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câncer  /  hipertensão / diabetegaleria 

REFERÊNCIAS

As referências a fontes de publicações científicas, atestando a  cancerogenicidade da carne são numerosas.

As fontes mais visitadas são: 

O principal sitio de informação científica biomédica na internet, a serviço do governo dos Estado Unidos: www.pubmed.gov  fazer busca por "meat cancer"

Google acadêmico em pesquisa sobre carne e câncer : http://scholar.google.com.br/scholar?q=meat++++cancer+&hl=pt-BR&lr=&btnG=Pesquisar&lr=

A carne é cancerígena por três motivos:

1) a presença do heme, a parte protéica da hemoglobina, na carne, que é cancerígena, independentemente sa origem e da maneira como foi processada a carne, fontes: http://scholar.google.com.br/scholar?hl=pt-BR&lr=&q=meat++++cancer++haem&btnG=Pesquisar&lr=

2) a presença das aminas heterocíclicas (HCA), substâncias, que se formam durante o cozimento da carne, fonte:   http://scholar.google.com.br/scholar?hl=pt-BR&lr=&q=meat++++cancer+++HCA&btnG=Pesquisar&lr=

3) a presença dos carboidratos policíclicos aromáticos (PAH), que se formam durante a fritura ou a exposição ao fogo aberto, fonte: http://scholar.google.com.br/scholar?hl=pt-BR&lr=&q=meat++++cancer+++PAH+&btnG=Pesquisar&lr=

 

A incidência do câncer é proporcional ao consumo de carne (vermelha e de aves):

O estado com maior consumo de carne per capita no Brasil é Rio Grande do Sul  e com menos consumo o Amazonas.

Para cada 100 mil habitantes no Estado de Rio Grande do Sul as mortes por câncer entre os homens são de 537,55 casos  e entre as mulheres de 546,84 casos, fonte: http://www.inca.gov.br/estimativa/2008/index.asp?link=tabelaestados.asp&UF=RS

Já no Estado de Amazonas entre os homens são 189,77, e entre as mulheres 200,89,  fonte: http://www.inca.gov.br/estimativa/2008/index.asp?link=tabelaestados.asp&UF=AM

Isto significa que morrem de câncer no Estado de Rio Grande Sul, entre os homens  283% e entre as mulheres 272% a mais,  do que no Estado de Amazonas.

 

Aqui reproduzimos, apenas como ilustração, algumas destas publicações.

Oncol Rep. 2007 Apr;17(4):807-11. Links

Diallyl sulfide inhibits PhIP-induced DNA strand breaks in normal human breast epithelial cells.

Wilson C, Aboyade-Cole A, Newell O,  Oriaku E, Thomas R.

Environmental Toxicology Program, College of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Tallahassee, FL 32307, USA.

Heterocyclic amines (HCAs) are formed when meat products such as beef, chicken, pork and fish are cooked at high temperatures. The most abundant HCA found in the human diet is  PhIP causes mammary carcinomas in female rats and mice, and is associated with an increased risk of developing colon, breast, and prostate cancer in humans. PhIP is metabolized by cytochrome P-450s producing N-OH-PhIP. The N-OH-PhIP can be esterified by phase II enzymes forming an arylnitrenium ion that binds to DNA causing adducts. Furthermore, N-OH-PhIP may be reduced by cytochrome b5 reductase producing superoxide anions and hydroxyl radicals causing DNA strand breaks. Diallyl sulfide (DAS) has been shown to prevent cancer in several animal models, presumably by metabolic modulation. We hypothesize that PhIP produces reactive oxygen species causing DNA strand breaks and that DAS will inhibit the formation of PhIP induced DNA strand breaks. To test this hypothesis we treated normal breast epithelial (MCF-10A) cells with PhIP, DAS and a combination of PhIP and DAS. The detection of lipid peroxides was used as a surrogate for ROS. Lipid peroxides were detected using a PeroxiDetect kit (Sigma). PhIP increased the production of lipid peroxides and DAS decreased the PhIP-induced peroxidation by 47%. To determine if PhIP causes DNA strand breaks in MCF-10A cells, cells were treated for 3, 6, 9, and 24 h with PhIP (100 microM), DAS (100 microM) and a combination of PhIP (100 microM) and DAS (100 microM). DNA strand breaks were evaluated using the Comet assay. PhIP produced DNA strand breaks in a dose- and time-dependent fashion. We have shown that DAS inhibits PhIP-induced DNA strand breaks by inhibiting the production of reactive oxygen species. Therefore, we propose that DAS can prevent PhIP-induced breast cancer.

