V javnosti se veliko govori o dejavnikih, ki negativno vplivajo na človekovo zdravje. Na nekatere, kot je na primer genetska nagnjenost k nekaterim boleznim, nimamo vpliva. Na druge pa lahko bistveno vplivamo s svojimi odločitvami. Odrečemo se lahko, na primer, škodljivemu kajenju. Osveščenost glede posledic kajenja je danes na Zahodu dokaj visoka. Težko bi namreč našli človeka, ki bi trdil, da kajenje ni škodljivo ali da je celo koristno.
Med zdravju škodljivimi dejavniki, na katere lahko vsakdo pomembno vpliva, je tudi prehrana. Tu pa je osveščenost ljudi veliko manjša. Zadnje čase narašča število znanstvenih raziskav, ki skušajo opredeliti rizična živila v naši prehrani. In v veliki večini raziskav se kot najbolj rizično živilo znova in znova pojavlja meso. Zato sta World Cancer Research Fund in American Institute for Cancer Research, ki v svetovnem merilu sodita med največje in najuglednejše ustanove na področju raziskovanja raka, v svojih priporočilih navedla, da obstaja "prepričljiva povezava med rdečim mesom, mesnimi izdelki in rakom debelega črevesa in danke". Njuni strokovnjaki pravijo, da je povezava med mesom in rakom po zaslugi novejših raziskav veliko močnejša kot je bila pred kakšnim desetletjem. Navajajo tudi, da raziskave kažejo na povezavo med prehranjevanjem z mesom in rakom prostate, pljuč, požiralnika, želodca in trebušne slinavke.
Omenjeni ustanovi sta objavili tudi zanimiv podatek, da je v ZDA osveščenost ljudi o povezavi med mesom in rakom le 35-odstotna. (V Sloveniji je ta odstotek verjetno še manjši, saj marsikdo domneva, da je meso vir zdravja).





Raziskave v ZDA - Harvardska medicinska fakulteta


Na harvardski medicinski fakulteti so prav tako izvedli raziskavo, s katero so želeli ugotoviti povezavo med hrano in rakom prostate. Spremljali so prek 50.000 moških, starih od 40 do 75 let v obdobju štirih let. Ugotovili so, da od maščob na raka prostate vpliva le maščoba živalskega izvora (tveganje se poveča za 63%), medtem ko maščoba rastlinskega izvora na povečanje ne vpliva. Živilo, ki se je izkazalo za največji faktor tveganja, je bilo rdeče meso (tveganje se poveča za 163%).



A prospective study of dietary fat and risk of prostate cancer, Giovannucci E, Rimm EB, Colditz GA, Stampfer MJ, Ascherio A, Chute CC, Willett WC, J Natl Cancer Inst. 1993 Oct 6;85(19):1538-40








A prospective study of dietary fat and risk of prostate cancer

Giovannucci E, Rimm EB, Colditz GA, Stampfer MJ, Ascherio A, Chute CC, Willett WC.

Channing Laboratory, Department of Medicine, Harvard Medical School, Boston, Mass.

Comment in: J Natl Cancer Inst. 1993 Oct 6;85(19):1538-40.

e-mail: edward.giovannucci@harvard.edu




BACKGROUND:

The strong correlation between national consumption of fat and national rate of mortality from prostate cancer has raised the hypothesis that dietary fat increases the risk of this malignancy. Case-control and cohort studies have not consistently supported this hypothesis. PURPOSE: We examined prospectively the relationship between prostate cancer and dietary fat, including specific fatty acids and dietary sources of fat. We examined the relationship of fat consumption to the incidence of advanced prostate cancer (stages C, D, or fatal cases) and to the total incidence of prostate cancer. METHODS: We used data from the Health Professionals Follow-up Study, which is a prospective cohort of 51529 U.S. men, aged 40 through 75, who completed a validated food-frequency questionnaire in 1986. We sent follow-up questionnaires to the entire cohort in 1988 and 1990 to document new cases of a variety of diseases and to update exposure information. As of January 31, 1990, 300 new cases of prostate cancer, including 126 advanced cases, were documented in 47855 participants initially free of diagnosed cancer. The Mantel-Haenszel summary estimator was used to adjust for age and other potentially confounding variables. Multiple logistic regression was used to estimate relative risks (RRs) when controlling simultaneously for more than two covariates. RESULTS: Total fat consumption was directly related to risk of advanced prostate cancer (age- and energy-adjusted RR = 1.79, with 95% confidence interval [CI] = 1.04-3.07, for high versus low quintile of intake; P [trend] = .06). This association was due primarily to animal fat (RR = 1.63; 95% CI = 0.95-2.78; P [trend] = .08), but not vegetable fat. Red meat represented the food group with the strongest positive association with advanced cancer (RR = 2.64; 95% CI = 1.21-5.77; P = .02). Fat from dairy products (with the exception of butter) or fish was unrelated to risk. Saturated fat, monounsaturated fat, and alpha-linolenic acid, but not linoleic acid, were associated with advanced prostate cancer risk; only the association with alpha-linolenic acid persisted when saturated fat, monounsaturated fat, linoleic acid, and alpha-linolenic acid were modeled simultaneously (multivariate RR = 3.43; 95% CI = 1.67-7.04; P [trend] = .002). CONCLUSION: The results support the hypothesis that animal fat, especially fat from red meat, is associated with an elevated risk of advanced prostate cancer. IMPLICATIONS: These findings support recommendations to lower intake of meat to reduce the risk of prostate cancer. The potential roles of carcinogens formed in cooking animal fat and of alpha-linolenic acid in the progression of prostate cancer need to be explored.

