Coffee And Cancer Risk

Here is a paper on coffee consumption and cancer risk from several years ago,  Bottom like is that there doesn't seem to be a big effect either way; coffee can cause decreased risk for some cancers, but possibly increased risk for childhood leukemia with maternal coffee drinking during pregnancy. The data are "limited and inconsistent" in some cases; overall it seems like a "wash" based on these findings, no big effect. Abstract:

We reviewed available evidence on coffee drinking and the risk of all cancers and selected cancers updated to May 2016. Coffee consumption is not associated with overall cancer risk. A meta-analysis reported a pooled relative risk (RR) for an increment of 1 cup of coffee/day of 1.00 [95% confidence interval (CI): 0.99-1.01] for all cancers. Coffee drinking is associated with a reduced risk of liver cancer. A meta-analysis of cohort studies found an RR for an increment of consumption of 1 cup/day of 0.85 (95% CI: 0.81-0.90) for liver cancer and a favorable effect on liver enzymes and cirrhosis. Another meta-analysis showed an inverse relation for endometrial cancer risk, with an RR of 0.92 (95% CI: 0.88-0.96) for an increment of 1 cup/day. A possible decreased risk was found in some studies for oral/pharyngeal cancer and for advanced prostate cancer. Although data are mixed, overall, there seems to be some favorable effect of coffee drinking on colorectal cancer in case-control studies, in the absence of a consistent relation in cohort studies. For bladder cancer, the results are not consistent; however, any possible direct association is not dose and duration related, and might depend on a residual confounding effect of smoking. A few studies suggest an increased risk of childhood leukemia after maternal coffee drinking during pregnancy, but data are limited and inconsistent. Although the results of studies are mixed, the overall evidence suggests no association of coffee intake with cancers of the stomach, pancreas, lung, breast, ovary, and prostate overall. Data are limited, with RR close to unity for other neoplasms, including those of the esophagus, small intestine, gallbladder and biliary tract, skin, kidney, brain, thyroid, as well as for soft tissue sarcoma and lymphohematopoietic cancer.

I don't drink coffee myself, but based on these data overall it seems not do any harm taking all risks together - although pregnant women may want to ask their doctor about the risk in that specific case.

Cancer Incidence In Different Parts Of The USA

Different forms of cancer seem more prevalent in some areas of the USA compared to others.  For example, read here. Part of abstract:

For many cancers, there were distinct clusters of counties with especially high mortality. The location of these clusters varied by type of cancer and were spread in different regions of the United States. Clusters of breast cancer were present in the southern belt and along the Mississippi River, while liver cancer was high along the Texas-Mexico border, and clusters of kidney cancer were observed in North and South Dakota and counties in West Virginia, Ohio, Indiana, Louisiana, Oklahoma, Texas, Alaska, and Illinois.
CONCLUSIONS AND RELEVANCE:
Cancer mortality declined overall in the United States between 1980 and 2014. Over this same period, there were important changes in trends, patterns, and differences in cancer mortality among US counties. These patterns may inform further research into improving prevention and treatment.

This differences can be due to genetic differences between demographic groups variably distributed in these regions, differences in lifestyle including diet and physical activity, different distribution of age groups in these regions, socioeconomic status and access to health care, etc.  As the authors state, hopefully this information can be useful in optimizing prevention and treatment.

Cancer Field Effect

Here is a paper on the cancer field effect, an idea that states than an entire area of a tissue can be altered in some way to predispose that area to develop cancer. Of interest is the possibility that diet, lifestyle (including smoking), etc. can alter the tissue microenvironment to create a "field of susceptibility" to cancer. Hopefully such research can fulfill the promise of "personalized prevention and treatment strategies for precision medicine;" however, until then, controlling diet and lifestyle to prevent cancer, to the best of your ability, is the optimal behavior modification to do.

The term 'field effect' (also known as field defect, field cancerization, or field carcinogenesis) has been used to describe a field of cellular and molecular alteration, which predisposes to the development of neoplasms within that territory. We explore an expanded, integrative concept, 'etiologic field effect', which asserts that various etiologic factors (the exposome including dietary, lifestyle, environmental, microbial, hormonal, and genetic factors) and their interactions (the interactome) contribute to a tissue microenvironmental milieu that constitutes a 'field of susceptibility' to neoplasia initiation, evolution, and progression. Importantly, etiological fields predate the acquisition of molecular aberrations commonly considered to indicate presence of filed effect. Inspired by molecular pathological epidemiology (MPE) research, which examines the influence of etiologic factors on cellular and molecular alterations during disease course, an etiologically focused approach to field effect can: (1) broaden the horizons of our inquiry into cancer susceptibility and progression at molecular, cellular, and environmental levels, during all stages of tumor evolution; (2) embrace host-environment-tumor interactions (including gene-environment interactions) occurring in the tumor microenvironment; and, (3) help explain intriguing observations, such as shared molecular features between bilateral primary breast carcinomas, and between synchronous colorectal cancers, where similar molecular changes are absent from intervening normal colon. MPE research has identified a number of endogenous and environmental exposures which can influence not only molecular signatures in the genome, epigenome, transcriptome, proteome, metabolome and interactome, but also host immunity and tumor behavior. We anticipate that future technological advances will allow the development of in vivo biosensors capable of detecting and quantifying 'etiologic field effect' as abnormal network pathology patterns of cellular and microenvironmental responses to endogenous and exogenous exposures. Through an 'etiologic field effect' paradigm, and holistic systems pathology (systems biology) approaches to cancer biology, we can improve personalized prevention and treatment strategies for precision medicine.

