scholarly journals Physical activity and cancer risk

2001 ◽  
Vol 60 (1) ◽  
pp. 107-113 ◽  
Author(s):  
Adrianne E. Hardman

Evidence is accumulating that high levels of physical activity are associated with a reduced risk of some cancers. This evidence is most consistent for colon cancer, which is reduced by 40–50 % among the most active individuals, compared with the least active. The effect is evident in men and women, and appears to be independent of important confounding factors. However, there may be important interactions with body fatness; a high BMI has been reported to be associated with an increased risk of colon cancer in sedentary men but not in physically-active men. Whilst the evidence on breast cancer is less consistent, case–control studies typically suggest a reduction of 25–30 % among the most active women, although several studies have found no effect. Potential mechanisms include systemic influences and others relevant only to site-specific cancers. One unifying hypothesis is that physical inactivity reduces insulin sensitivity, leading to a growth-promotional environment which may facilitate neoplasia. The non-specific immune system may be improved by physical activity, possibly through the summative effects of repeated exercise bouts. Regular exercise, even at a recreational level, probably reduces exposure to oestrogen and thus decreases the risk of breast cancer. Increased colonic peristalsis, and thus reduced bowel transit time, might partly explain the lower risk of colon cancer in active people. Physical activity emerges as one of the few modifiable risk factors for some cancers and, as such, justifies further study.

Author(s):  
Shuwaathi Thamil Manni ◽  
Amuthaganesh Mathialagan ◽  
Kanakeswary Karisnan ◽  
Calvin P. Noris

Physical activity (PA) and metabolic syndrome (MetS) have emerged as crucial factors in facilitating the incidence of postmenopausal (PM) breast cancer (BC). The association of PA, MetS and its components with PM BC was explored in this study. PRISMA guideline was followed and online databases were searched comprehensively to find relevant cohort and case-control studies until 18 February 2021 using keywords such as “physical activity”, “metabolic syndrome” and “breast cancer”. Eligible studies evaluating BC in postmenopausal women with a clear definition and measure of PA, MetS and its individual components were selected. A total of twenty-three articles related to PA and fifteen articles for MetS met the eligibility criteria and were assessed thoroughly. PA and MetS were significantly associated with PM BC. There was evidence of dose-response effect of PA and Mets on PM BC. Obesity, diabetes and dyslipidaemia were independently associated with PM BC and posed an increased risk on PM BC whereas the association of HPTN with PM BC was not prominent. Consistent and sustained long term PA throughout one’s lifetime was observed to decrease PM BC risk whereas increasing number of MetS components increased the risk of PM BC. Routine screening for PM women with ≥2 MetS components and obese or overweight women with any of the MetS components may be beneficial in early BC detection. Lifestyle modifications with emphasis on long term PA would be beneficial to public health in preventing and improving MetS outcomes as well as a primary prevention of sporadic PM BC.


2019 ◽  
Vol 78 (1) ◽  
pp. 1-18 ◽  
Author(s):  
Khemayanto Hidayat ◽  
Hui-Juan Zhou ◽  
Bi-Min Shi

Abstract Context Excess weight has been linked to increased risks of 13 types of cancers. Physical activity is a non-nutritional modifiable lifestyle factor that is not only crucial for weight control but is also known to regulate hormones and metabolic pathways that may contribute to carcinogenesis. There is solid evidence that being physically active during middle and late adulthood lowers the risks of 3 obesity-related cancers, namely breast cancer, colon cancer, and endometrial cancer. However, the associations between physical activity at a young age (childhood, adolescence, and young adulthood; age 5 to ≤30 yr) and lifetime physical activity and the risks of breast cancer, colon cancer, and endometrial cancer are less defined. Objective The present systematic review and meta-analysis of observational studies was performed in accordance with the MOOSE guidelines to determine whether physical activity at a young age and lifetime physical activity may lower the risks of breast cancer, colon cancer, and endometrial cancer. Data sources The PubMed and Web of Science databases were searched for relevant observational studies published from inception to July 2018. Study selection Observational studies (prospective cohort, case-cohort, nested case-control, historical cohort, and case-control) were considered relevant if they investigated the association between physical activity at a young age or lifetime physical activity and the risks of developing selected cancers. Data extraction A random-effects meta-analysis was performed to generate the summary relative risk (RR) with 95%CI for the highest vs the lowest category of physical activity of any type. Results Eighty publications were included in the present meta-analysis. Higher physical activity at a young age was associated with lower risks of breast cancer (RR 0.81, 95%CI 0.76, 0.87) and colon cancer (RR 0.67, 95%CI 0.50, 0.88). Similarly, lifetime physical activity was inversely associated with the risks of breast cancer (RR 0.79, 95%CI 0.72, 0.86) and colon cancer (RR 0.75, 95%CI 0.69, 0.82). For breast cancer, menopausal status did not appear to modify the observed inverse association. The benefit with respect to endometrial cancer risk reduction was only observed with higher lifetime physical activity (RR 0.77, 95%CI 0.67, 0.88), not with higher physical activity at a young age (RR 0.89, 95%CI 0.73, 1.07). Conclusions Being physically active over a lifetime, starting from early childhood, may lower the risks of developing breast cancer, colon cancer, and endometrial cancer.


