cancer incidence attributed to
diet in Athens, Greece. Eur J Cancer Prev 2000;9:119-23.
44. U.S. Department of Agriculture and Department of Health
and Human Services. Nutrition and Your Health: Dietary Guidelines
for Americans, 5th Edition. Home and Garden Bulletin
No. 232. U.S. Department of Agriculture, Washington, D.C., 2000,
45. Smith-Warner SA, Spiegelman D, Yuan SS, van den Brandt
PA, Folsom AR, Goldbohm A, Graham S, Holmberg L, Howe GR, Marshall
JR, Miller AB, Potter JD, Speizer FE, Willett WC, Wolk A, Hunter
DJ. Alcohol and breast cancer among women: a pooled analysis of
cohort studies. JAMA 1998;279:535-40.
46. World Cancer Research Fund/American Institute for Cancer
Research. Food, Nutrition, and the Prevention of Cancer: A Global
Perspective. American Institute for Cancer Research, Washington,
D.C., 1997, pp. 270-74.
47. Welten DC, Kemper HCG, Post GB, Van Staveren WA. A meta-analysis
of the effect of calcium intake on bone mass in young and middle-aged
females and males. J Nutr 1995;125:2802-13.
48. Holt PR, Attilsoy EO, Gilman J, Guss J, Moss SF, Newmark
H, Fan K, Yang K, Lipkin M. Modulation of abnormal colonic epithelial
cell proliferation and differentiation by low-fat dairy foods: a
randomized controlled trial. JAMA 1998;280:1074-9.
49. Walker ARP, Segal I. Low-fat dairy foods and colonic
epithelial cell proliferation (letter). JAMA 1999;281:1274.
50. Griffith LE, Guyatt GH, Cook RJ, Bucher HC, Cook DJ.
The influence of dietary and nondietary calcium supplementation
on blood pressure: an updated metaanalysis of randomized controlled
trials. Am J Hypertension 1999;12:84-92.
51. Sacks FM, Appel LJ, Moore TJ, Obarzanek E, Vollmer WM,
Svetkey LP, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH,
Karanja N. A dietary approach to prevent hypertension: a review
of the Dietary Approaches to Stop Hypertension (DASH) study. Clin
Cardiol 1999;22(suppl III):III-6-III-10.
Table 1. Case-Control Studies of Dairy Product Intake and Prostate Cancer
Author, Year, Location
|No. of Cases
||Findings Related to Dairy Intake RR (95% CI), where
|Rotkin, 1977, USA
||Cases consumed more dairy (ns)
|Schuman et al., 1982, USA
||Cases consumed more dairy (ns)
|Mishima et al., 1985, Japan
||Cases consumed more dairy (ns)
|Talamini et al., 1986, Italy
||milk/dairy>5/wk vs less
|Mettlin et al., 1989, USA
||milk 3 servings/d vs none
|Talamini et al., 1992, Italy
||milk>10/wk vs <2/wk
|De Stefani et al., 1995, Uruguay
||milk>2 servings/d vs <1/d
|Hayes et al., 1996, USA
|milk: h vs 1 quartile
milk: h vs 1 quartile
|Grönberg et al., 1996, Sweden
||milk: >5 servings/d vs 0 servings/d
|Ewings et al., 1996, UK
||>7 pints/wk (ns) vs <3 pints/wk
|Chan et al., 1998b, Sweden
||dairy>4.5 servings/d vs <2.5 servings/d
|Tzonou et al., 1999, Greece
Table 2. Cohort Studies of Dairy Product Intake and Prostate Cancer
Author, Year, Location
|Size of Cohort Cases/
|Findings Related to Dairy Intake RR (95% CI), where
|Hirayama, 1979, Japan
|milk daily vs rarely or never (ns)
|Snowdon et al., 1984, USA
|milk>3 servings/d vs <1/d
(multivariate: 1.5, P<0.10)
|Mills et al., 1989, USA
|milk>daily vs never
|Thompson et al., 1989, USA
|Severson et al., 1989, USA
|milk>5 servings/wk vs <1 serving/wk
|Hsing et al., 1990, USA
|dairy>86 servings/mo vs <26 servings/mo
|LeMarchand et al., 1994, USA (Hawaii)
|milk, high vs low tertile
|Veierřd et al., 1997, Norway
|milk, not quantified (na)
|Giovannucci et al., 1998a, USA
|milk>2 servings/d vs none
|Schuurman et al., 1999, Netherlands
|milk, high vs low quintile
1.12 (0.81-1.56) Ptrend=0.02
|Chan et al, 2000, USA
|dairy>2.5 servings/d vs <0.5 serving/d