V javnosti se veliko govori o dejavnikih, ki negativno vplivajo na človekovo zdravje. Na nekatere, kot je na primer genetska nagnjenost k nekaterim boleznim, nimamo vpliva. Na druge pa lahko bistveno vplivamo s svojimi odločitvami. Odrečemo se lahko, na primer, škodljivemu kajenju. Osveščenost glede posledic kajenja je danes na Zahodu dokaj visoka. Težko bi namreč našli človeka, ki bi trdil, da kajenje ni škodljivo ali da je celo koristno.
Med zdravju škodljivimi dejavniki, na katere lahko vsakdo pomembno vpliva, je tudi prehrana. Tu pa je osveščenost ljudi veliko manjša. Zadnje čase narašča število znanstvenih raziskav, ki skušajo opredeliti rizična živila v naši prehrani. In v veliki večini raziskav se kot najbolj rizično živilo znova in znova pojavlja meso. Zato sta World Cancer Research Fund in American Institute for Cancer Research, ki v svetovnem merilu sodita med največje in najuglednejše ustanove na področju raziskovanja raka, v svojih priporočilih navedla, da obstaja "prepričljiva povezava med rdečim mesom, mesnimi izdelki in rakom debelega črevesa in danke". Njuni strokovnjaki pravijo, da je povezava med mesom in rakom po zaslugi novejših raziskav veliko močnejša kot je bila pred kakšnim desetletjem. Navajajo tudi, da raziskave kažejo na povezavo med prehranjevanjem z mesom in rakom prostate, pljuč, požiralnika, želodca in trebušne slinavke.
Omenjeni ustanovi sta objavili tudi zanimiv podatek, da je v ZDA osveščenost ljudi o povezavi med mesom in rakom le 35-odstotna. (V Sloveniji je ta odstotek verjetno še manjši, saj marsikdo domneva, da je meso vir zdravja).



Raziskave v ZDA - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland

Zanimiva je raziskava iz ZDA, kjer so prav tako ugotavljali pojavnost raka prostate, najpogostejše oblike raka med moškimi. Želeli so odkriti vzrok večje pogostnosti te bolezni med Američani črnskega rodu. Ugotovili so močno povezavo med maščobami živalskega izvora in večjo pojavnostjo raka prostate. Tveganje za belce, ki uživajo več maščob živalskega izvora, se je povečalo za 120-160%, povečanje tveganja za črnce pa se giblje med 120% in 320%.



Dietary factors and risks for prostate cancer among blacks and whites in the United States Cancer, Hayes RB, Ziegler RG, Gridley G. Et. Al. Epidemiol Biomarkers Prev. 1999 Jan;8(1):25-34.




Dietary factors and risks for prostate cancer among blacks and whites in the United States.

Cancer Epidemiol Biomarkers Prev. 1999 Jan;8(1):25-34.

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.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20892, USA. hayesr@epndce.nci.nih.gov



Prostate cancer is the most common malignancy in men in the United States, with substantially higher rates among American blacks than whites. We carried out a population-based case-control study in three geographic areas of the United States to evaluate the reasons for the racial disparity in incidence rates. A total of 932 men (449 black men and 483 white men) who had been newly diagnosed with pathologically confirmed prostate cancer and 1201 controls (543 black men and 658 white men) were interviewed in person to elicit information on potential risk factors. This report evaluates the impact of dietary factors, particularly the consumption of animal products and animal fat, on the risk of prostate cancer among blacks and whites in the United States. Increased consumption (grams/day) of foods high in animal fat was linked to prostate cancer (independent of intake of other calories) among American blacks [by quartile of intake, odds ratio (OR) = 1.0 (referent), 1.5, 2.1, and 2.0; Ptrend = 0.007], but not among American whites [by quartile of intake, OR = 1.0 (referent), 1.6, 1.5, and 1.1; Ptrend = 0.90]. However, risks for advanced prostate cancer were higher with greater intake of foods high in animal fat among blacks [by quartile of intake, OR = 1.0 (referent), 2.2, 4.2, and 3.1; Ptrend = 0.006] and whites [by quartile of intake, OR = 1.0 (referent), 2.2, 2.6, and 2.4; Ptrend = 0.02]. Increased intake of animal fat as a proportion of total caloric intake also showed positive but weaker associations with advanced prostate cancer among blacks (Ptrend = 0.13) and whites (Ptrend = 0.08). No clear associations were found with vitamin A, calcium, or specific lycopene-rich foods. The study linked greater consumption of fat from animal sources to increased risk for prostate cancer among American blacks and to advanced prostate cancer among American blacks and whites. A reduction of fat from animal sources in the diet could lead to decreased incidence and mortality rates for prostate cancer, particularly among American blacks.