 

Cancer Epidemiol Biomarkers Prev. 2007 Mar 2; [Epub ahead of print]Click here to read  Links

Obesity, Diet and Risk of Non-Hodgkin Lymphoma.

Skibola CF.

Division of Environmental Health Sciences, School of Public Health, 140 Earl Warren Hall University of California, Berkeley, California.

Non-Hodgkin lymphoma (NHL) represents a group of heterogeneous diseases that significantly vary in their causes, molecular profiles, and natural progression. In 2007, there will be approximately 59,000 newly diagnosed NHL cases in the United States and over 300,000 cases worldwide. Although new therapeutic regimens are minimizing the number of deaths related to NHL, causes for the majority of lymphomas remain undetermined. Recent studies suggest that dietary factors may contribute to the rising rates of NHL. This review will summarize epidemiologic reports that have studied the relationship between obesity, physical activity, and diet and risk of NHL. Based on a number of case-control and prospective cohort studies, overweight/obesity probably increases the risk of NHL, whereas moderate physical activity may reduce risk. Several studies support an inverse association between intakes of vegetables and NHL risk, particularly for the consumption of cruciferous vegetables. This may relate to the induction of apoptosis and growth arrest in preneoplastic and neoplastic cells, two important actions of isothiocyanates found in cruciferous vegetables. Studies also suggest that fish intake may be inversely associated with risk of NHL, although findings have not been entirely consistent. This may relate to the high organochlorine content in some fish that could override a protective effect. High consumption of fats, meat, and dairy products also may increase lymphoma risk. The accumulated scientific evidence concerning the associations between obesity, diet, and NHL suggests several identified modifiable risk factors that might be recommended to decrease lymphoma risk. (Cancer Epidemiol Biomarkers Prev 2007;16(3):392-5).

 

Cancer Causes Control. 2007 Feb;18(1):41-50. Links

Meat and dairy consumption and subsequent risk of prostate cancer in a US cohort study.

Rohrmann S, Platz EA, Kavanaugh CJ, Thuita L, Hoffman SC, Helzlsouer KJ.

Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe St., Rm. E 6138, Baltimore, MD 21205, USA.

OBJECTIVE: To evaluate the association of meat and dairy food consumption with subsequent risk of prostate cancer. METHODS: In 1989, 3,892 men 35+ years old, who participated in CLUE II study of Washington County, MD, completed an abbreviated Block food frequency questionnaire. Intake of meat and dairy related foods was calculated using consumption frequency and portion size. Incident prostate cancer cases (n = 199) were ascertained through October 2004. Cox proportional hazards regression was used to calculate hazard ratios (HR) of total and advanced (SEER states three and four; n = 54) prostate cancer and 95% confidence intervals (CI) adjusted for age, BMI at age 21, and intake of energy, saturated fat, and tomato products. RESULTS: Intakes of total mean (HR = 0.90, 95% CI 0.60-1.33, comparing highest to lowest tertile) and red meat (HR = 0.87, 95% CI 0.59-1.32) were not statistically significantly associated with prostate cancer. However, processed meat consumption was associated with a non-statistically significant higher risk of total (5+ vs. < or =1 servings/week: HR = 2.24; 95% CI 0.90-5.59) prostate cancer. There was no association across tertiles of dairy or calcium with total prostate cancer, although compared tp < or =1 servings/week consumption of 5+ servings/week of dairy foods was associated with an increased risk of prostate cancer (HR = 1.65, 98% CI 1.02-2.66). CONCLUSION: Overall, consumption of processed meat, but not total meat or red meat, was associated with a possible increased risk of total prostate cancer in this prospective study. Higher intake of dairy foods but not calcium was positively associated with prostate cancer. Further investigation into the mechanisms by which processed meat and dairy consumption might increase the risk of prostate cancer is suggested.