Red Meat and Pancreatic Cancer

Consistent with previous concerns about red meat and cancer, a new study suggests consuming heme iron from red meat increases the risk for pancreatic cancer:
 

Several studies on pancreatic cancer have reported significant positive associations for intake of red meat but null associations for heme iron. We assessed total, red, white, and processed meat intake, meat cooking methods and doneness, and heme iron and mutagen intake in relation to pancreatic cancer...Pancreatic cancer risk significantly increased with intake of total meat (Q5 vs. Q1 HR=1.20, 95% CI 1.02-1.42, p-trend=0.03), red meat (HR=1.22, 95% CI 1.01-1.48, p-trend=0.02), high-temperature cooked meat (HR=1.21, 95% CI 1.00-1.45, p-trend=0.02), grilled/barbequed meat (HR=1.24, 95% CI 1.03-1.50, p-trend=0.007), well/very well done meat (HR=1.32, 95% CI 1.10-1.58, p-trend = 0.005), and heme iron from red meat (Q4 vs. Q1 HR=1.21, 95% CI 1.01-1.45, p-trend=0.04)...Additional studies should confirm our findings that consuming heme iron from red meat increases pancreatic cancer risk. 

Once again, we see evidence that reducing red meat consumption is likely helpful for cancer prevention.

Blindness and Cancer Risk

This is an interesting paper.
 

Melatonin is a hormone primarily produced by the pineal gland at night and is suppressed by exposure to light. Experimental studies have indicated that melatonin may protect against cancer development. In the majority of totally blind people, melatonin is never suppressed by light exposure. The aim of this study was to test the hypothesis that blind people have a decreased cancer incidence, and that this effect is more pronounced in the totally blind than in the severely visually impaired. We identified a cohort of 1,567 totally blind and 13,292 severely visually impaired subjects and obtained information about cancer incidence from the Swedish Cancer Registry. We calculated standardized incidence ratios (SIRs) based on the number of person-years and incidence rates specific for national age, sex, and calendar year. Totally blind people had a lower incidence of all cancers combined [SIR = 0.69; 95% confidence interval (CI) = 0.59-0.82]. The risk reduction was observed in both men and women and was equally pronounced in hormone-dependent tumors as in other types of cancer. In the severely visually impaired, SIR was 0.95 (95% CI = 0.91-1.00). The findings support the hypothesis that blind people have a lower cancer incidence, although other explanations than the higher melatonin exposure must also be considered.

When such epidemiological findings are observed, it is extremely important to follow up and find out why this occurs. And that of course applies not only to this particular finding, but in general to every observation where a specific population has a greater or lesser incidence of some disease. Figuring out why incidence varies could be the first step to designing approaches for prevention and therapy.

Rats and Colon Cancer

A study shows that dietary risk factors thought to contribute to colon cancer in humans induce early stage colonic lesions in rats.

Epidemiological studies have demonstrated clear associations between specific dietary and environmental risk factors and incidence of colorectal cancer, but the mechanisms responsible for these associations are not known. An animal model could facilitate such an understanding.

Both genotoxic and nongenotoxic carcinogens induce aberrant crypt foci (ACF) in the colons of F344 rats. F344 rats were provided with diets that contained putative risk factors for CRC: low calcium and low vitamin D, high iron, high fructose, and decreased light (UV) exposure or a control diet for 14 wk. The rats were then assessed with biochemical measures and by topological examination for evidence of colon abnormalities. Circulating ionized calcium was decreased from 2.85 to 1.69 mmol/L, and ACF were increased from 0.7 to 13.6 lesions/colon (both P < 0.001).

Rats exposed to the multiple environmental conditions associated with colon cancer, developed ACF similar to the heterogeneous or ill-defined ACF in the human colon. Heterogeneous ACF are the type most frequently seen in humans, and are also seen in rats shortly after exposure to the non-genotoxic colon carcinogen, dextran sulfate sodium. The rodent model could be used to assess the pathways from diet and environment to colon cancer and to provide guidance for clinical studies.

Consider carefully the results with "high fructose" - do we really need high fructose corn syrup in our diets? Also, the "high iron" is another warning shot about red meat.