PMID: 9950236 [PubMed - indexed for MEDLINE]



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V javnosti se veliko govori o dejavnikih, ki negativno vplivajo na človekovo zdravje. Na nekatere, kot je na primer genetska nagnjenost k nekaterim boleznim, nimamo vpliva. Na druge pa lahko bistveno vplivamo s svojimi odločitvami. Odrečemo se lahko, na primer, škodljivemu kajenju. Osveščenost glede posledic kajenja je danes na Zahodu dokaj visoka. Težko bi namreč našli človeka, ki bi trdil, da kajenje ni škodljivo ali da je celo koristno.
Med zdravju škodljivimi dejavniki, na katere lahko vsakdo pomembno vpliva, je tudi prehrana. Tu pa je osveščenost ljudi veliko manjša. Zadnje čase narašča število znanstvenih raziskav, ki skušajo opredeliti rizična živila v naši prehrani. In v veliki večini raziskav se kot najbolj rizično živilo znova in znova pojavlja meso. Zato sta World Cancer Research Fund in American Institute for Cancer Research, ki v svetovnem merilu sodita med največje in najuglednejše ustanove na področju raziskovanja raka, v svojih priporočilih navedla, da obstaja "prepričljiva povezava med rdečim mesom, mesnimi izdelki in rakom debelega črevesa in danke". Njuni strokovnjaki pravijo, da je povezava med mesom in rakom po zaslugi novejših raziskav veliko močnejša kot je bila pred kakšnim desetletjem. Navajajo tudi, da raziskave kažejo na povezavo med prehranjevanjem z mesom in rakom prostate, pljuč, požiralnika, želodca in trebušne slinavke.
Omenjeni ustanovi sta objavili tudi zanimiv podatek, da je v ZDA osveščenost ljudi o povezavi med mesom in rakom le 35-odstotna. (V Sloveniji je ta odstotek verjetno še manjši, saj marsikdo domneva, da je meso vir zdravja).




Urugvajske raziskave


V Montevideu so izvedli raziskavo, ki je skušala ugotoviti povezavo med posameznimi skupinami živil in pojavnostjo raka prostate. Pri analizi se je kot največji faktor tveganja pokazalo meso (povečanje tveganja za 100%) ter skupna količina zaužitih kalorij (povečanje tveganja za 90%). Kot rizična sta se pokazala še skupna količina zaužitih maščob ter uživanje slaščic. Nasprotno pa uživanje sadja in zelenjave zmanjša možnost nastanka raka prostate za 50%.



Foods, nutrients and prostate cancer: a case-control study in Uruguay, H Deneo-Pellegrini, E De Stefani, A Ronco and M Mendilaharsu, British Journal of Cancer (1999) 80, 591-597






Meat intake, heterocyclic amines, and risk of breast cancer: a case-control study in Uruguay.

De Stefani E, Ronco A, Mendilaharsu M, Guidobono M - Registro Nacional de Cáncer, Montevideo, Uruguay
Deneo-Pellegrini H. - Department of Pathology, Instituto Nacional de Oncología, Montevideo, Uruguay

Registro Nacional de Cancer, Department 402, Montevideo, Uruguay.



A case–control study of diet and prostate cancer was conducted in Montevideo, Uruguay involving 175 cases and 233 controls. When the highest quartile of intake was compared with the lowest, positive findings were obtained for red meat intake (OR 2.0, 95% CI 1.1–3.8), desserts (OR 1.8, 95% CI 0.9–3.3), total energy (OR 1.9, 95% CI 1.0–3.4) and total fat intake (OR 1.8, 95% CI 0.9–3.4). On the other hand, vegetables and fruits (OR 0.5, 95% CI 0.3–0.9), vitamin C (OR 0.4, 95% 0.2–0.8) and vitamin E (OR 0.6, 95% CI 0.3–1.1) were associated with reduced risks of prostate cancer. Possible mechanisms are discussed.