2020 ◽  
Vol 11 (SPL1) ◽  
pp. 934-937
Author(s):  
Tasneem M. Lakkadsha ◽  
Kiran Kumar ◽  
Waqar M. Naqvi ◽  
Pratik Phansopkar

In January 2020, we met with COVID-19 (aka SARS-Co-V-2 and/or Corona virus) on our news channels all the way from china. Little did we know that it would shake up our lives in such a manner that we had heard only in a movie or read in history books. Currently we are all in some sort of lockdown, be it in hospital/home or in our minds. Being there, most of us are facing certain kind of misery, be it emotional, mental, physical or social. To be expansive the most common stresses that have been addressed by people on mass media platform are feeling of depression and isolation caused by being away from family and friends, some are complaining of losing their enthusiasm, some of gaining weight, some of losing it and many more. Going through a pandemic is also helping people in some or the other way, one of which is being concerned about their health and habits to keep themselves fit and away from serious comorbidities which can stem out from physical inactivity and heightened stress levels. There are many ways to stay fit at home without any complex gym equipment, but far less is known about it. Thus, an understanding of methods through which one can become physically active with least complexity, easy availability, and appropriate utilization is need of the hour.


Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1378
Author(s):  
Tú Nguyen-Dumont ◽  
James G. Dowty ◽  
Jason A. Steen ◽  
Anne-Laure Renault ◽  
Fleur Hammet ◽  
...  

Case-control studies of breast cancer have consistently shown that pathogenic variants in CHEK2 are associated with about a 3-fold increased risk of breast cancer. Information about the recurrent protein-truncating variant CHEK2 c.1100delC dominates this estimate. There have been no formal estimates of age-specific cumulative risk of breast cancer for all CHEK2 pathogenic (including likely pathogenic) variants combined. We conducted a population-based case-control-family study of pathogenic CHEK2 variants (26 families, 1071 relatives) and estimated the age-specific cumulative risk of breast cancer using segregation analysis. The estimated hazard ratio for carriers of pathogenic CHEK2 variants (combined) was 4.9 (95% CI 2.5–9.5) relative to non-carriers. The HR for carriers of the CHEK2 c.1100delC variant was estimated to be 3.5 (95% CI 1.02–11.6) and the HR for carriers of all other CHEK2 variants combined was estimated to be 5.7 (95% CI 2.5–12.9). The age-specific cumulative risk of breast cancer was estimated to be 18% (95% CI 11–30%) and 33% (95% CI 21–48%) to age 60 and 80 years, respectively. These findings provide important information for the clinical management of breast cancer risk for women carrying pathogenic variants in CHEK2.


2021 ◽  
Vol 118 (50) ◽  
pp. e2107621118
Author(s):  
Daniel E. Lieberman ◽  
Timothy M. Kistner ◽  
Daniel Richard ◽  
I-Min Lee ◽  
Aaron L. Baggish

The proximate mechanisms by which physical activity (PA) slows senescence and decreases morbidity and mortality have been extensively documented. However, we lack an ultimate, evolutionary explanation for why lifelong PA, particularly during middle and older age, promotes health. As the growing worldwide epidemic of physical inactivity accelerates the prevalence of noncommunicable diseases among aging populations, integrating evolutionary and biomedical perspectives can foster new insights into how and why lifelong PA helps preserve health and extend lifespans. Building on previous life-history research, we assess the evidence that humans were selected not just to live several decades after they cease reproducing but also to be moderately physically active during those postreproductive years. We next review the longstanding hypothesis that PA promotes health by allocating energy away from potentially harmful overinvestments in fat storage and reproductive tissues and propose the novel hypothesis that PA also stimulates energy allocation toward repair and maintenance processes. We hypothesize that selection in humans for lifelong PA, including during postreproductive years to provision offspring, promoted selection for both energy allocation pathways which synergistically slow senescence and reduce vulnerability to many forms of chronic diseases. As a result, extended human healthspans and lifespans are both a cause and an effect of habitual PA, helping explain why lack of lifelong PA in humans can increase disease risk and reduce longevity.


2020 ◽  
Vol 7 (1) ◽  
pp. e000413
Author(s):  
Kasper Adelborg ◽  
Dóra Körmendiné Farkas ◽  
Jens Sundbøll ◽  
Lidia Schapira ◽  
Suzanne Tamang ◽  
...  

ObjectiveWe examined the risk of primary gastrointestinal cancers in women with breast cancer and compared this risk with that of the general population.DesignUsing population-based Danish registries, we conducted a cohort study of women with incident non-metastatic breast cancer (1990–2017). We computed cumulative cancer incidences and standardised incidence ratios (SIRs).ResultsAmong 84 972 patients with breast cancer, we observed 2340 gastrointestinal cancers. After 20 years of follow-up, the cumulative incidence of gastrointestinal cancers was 4%, driven mainly by colon cancers. Only risk of stomach cancer was continually increased beyond 1 year following breast cancer. The SIR for colon cancer was neutral during 2–5 years of follow-up and approximately 1.2-fold increased thereafter. For cancer of the oesophagus, the SIR was increased only during 6–10 years. There was a weak association with pancreas cancer beyond 10 years. Between 1990–2006 and 2007–2017, the 1–10 years SIR estimate decreased and reached unity for upper gastrointestinal cancers (oesophagus, stomach, and small intestine). For lower gastrointestinal cancers (colon, rectum, and anal canal), the SIR estimate was increased only after 2007. No temporal effects were observed for the remaining gastrointestinal cancers. Treatment effects were negligible.ConclusionBreast cancer survivors were at increased risk of oesophagus and stomach cancer, but only before 2007. The risk of colon cancer was increased, but only after 2007.


Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5654
Author(s):  
Agnieszka Barańska ◽  
Agata Błaszczuk ◽  
Wiesław Kanadys ◽  
Maria Malm ◽  
Katarzyna Drop ◽  
...  

To perform a meta-analysis of case-control studies that addressed the association between oral contraceptive pills (OC) use and breast cancer (BrCa), PubMED (MEDLINE), Embase, and the Cochrane Library were searched to identify case-control studies of OC and BrCa published between 2009 and 2020. We used the DerSimonian–Laird method to compute pooled odds ratios (ORs) and confidence intervals (CIs), and the Mantel–Haenszel test to assess the association between OC use and cancer. Forty-two studies were identified that met the inclusion criteria and we included a total of 110,580 women (30,778 into the BrCa group and 79,802 into the control group, of which 15,722 and 38,334 were using OC, respectively). The conducted meta-analysis showed that the use of OC was associated with a significantly increased risk of BrCa in general, OR = 1.15, 95% CI: 1.01 to 1.31, p = 0.0358. Regarding other risk factors for BrCa, we found that increased risk was associated significantly with early menarche, nulliparous, non-breastfeeding, older age at first parity, postmenopause, obesity, smoking, and family history of BrCa. Despite our conclusion that birth control pills increase the cancer risk being supported by extensive previous studies and meta-analyzes, further confirmation is required.


2009 ◽  
Vol 9 (1) ◽  
Author(s):  
Larissa A Korde ◽  
Amy Micheli ◽  
Ashley W Smith ◽  
David Venzon ◽  
Sheila A Prindiville ◽  
...  

2007 ◽  
Vol 28 (2) ◽  
pp. 146-157 ◽  
Author(s):  
Frank W. Booth ◽  
Simon J. Lees

Currently our society is faced with the challenge of understanding the biological basis for the epidemics of obesity and many chronic diseases, including Type 2 diabetes. Physical inactivity increases the relative risk of coronary artery disease by 45%, stroke by 60%, hypertension by 30%, and osteoporosis by 59%. Moreover, physical inactivity is cited as an actual cause of chronic disease by the US Centers of Disease Control. Physical activity was obligatory for survival for the Homo genus for hundreds of thousands of years. This review will present evidence that suggests that metabolic pathways selected during the evolution of the human genome are inevitably linked to physical activity. Furthermore, as with many other environmental interactions, cycles of physical activity and inactivity interact with genes resulting in a functional outcome appropriate for the environment. However, as humans are less physically active, there is a maladaptive response that leads to metabolic dysfunction and many chronic diseases. How and why these interactions occur are fundamental questions in biology. Finally, a perspective to future research in physical inactivity-gene interaction is presented. This information is necessary to provide the molecular evidence required to further promote the primary prevention of chronic diseases through physical activity, identify those molecules that will allow early disease detection, and provide society with the molecular information needed to counter the current strategy of adding physical inactivity into our lives.


2004 ◽  
Vol 29 (4) ◽  
pp. 447-460 ◽  
Author(s):  
Simon J. Lees ◽  
Frank W. Booth

Sedentary death syndrome (SeDS) is a major public health burden due to its causing multiple chronic diseases and millions of premature deaths each year. Despite the impact of physical inactivity, very little is known about the actual causes of physical inactivity-induced chronic diseases. It is important to study the mechanisms underlying molecular changes related to physical inactivity in order to better understand the scientific basis of individualized exercise prescription and the rapies for chronic diseases, and to support improved public health efforts by providing molecular proof that physical inactivity is an actual cause of chronic diseases. Physical activity has a genetic basis. A subpopulation of genes, which have functioned to support physical activity for survival through most of humankind's existence, require daily exercise to maintain long-term health and vitality. Type 2 diabetes (T2D) is an example of a SeDS condition, as it is almost entirely preventable with physical activity. To determine the true role of physical inactivity in the development and progression of T2D, information is presented which indicates that comparisons should be made to physically active controls, rather than sedentary controls, as this population is the healthiest. Use of sedentary subjects as the control group has led to potentially misleading interpretations. If physically active individuals were designated as the control group, a different interpretation would have been drawn. It is thought that there is no difference in GLUT4 concentration between T2D and sedentary groups. However, GLUT4 expression is higher in active controls than in sedentary and T2D groups. Therefore, to obtain causal mechanisms for SeDS in order to allow for scientifically based prevention and therapy strategies, physically active subjects must serve as the control group. Key words: physical inactivity, chronic diseases, diabetes, glucose


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