 

Recent Results Cancer Res. 2007;174:179-87. Links

Prevention and early detection of colorectal cancer--new horizons.  Rennert G.

CHS National Cancer Control Center, Carmel Medical Center, Haifa, Israel.

Colorectal cancer is potentially one of the most preventable malignancies. Nutritional awareness (low fat, low red meat, high fruits and vegetables) and regular physical activity have major potential for primary prevention of this malignancy, while early detection technologies have the potential of both influencing mortality from colorectal cancer as well as enhancing primary prevention through detection and removal of lesions that could potentially develop into cancer. While the potential for prevention is large, its materialization is far from being optimal. The large-scale lifestyle changes in the population necessary to reduce colorectal cancer rates are hard to achieve, and most of the early detection technologies are either invasive or otherwise nonappealing to the population. Thus, without abandoning the proven prevention methods, new avenues need to be investigated to deal with this malignancy, which carries both high morbidity and high mortality. Such new avenues can now be followed, both in prevention and detection. Chemoprevention, or the use of medications to prevent disease, has now been extensively explored in colorectal cancer. Some of these interventions, such as supplemental fibers, have failed to demonstrate the anticipated effect, while others such as calcium supplementation have been shown to reduce formation of premalignant lesions, polyps, or adenomas. Data accumulating in recent years have suggested that aspirin, nonsteroidal anti-inflammatory drugs, and selective COX-II inhibitors all have a potential to reduce both colorectal cancer and colorectal adenomas. Issues of safety and therapeutic indexes have recently come up as barriers to the use of COX-II inhibitors, and have again drawn attention to aspirin as a potential drug of choice. Association studies have also shown a major potential role for statins in colorectal cancer prevention. New methodologies in cancer detection involve the introduction of colonography or virtual colonoscopy, and the development of methods of detection of genetic somatic mutations in feces or peripheral blood. While radiological techniques currently avoid the need for premedication and are less invasive, they currently still require similar gut cleansing to colonoscopy, can also lead to perforation, are costly, and carry a non-negligible exposure to radiation. Genetic analysis of the stool for mutations in tumor cells is evolving as a promising technique, struggling to achieve both high sensitivity and high specificity with the right combination of mutations sought. With all of these developments taking place, the near future will undoubtedly bring about the expected reduction in colorectal cancer mortality.

 

Eur J Clin Nutr. 2007 Feb 7; [Epub ahead of print]Click here to read  Links

Comparative fracture risk in vegetarians and nonvegetarians in EPIC-Oxford.  Appleby P, Roddam A, Allen N, Key T.

1Cancer Research UK Epidemiology Unit, Nuffield Department of Clinical Medicine, University of Oxford, Roosevelt Drive, Oxford, UK.

Objective:To compare fracture rates in four diet groups (meat eaters, fish eaters, vegetarians and vegans) in the Oxford cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford).Design:Prospective cohort study of self-reported fracture risk at follow-up.Setting:The United Kingdom.Subjects:A total of 7947 men and 26 749 women aged 20-89 years, including 19 249 meat eaters, 4901 fish eaters, 9420 vegetarians and 1126 vegans, recruited by postal methods and through general practice surgeries.Methods:Cox regression.Results:Over an average of 5.2 years of follow-up, 343 men and 1555 women reported one or more fractures. Compared with meat eaters, fracture incidence rate ratios in men and women combined adjusted for sex, age and non-dietary factors were 1.01 (95% CI 0.88-1.17) for fish eaters, 1.00 (0.89-1.13) for vegetarians and 1.30 (1.02-1.66) for vegans. After further adjustment for dietary energy and calcium intake the incidence rate ratio among vegans compared with meat eaters was 1.15 (0.89-1.49). Among subjects consuming at least 525 mg/day calcium the corresponding incidence rate ratios were 1.05 (0.90-1.21) for fish eaters, 1.02 (0.90-1.15) for vegetarians and 1.00 (0.69-1.44) for vegans.Conclusions:In this population, fracture risk was similar for meat eaters, fish eaters and vegetarians. The higher fracture risk in the vegans appeared to be a consequence of their considerably lower mean calcium intake. An adequate calcium intake is essential for bone health, irrespective of dietary preferences.Sponsorship:The EPIC-Oxford study is supported by The Medical Research Council and Cancer Research UK.European Journal of Clinical Nutrition advance online publication, 7 February 2007; doi:10.1038/sj.ejcn.1602659.