To examine whether meat intake modifies breast-cancer risk, a case-control study was conducted in Uruguay. Dietary patterns were assessed in detail (for cases, before diagnosis or symptoms occurred) using a food frequency questionnaire involving 64 food items, which allowed total energy intake to be calculated. Nutrient residuals were calculated through regression analysis. After adjustment for potential confounders (which included family history of breast cancer, menopausal status, body-mass index, total energy and total alcohol intake), an increased risk associated with consumption of total meat intake, red meat intake, total fat and saturated fat intake was observed. The strongest effect was observed for red meat intake (OR 4.2, 95% CL 2.3-7.7) for consumption in the upper quartile, after controlling for protein and fat intake. This suggests an independent effect for meat. Since experimental studies have shown a strong effect of heterocyclic amines in rat mammary carcinogenesis, further studies should be performed in human epidemiology, perhaps using biomarkers of heterocyclic amine exposure.



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Whittemore, A. S., Kolonel, L. N., Wu, A. H., John, E. M., Gallagher, R. P., Howe, G. R., Burch, J. D., Hankin, J., Dreon, D. M., West, D. W., Teh, C-Z & Paffenbarger, R. S. (1995). Prostate cancer in relation to diet, physical activity, and body size in blacks, whites, and Asians in the United States and Canada. J Natl Cancer Inst 87: 652–661.

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V javnosti se veliko govori o dejavnikih, ki negativno vplivajo na človekovo zdravje. Na nekatere, kot je na primer genetska nagnjenost k nekaterim boleznim, nimamo vpliva. Na druge pa lahko bistveno vplivamo s svojimi odločitvami. Odrečemo se lahko, na primer, škodljivemu kajenju. Osveščenost glede posledic kajenja je danes na Zahodu dokaj visoka. Težko bi namreč našli človeka, ki bi trdil, da kajenje ni škodljivo ali da je celo koristno.
Med zdravju škodljivimi dejavniki, na katere lahko vsakdo pomembno vpliva, je tudi prehrana. Tu pa je osveščenost ljudi veliko manjša. Zadnje čase narašča število znanstvenih raziskav, ki skušajo opredeliti rizična živila v naši prehrani. In v veliki večini raziskav se kot najbolj rizično živilo znova in znova pojavlja meso. Zato sta World Cancer Research Fund in American Institute for Cancer Research, ki v svetovnem merilu sodita med največje in najuglednejše ustanove na področju raziskovanja raka, v svojih priporočilih navedla, da obstaja "prepričljiva povezava med rdečim mesom, mesnimi izdelki in rakom debelega črevesa in danke". Njuni strokovnjaki pravijo, da je povezava med mesom in rakom po zaslugi novejših raziskav veliko močnejša kot je bila pred kakšnim desetletjem. Navajajo tudi, da raziskave kažejo na povezavo med prehranjevanjem z mesom in rakom prostate, pljuč, požiralnika, želodca in trebušne slinavke.
Omenjeni ustanovi sta objavili tudi zanimiv podatek, da je v ZDA osveščenost ljudi o povezavi med mesom in rakom le 35-odstotna. (V Sloveniji je ta odstotek verjetno še manjši, saj marsikdo domneva, da je meso vir zdravja).



Raziskave v ZDA - Johns Hopkins University


Na Johns Hopkins University v ZDA so podobno kot na Švedskem izvedli obsežno meta-analizo študij, kjer so iskali povezavo med zaužitjem posameznih maščob (nasičenih, nenasičenih, večkrat nasičenih itd.) ter mesom in pojavnostjo raka prostate. Ugotavljajo, da so podatki za posamezne maščobe manj konsistentni, vendar kažejo na povezavo med rakom prostate in nasičenimi maščobami ter maščobami živalskega izvora. Nadaljnja analiza pokaže, da so podatki raziskav, ki povezujejo meso in rak prostate precej bolj konsistentni. Velika večina proučenih raziskav namreč kaže močno povezavo med mesom in rakom prostate, saj določajo faktor povečanja tveganja za 30% ali več.



Fat, Meat, and Prostate Cancer, Laurence N. Kolonel, Epidemiol Rev 2001;23:72-81



Johns Hopkins University Bloomberg School of Public Health

Fat, Meat, and Prostate Cancer

Laurence N. Kolonel



INTRODUCTION

For more than 25 years, epidemiologic studies have reported on the relation of dietary fat to the risk of prostate cancer. Indeed, fat per se, or food sources of fat, has probably been the most studied of all dietary factors with regard to this cancer site. Despite this extensive investigative effort, the role of dietary fat in prostate cancer remains unclear.
The hypothesis that dietary fat increases the risk of prostate cancer grew out of early ecologic studies that showed a positive correlation between prostate cancer mortality and per capita intake of fat, meat, and milk in international comparisons (1, 2). These findings were consistent with the recognition that prostate cancer risk is modifiable, as evidenced by such observations as the changing incidence and mortality rates in Japanese migrants to Hawaii and the substantial variations in incidence among ethnically similar populations in different geographic locations, e.g., Chinese men in different countries of Asia and the United States (3, 4).
Fat and meat are considered together in this presentation because most research has been done in Western populations (United States, Canada, and Europe) where meat is an important contributor to total and saturated fat intake. Many investigators, therefore, interpreted associations with meat intake to reflect an effect of dietary fat. However, other constituents of meat could also contribute to a carcinogenic effect, as discussed below.