New Cancer Study

Striking back at an earlier paper that seemed to suggest that cancer is due to “bad luck” a new study demonstrates the powerful role of lifestyle on cancer development.  From the news story:

Most researchers agree cancer is likely caused by the body's stem cells dividing at uncontrollable rates. A study published in the journal Science back in January appeared to show two-thirds of cancer types were victims of bad luck, or chance mutations.

But a new study, which included some of the same data as the January study, argues only as much as 30 percent of cancers fall under the so-called "bad luck hypothesis."

Instead, the main causes were found to be external. Causes include diet, alcohol and cigarette use, sunburns, viruses, pollution and more –– including some factors that haven't been identified yet. The director of Stony Brook Cancer Center, from the university that conducted the study, told the BBC if intrinsic risk is like Russian roulette, "... then maybe one in six will get cancer. Now, what a smoker does is add two or three more bullets to that revolver. And now, they pull the trigger." The researchers noted in their paper at least nine other studies have shown evidence against the "bad luck hypothesis," but they say theirs is the first to quantitatively appraise the relative contribution of extrinsic factors. The finding could significantly alter how cancer is both treated and prevented.

The paper is here. This is the abstract:
 

Recent research has highlighted a strong correlation between tissue-specific cancer risk and the lifetime number of tissue-specific stem-cell divisions. Whether such correlation implies a high unavoidable intrinsic cancer risk has become a key public health debate with the dissemination of the ‘bad luck’ hypothesis. Here we provide evidence that intrinsic risk factors contribute only modestly (less than ~10–30% of lifetime risk) to cancer development. First, we demonstrate that the correlation between stem-cell division and cancer risk does not distinguish between the effects of intrinsic and extrinsic factors. We then show that intrinsic risk is better estimated by the lower bound risk controlling for total stem-cell divisions. Finally, we show that the rates of endogenous mutation accumulation by intrinsic processes are not sufficient to account for the observed cancer risks. Collectively, we conclude that cancer risk is heavily influenced by extrinsic factors. These results are important for strategizing cancer prevention, research and public health.

And their important conclusion:

…a consistent estimate of contribution of extrinsic factors of > 70–90% in most common cancer types. This is consistent with the overall conclusion regarding the role of extrinsic factors in cancer development.

Therefore, the important actionables remain consistent for cancer prevention: a healthy diet, avoid smoking, and get sufficient physical activity.

People Do Not Want To Know Their Cancer Risk?

Here is a study that suggests that many people don’t want to know their personal cancer risk; reasons for this are given as well.

Based on our representative sample, 39% of the population indicated that they agreed or strongly agreed that they would "rather not know [their] chance of getting cancer." This preference was stronger among older participants, female participants, and participants with lower levels of education. Preferring to avoid cancer risk information was stronger among participants who agreed with the beliefs that everything causes cancer, that there's not much one can do to prevent cancer, and that there are too many recommendations to follow. Finally, the preference to avoid cancer risk information was associated with lower levels of screening for colon cancer.

Note several things here. First, in certain populations at higher risk for cancer (older, less educated), there is an increased prevalence of the “I rather would not know” mentality.  We also see the cost of the media distorting and exaggerating various studies that come out – some of them occasionally contradictory – about cancer risk and health.

The constant drumbeat of scare articles about various things that may cause cancer is not helpful. There are some well-documented and important factors: smoking, obesity, diet, radon, certain viruses – and these should be publicized MORE. On the other hand, the constant stream of poorly documented speculation, often refuted by new studies, does more harm than good. It is like the “boy who cried wolf” story, straining credibility, and also giving the impression that since every daily activity causes cancer, then, “what can you do?” Of course, if new cancer-causing agents are discovered and are well-documented, then this needs to be publicized. But ill-documented sensationalism for the sake of “page hits” is irresponsible.

Related to this is the confusion of recommendations, which mirror in their complexity and contradictions the endless stories of new and often esoteric causes of cancer

Then there is the attitude of “there’s not much I can do to prevent cancer” which is in part due to recent articles claiming that “most cancers are due to genetic bad luck.”

What happens is that people skip over the part about screening, they skip over the part about those cancers that are affected by environmental factors (and they will not be aware of flaws in the interpretation of the study), and they will shrug their shoulders, smoke that cigarette while eating a deep-fried Twinkie and trust in their “good luck.” This is of course inconsistent with the “everything in the environment causes cancer” idea, but then this is the problem – extremes of opinion in one direction or another.

This has real-life consequences, such as lower levels of colon cancer screening, and, likely, continued bad health habits. And I believe this not only applies to cancer, but other problems as well: obesity, diabetes, etc. Human nature is to avoid thinking about potential bad news and to avoid hearing things that may be unpleasant or which go against currently held beliefs or which might result in undesired changes in habits (change in diet, exercise, etc.). Therefore, the scientific, medical, and media communities need to be cognizant of this, and to present to the public solidly documented and easy-to-understand pieces of information, particularly those that concentrate on major risk factors, and which avoid sensationalism for its own sake and large amounts of background “noise” static obscuring the most important messages about health and cancer risk.