 

Br J Ind Med. 1989 Mar;46(3):188-91. Links

Lung cancer in the meat industry. Coggon D, Pannett B, Pippard EC, Winter PD.

Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, UK.

Routine statistics of occupational mortality and incidence of cancer have consistently shown high rates of lung cancer in butchers. Possible explanations include infection by carcinogenic papilloma viruses, exposure to polycyclic aromatic hydrocarbons and nitrites in the preservation of meat, or a confounding effect of tobacco. To explore these possibilities, we have examined the mortality of 1610 men employed at three British companies processing pork, beef, lamb, bacon, and other meat products. The overall death rate was less than in the national population (271 deaths observed, 310 expected) but there was an excess of deaths from cancer (87 observed, 80 expected), and in particular from lung cancer (42 observed, 32 expected). The risk of lung cancer was concentrated in subjects exposed to recently slaughtered meat, especially after an interval of 10 or more years. These findings increase suspicions of a risk of lung cancer in butchers, although further information is needed about smoking habits in the meat industry. If there is a hazard infection by a papilloma virus would seem the most likely cause.

 

 September/October 2006

An Update of Broward County Air Licensing for Remediation Systems

An Official Bimonthly Publication of Broward County’s

Environmental Protection Department

Polycyclic aromatic hydrocarbons, commonly referred to as PAHs, are carcinogenic organic molecules consisting of three or

more rings containing carbon and hydrogen which are a by-product of fossil fuel combustion. PAHs are also by-products of

incomplete burning of organic substances such as tobacco and charbroiled meat. Common sources of PAHs are asphalt for

road construction, crude oil, coal, coal tar pitch, creosote, and roofing tar. PAHs with four benzene rings are considered light

PAHs, while PAHs with more than four rings are considered heavy PAHs, making them more stable and more toxic.

Out of the more than 100 different PAHs, the Agency for Toxic Substance & Disease Registry has identified the following

PAHs to be considered as a group: acenaphthene, acenaphthylene, anthracene, benzo(a)anthracene, benzo(a)pyrene,

benzo(e)pyrene, benzo(b)fluoranthene, benzo(g,h,i)perylene, benzo(j)fluoranthene, benzo(k)fluoranthene, chrysene,

dibenz(a,h)anthracene, fluoranthene, fluorine, indeno(1,2,3-c,d)pyrene, phenanthrene, and pyrene. The PAHs listed in this

group are well known and readily available, exhibit harmful effects, and were found at hazardous waste sites on the National

Priority List with the highest concentrations.

In short, toxicity values are derived from primary sources when information is available. However, when toxicity information

is not available, alternative approaches are used to determine CTLs, which include, among other sources, toxicity equivalency

factors (TEFs).

The TEF approach was chosen to determine SCTLs for: Benzo(a)pyrene, Benz(a)anthracene, Benzo(b)fluoranthene,

Benzo(k)fluoranthene, Chrysene, Dibenzo(a,h)anthracene, and Indeno(1,2,3cd)pyrene. The TEF approach is defined by the

University of Florida Center for Environmental Health & Human Toxicology as the numerical expression of the potencies of

a series of related compounds relative to the potency of a reference or index chemical. Benzo(a)pyrene (BaP) was chosen as

the index chemical because its toxicity is well known as the first discovered chemical carcinogen. BaP concentrations in

charbroiled meat can range from 2.60 to 11.20 ug/kg, while the smoke resulting from one cigarette can range from 18 to 50

ng/cigarette. BaP is strictly produced during incomplete burning, and as a result has no industrial uses.