FAT

Because fat is such a major contributor to energy intake in Western populations, these two dietary components tend to be highly correlated and an independent effect of fat may
be difficult to establish. Early epidemiologic studies of diet and prostate cancer were based on dietary assessment methods that did not permit the calculation of total caloric intake,
so that neither the effect of energy nor adjustment for energy intake was possible. This limitation has been overcome in many recent studies in which dietary histories were sufficiently complete for the computation of total caloric intakes.

Although a positive effect of energy per se was reported in a few of these investigations (5-7), including one study of latent prostate cancer (8), most studies found no effect of energy independent of fat (9-15). Nevertheless, it is noteworthy that experimental studies in rodents have shown a reduction in prostate tumor growth from energy restriction (16).
In epidemiologic studies of prostate cancer, fatty acids have been classified in several different ways, including total fat, animal versus vegetable fat, and saturated versus
unsaturated fat. Unsaturated fatty acids have sometimes been grouped into monounsaturated versus polyunsaturated fats, and polyunsaturated fatty acids have been further subdivided into co-6 and (O-3 fatty acids. Fatty acids can differ in their biologic properties depending on the degree of saturation and length of the carbon chain. Thus, not all fat components would be expected to carry the same risk for cancer.

Total, saturated, and animal fat

Data from several ecologic studies have shown positive correlations (r > 0.6) between per capita intake of total, saturated, or animal fat and prostate cancer incidence or mortality
(1, 2, 17-19). The findings for these fat components from case-control and cohort studies are summarized in table 1. Although several case-control studies found positive associations (odds ratio (OR) >1.3) between total fat intake and the risk of prostate cancer (7, 9, 10, 20-22, 24, 27, 29), only slightly fewer failed to find this relation (5, 12-14, 23,
26, 30). Most studies found stronger associations for saturated or animal fat than for total fat (9, 11, 20, 24, 25, 28, 30). Of the five case-control studies in table 1 that examined
total fat intake with adjustment for total energy intake (5, 7, 10, 12, 13), only two (7, 10) found an increased risk.
Similarly, of the eight case-control studies that examined animal or saturated fat with adjustment for total energy intake (5-7, 10-13, 31), only two (10, 11) showed an increased risk.
Because cohort studies of diet and cancer avoid the problem of recall bias and are less prone than case-control studies to other selection biases, they are generally given more
weight in overall assessments of the literature. Three such studies, all of which adjusted for energy intake (15, 33, 34), examined total fat and prostate cancer; two of these studies
(33, 34) found a positive association (relative risk > 1.3).
Four cohort studies examined animal or saturated fat and prostate cancer (15, 32-34), all with adjustment for energy intake. Only one of these studies (33) found a positive association with saturated fat, but two (32, 33) reported positive associations with animal fat. Although most studies did not stratify the cases by stage or other measures of disease progression, it is notable that the association with total and saturated fat was stronger for the advanced cases in some reports (9, 11,27,33).
Two recent studies reported on the relation of dietary fat to latent prostate cancer (8, 15). Neither study found a significant association between total or saturated fat and prostate cancer after adjustment for energy intake.

Unsaturated fat

The data regarding unsaturated fat are more limited. A few ecologic studies examined monounsaturated and polyunsaturated fat intake based on per capita intake data (19, 35) or analysis of fatty acids in adipose tissue (36); none of these studies found more than weak correlations.

The results from case-control and cohort studies are shown in table 2. Three case-control studies (27, 30, 39), one of which adjusted for energy intake (39), found positive associations (p > 1.3) of monounsaturated fat intake with prostate cancer risk, but five others (5, 6, 12, 13, 31), all of which adjusted for energy intake, did not. Of the three
cohort studies that examined monounsaturated fat (15, 33, 34), all found positive associations after adjustment for energy intake. Of the two reports on latent prostate cancer (8, 15), one found a positive association with intake of monounsaturated fat; a similar effect was seen for the nonlatent tumors in this study.
Three case-control studies (12, 27, 31), two of which (12, 31) included energy adjustment, found positive associations between polyunsaturated fat intake, or measurement in blood samples, and prostate cancer, whereas four studies (5, 6, 13, 30), three of which included energy adjustment (5, 6, 13), did not. Two reports based on latent prostate cancer (8, 15) found no association of polyunsaturated fat intake with prostate cancer risk. One of these studies (15) also examined trans unsaturated fatty acids and found no effect on prostate cancer risk.
Analyses based on groupings of fatty acids, such as polyunsaturated fat, could mask an effect specific to a single fatty acid. Several recent studies have examined specific polyunsaturated fatty acids, based either on dietary intake data or biochemical measurements in blood or adipose tissue (5, 15, 30, 33, 37^0). The results for the major
polyunsaturated fatty acid, linoleic acid (u>6), and its derivative, a-linolenic acid ((0-3, obtained from terrestrial food sources), as well as for two of the major long-chain (0-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid, found in fish oils) are also shown in table 2. Most studies found no increased risk associated with linoleic acid (5, 15, 30, 33, 39,40), but five (30, 33, 37, 39, 40) of seven (5, 15, 30, 33, 37, 39, 40) studies that examined a-linolenic acid found a positive association. Some of the discrepancies in the results of different studies could be related to the use of different data sources (diet histories, adipose tissue, erythrocyte membranes, serum phospholipids, plasma cholesterol ester fatty acids). In one study, linoleic, but not a-linolenic, acid was associated with a statistically nonsignificant increased risk of latent prostate cancer (odds ratio = 1.6 for highest relative to lowest intake quartile) (8).
Eicosapentaenoic acid was associated with decreased risk (odds ratio < 0.7) in two case-control studies based on biochemical analyses (37, 38), though three other studies,
including two cohort studies, did not show this relation (15, 30,40). Notably, neither of two studies that estimated eicosapentaenoic acid intake from diet histories found any effect
(15, 38). Findings for docosahexaenoic acid are similar to those for eicosapentaenoic acid, with the exception of one study (30) which found an inverse relation for the former
but not the latter fatty acid.

MEAT

The data on meat and prostate cancer are more consistent than those on fat. The findings from case-control and cohort studies are summarized in table 3. Sixteen (7, 9, 25, 28, 29, 32-34, 40, 42, 44-46, 48, 50, 52) of the 22 studies in the table show a positive relation, with all but one (42) showing risk ratios of 1.3 or more. In addition, several ecologic studies have reported a similar positive relation (1, 2, 53). Most studies reported on meat as a single category. Of the eight studies in table 3 that distinguished red meat as a group, or that included specific red meat items (mostly beef or pork) (7, 9, 33, 34, 40, 42, 47, 52), all but one (47) found positive associations, six of which showed risk ratios of 1.3 or more. Two reports (7, 52) examined processed meats, a dietary source of exposure to nitrites; neither study found an association of prostate cancer with this food item.
The basis for this association between prostate cancer and high consumption of red meat is not known. Initially, the finding was thought to reflect a high exposure to dietary fat,
especially saturated fat, since meat and dairy products are the major contributors to fat intake in the western diet.
However, because the findings on dietary fat and prostate cancer, as reviewed above, are inconsistent, other explanations for the association need to be considered. There are
several possibilities: 1) In the American diet, red meat is a major source of zinc, which is essential for testosterone synthesis and may have other effects in the prostate (see the
review of selenium and zinc in this issue of Epidemiologic Reviews). 2) Diets high in meat and other animal products may be relatively deficient in certain anticarcinogenic constituents found primarily in plant foods (see the reviews of fruits and vegetables, and phytochemicals also in this issue of Epidemiologic Reviews). 3) Most intriguingly, many
meats are cooked at high temperatures, such as by panfrying, grilling, or barbecuing. Cooking meats at high temperatures can result in the formation of heterocyclic amines
which are potent carcinogens in animals (54), including the rat prostate (55). Furthermore, when meats are cooked on charcoal grills, rendered fat is pyrolized by the coals, leading
to the deposition of polycyclic aromatic hydrocarbons, which are also carcinogenic in animals, on the outer surface of the meat (56). Because the levels of these compounds in
the diets of individuals cannot be easily assessed, few epidemiologic studies have yet reported on their relation to cancer. In a recent study on prostate cancer, heterocyclic
amine intake from cooked meat was estimated; however, the study did not lead to a clear result (57).

ANIMAL AND IN VITRO STUDIES

Despite difficulties in developing a suitable animal model for the study of prostate cancer, several animal and in vitro studies support the fat-cancer hypothesis (58). In one of the earliest studies, a high fat diet was found to increase prostate cancer incidence and to shorten the latency period in Lobund-Wistar rats treated with exogenous testosterone to induce the tumors (59). Conversely, prostate tumor growth rate was reduced by a fat-free diet in Dunning rats (60) or by lowering dietary fat intake in athymic nude mice injected with LNCaP cells (a human prostate cancer cell line) (61). However, some other studies
in rodent models failed to reproduce these findings (62, 63). In a recent report (16), tumor growth of androgenresponsive carcinomas in rats was shown to be reduced by restriction of energy rather than fat. With regard to specific types of fat, fish oils containing high levels of co-3 fatty acids, such as eicosapentaenoic and docosahexaenoic acids, generally suppressed prostate tumor growth in rodents, whereas other polyunsaturated fatty acids, including linoleic (co-6) and a-linolenic (co-3), promoted tumor growth (64, 65). Since most animal studies have been conducted in rodents, whose prostate glands differ anatomically from that of humans, extrapolation of these findings to humans is particularly tenuous.