 

 

Carcinogenesis. 2007 Feb 2; [Epub ahead of print]Click here to read  Links

Processed meat intake, CYP2A6 activity, and risk of colorectal adenoma.Ward MH, Cross AJ, Divan H, Kulldorff M, Nowell-Kadlubar S, Kadlubar FF, Sinha R.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services.

Red and processed meat intake is associated with increased risks of both colorectal adenoma and cancer. Processed meats contain nitrate and nitrite, precursors of N-nitroso compounds (NOC); furthermore, meats cooked at high-temperatures contain heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH). Specific NOC, HCA, and PAH are mutagens and animal carcinogens. We conducted a case-control study of 146 cases of colorectal adenoma, diagnosed at sigmoidoscopy or colonoscopy, and 228 polyp-free controls. We calculated odds ratios (and 95% confidence intervals) and found a 2-fold increased risk in the highest, compared to the lowest, quartile of processed meat intake (95% CI = 1.0-4.0). We estimated nitrate and nitrite intake from meat using published data from the literature as well as from actual measurements of meats analyzed recently. We evaluated the interaction of processed meat and nitrate plus nitrite intake with CYP2A6 activity, an enzyme able to metabolize some NOC to their carcinogenic form. Results for both methods of estimating nitrate and nitrite intake were similar; compared with the lowest, the highest quartile was associated with a two-fold elevated risk (95% CI = 1.0-3.9). Adjustment for the HCA MeIQx attenuated the association (OR=1.6, 95% CI = 0.8-3.2), but other HCA and a PAH had minimal effect. Higher CYP2A6 activity was not associated with risk and there was no evidence of an interaction between CYP2A6 activity with nitrate and nitrite intake. Our results suggest that nitrite and nitrate intake from processed meat intake increases the risk of colorectal adenoma after accounting for HCA and PAH.

 

Carcinogenesis. 2007 Feb 2; [Epub ahead of print]Click here to read  Links

Leukocyte Polycyclic Aromatic Hydrocarbon-DNA Adduct Formation and Colorectal Adenoma.Gunter MJ, Divi RL, Kulldorff M, Vermeulen R, Haverkos KJ, Kuo MM, Strickland P, Poirier MC,Rothman N, Sinha R.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD, USA.

Consumption of charbroiled red meat and meat-derived polycyclic aromatic hydrocarbons (PAHs) has been associated with risk of colorectal adenoma, a precursor of colorectal cancer. Furthermore, leukocyte PAH-DNA adduct levels have been demonstrated to increase in response to charbroiled red meat intake but to date there have been no studies that have investigated the relationship between leukocyte PAH-DNA adduct levels and risk of colorectal adenoma. We investigated the relation of leukocyte PAH-DNA adduct formation and colorectal adenoma in a clinic-based case-control study of colorectal adenomas. The study comprised 82 cases of colorectal adenoma and 111 polyp-free controls, none of whom were current smokers. Leukocyte PAH-DNA adducts were measured by a sensitive chemiluminescence immunoassay (CIA) using an antiserum elicited against DNA modified with (+/-)-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene (BPDE) that recognizes several PAHs bound to human DNA. Leukocyte PAH-DNA adduct levels were higher among colorectal adenoma cases (median, 1.4 adducts per 10(8) nucleotides) than polyp-free controls (median, 1.2 adducts per 10(8) nucleotides) (P = 0.02). There was a positive association between PAH-DNA adduct level and adenoma prevalence: each unit increase in PAH-DNA adduct level (per 10(8) nucleotides) was associated with an odds ratio of 1.5 (95% confidence interval [CI], 1.1-2.2). In addition, a comparison of the lowest quartile for PAH-DNA adduct level with the highest quartile yielded an odds ratio of 2.8 (95%CI, 1.2-6.5; P(trend) = 0.048) for risk of colorectal adenoma. These data support a link between PAH exposure and colorectal adenoma.

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