BIOLOGIC MECHANISMS

A number of plausible mechanisms by which dietary fat could contribute to carcinogenesis in the prostate gland have been proposed (58): 1) oxidation of polyunsaturated fatty
acids leads to the formation of lipid radicals and hydroperoxides that can produce DNA damage; 2) a high fat diet increases circulating levels of endogenous androgens that
may contribute to the development of prostatic tumors (see the review on hormonal risk factors in this issue of Epidemiologic Reviews; 3) polyunsaturated fatty acids inhibit gap-junctional communication between cells, which is essential for normal control of tissue growth; 4) fatty acids can alter the activities of signal transduction molecules that are necessary for cellular growth control; 5) eicosanoids (prostaglandins and leukotrienes) are formed from arachidonic acid, and may influence prostate tumor cell growth; and 6) fatty acids may decrease the immune responsiveness of prostatic tissue.
Heterocyclic amines and polycyclic aromatic hydrocarbons may induce cancer directly by formation of DNA adducts, though supportive data are limited and other factors may be involved (54, 66). Biologically plausible mechanisms for the carcinogenic effects of other meat constituents can be found in the reviews noted in the section above on Meat.

ASSESSMENT

Conclusions

Figure 1 summarizes the relative risks/odds ratios for the various studies in tables 1-3. The findings from casecontrol studies are distinguished from those of cohort studies, and statistically significant risk ratios are noted. As seen in figure 1, most studies of total and saturated or animal fat reported risk ratios greater than 1.3, though none of the results from cohort studies were statistically significant.
The substantial proportion of studies with a positive finding, however, makes it difficult to dismiss the possibility that total or saturated fat may play a role, perhaps indirect, in the etiology of prostate cancer. Attributable risk estimates from two reports (11, 67) suggest that about 20-25 percent of the incidence of prostate cancer among US Caucasian-Americans and African-Americans, and about 5-10 percent among Asian-Americans, may be due to high levels of saturated fat intake. However, less than 10 percent of the African-American versus Caucasian-American, and only about 15 percent of the Caucasian-
American versus Asian-American, differences in incidence of prostate cancer could be attributed to differences in theirsaturated fat intakes (11).
The findings for monounsaturated fat suggest a possible positive relation to prostate cancer, though the number of studies is fewer than for total or saturated fat. For total
polyunsaturated fat, the risk ratios are more evenly spread above and below 1.0, though two case-control studies reported odds ratios greater than 2.0. The inconsistency in the overall findings for polyunsaturated fat may reflect different effects for specific fatty acids, as the results for alinolenic acid are supportive of a positive association, whereas those for eicosapentaenoic acid suggest a possible inverse association. Furthermore, the ratio of fat types, such a co-6 to co-3 polyunsaturated fatty acids, or possibly saturated to unsaturated fatty acids, may be more critical, as suggested in one report (30). The data on meat, like total fat, are heavily weighted with studies showing a positive relation to prostate cancer. All of the statistically significant findings are risk ratios above 1.3 and include the results from three cohort analyses. As noted earlier, the meat effect could reflect several constituents other than fat, including compounds produced during the cooking process.

Research needs

It does not seem likely that incremental improvements in the methods of dietary assessment in the next several years will substantially clarify the relations discussed in
this review. More specific examination of particular subgroups of fats, such as the ratio of co-6 to co-3 fatty acids or the balance of saturated and unsaturated fats in the diet,
may yield useful insights. Although fatty acids can be measured in serum, other biomarkers that could better reflect long-term and absolute fat intake (especially if they could distinguish fat intake at different periods of life) would be useful; such markers have yet to be identified.
Research efforts to determine the role of diet, especially dietary fat, in explaining the large interracial differences in prostate cancer incidence should continue. More studies that distinguish between latent and overt cases should be encouraged, as only the latter have health consequences, and the proportion of very early prostate cancers being identified through the widespread use of prostate-specific antigen screening has greatly increased
(68). If clinical tumors evolve from latent tumors, then the identification of factors that promote the progression of latent tumors should be of paramount interest. Because
dietary fat appears to act as a cancer promoter (69), it could play a role in this sequence. However, the findings of one cohort study that compared latent with nonlatent tumors (15) suggested that the relation of fat to prostate cancer does not differ substantially between these two groups of cases.
Studies that carefully examine interactions between dietary fat and other dietary or nondietary risk factors may help clarify some of the specific effects of fat on carcinogenesis
in the prostate. This research should include investigations of gene-environment interactions, such as may occur between intake of specific fat components or red meat
consumption (including methods of preparation) and polymorphisms in genes encoding cytochrome P450 and other enzymes involved in the metabolism of heteocyclic amines,
polycyclic aromatic hydrocarbons, and fatty acids (e.g., CYP1A2, NAT2, GSTP1). Although analyses of some candidate polymorphisms did not show significant relations to prostate cancer risk in a recent study (70), interactions with dietary exposures were not included. Studies with sufficient power to examine such interactions will require very large sample sizes that should be available in the next several years from some of the ongoing cancer cohorts in the United States and Europe.

ACKNOWLEDGMENTS

This work was supported in part by grants 5 R01
CA54281 and 2 P01-CA33619 from the US National
Cancer Institute.

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Originalna objava v Epidemiologic Reviews (vsebuje vse tabele in dodatne podatke)

http://epirev.oxfordjournals.org/cgi/rep
rint/23/1/72

V javnosti se veliko govori o dejavnikih, ki negativno vplivajo na človekovo zdravje. Na nekatere, kot je na primer genetska nagnjenost k nekaterim boleznim, nimamo vpliva. Na druge pa lahko bistveno vplivamo s svojimi odločitvami. Odrečemo se lahko, na primer, škodljivemu kajenju. Osveščenost glede posledic kajenja je danes na Zahodu dokaj visoka. Težko bi namreč našli človeka, ki bi trdil, da kajenje ni škodljivo ali da je celo koristno.
Med zdravju škodljivimi dejavniki, na katere lahko vsakdo pomembno vpliva, je tudi prehrana. Tu pa je osveščenost ljudi veliko manjša. Zadnje čase narašča število znanstvenih raziskav, ki skušajo opredeliti rizična živila v naši prehrani. In v veliki večini raziskav se kot najbolj rizično živilo znova in znova pojavlja meso. Zato sta World Cancer Research Fund in American Institute for Cancer Research, ki v svetovnem merilu sodita med največje in najuglednejše ustanove na področju raziskovanja raka, v svojih priporočilih navedla, da obstaja "prepričljiva povezava med rdečim mesom, mesnimi izdelki in rakom debelega črevesa in danke". Njuni strokovnjaki pravijo, da je povezava med mesom in rakom po zaslugi novejših raziskav veliko močnejša kot je bila pred kakšnim desetletjem. Navajajo tudi, da raziskave kažejo na povezavo med prehranjevanjem z mesom in rakom prostate, pljuč, požiralnika, želodca in trebušne slinavke.
Omenjeni ustanovi sta objavili tudi zanimiv podatek, da je v ZDA osveščenost ljudi o povezavi med mesom in rakom le 35-odstotna. (V Sloveniji je ta odstotek verjetno še manjši, saj marsikdo domneva, da je meso vir zdravja).



Švedske raziskave

Na švedskem Karolinska Institutet v Stockholmu so pripravili meta-analizo več raziskav na temo mesa in raka želodca. Rezultate petnajstih raziskav so združili v dve skupini in ugotavljali povezavo med dozo in odzivom (dose-response). Ta je pokazala, da se možnost raka želodca na vsakih dnevno zaužitih 30 g mesnih izdelkov v prvi skupini raziskav poveča za 38% (študije primerov) in v drugi skupini za 15% (kohortne študije).



Processed Meat Consumption and Stomach Cancer Risk: A Meta-Analysis, Susanna C. Larsson, Nicola Orsini, Alicja Wolk, JNCI Journal of the National Cancer Institute 2006 98(15):1078-1087¸





Susanna C. Larsson, Nicola Orsini, Alicja Wolk


Affiliation of authors: Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

Correspondence to: Susanna C. Larsson, MSc, Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE-171 77, Stockholm, Sweden (e-mail: Susanna.Larsson@ki.se), Nicola Orsini(Nicola.Orsini@ki.se) .



Background:

The relationship between processed meat consumption and the risk of stomach cancer is controversial. We conducted a meta-analysis to summarize available evidence from cohort and case–control studies on this issue. Methods: We searched Medline for studies of processed meat consumption and stomach cancer published from January 1966 through March 2006. Random-effects models were used to pool the relative risks from individual studies. All statistical tests were two-sided. Results: Six prospective cohort studies (involving 2209 stomach cancer patients) and nine case–control studies (2495 case patients) were eligible for inclusion in the dose–response meta-analysis of processed meat consumption. The estimated summary relative risks of stomach cancer for an increase in processed meat consumption of 30 g/day, approximately half of an average serving, were 1.15 (95% confidence interval [CI] = 1.04 to 1.27) for the cohort studies and 1.38 (95% CI = 1.19 to 1.60) for the case–control studies. There was no statistically significant heterogeneity among the cohort studies (P = .42) or among the case–control studies (P = .19). In three cohort and four case–control studies that examined the association between bacon consumption and stomach cancer, the summary relative risk was 1.37 (95% CI = 1.17 to 1.61) for the highest versus lowest intake categories of bacon, without heterogeneity among these studies (P = .66). Conclusion: Increased consumption of processed meat is associated with an increased risk of stomach cancer. However, the possibility that the association may be confounded or modified by other factors cannot be ruled out.