Don’t keep still – cutting your cancer risk – a brief paper explaining what is far more than just an exercise issue.

By Dr Chris Barnes, Manager Bangor Scientific and Educational Consultants, June 2017, e-mail, manager@bsec-wales.co.uk

Introduction

It has long been established that exercise reduces the risk of heart disease (http://circ.ahajournals.org/content/107/24/3109.short) and type 2 diabetes https://link.springer.com/article/10.1007/BF00400196

More recently it has been established that a sedentary life style increases the risk of certain cancers (Schmidt et al 2014) and that the converse is true.

However, when we examine the in detail time, place and situation with regard to sedentary risk, we find that some situations such as watching television, for example, are more risky than others.

The other place where we are relatively still for long periods , other than for making involuntary movements is in our beds. It has recently been established that in adults sleeping too long i.e. greater than about 8.5 hours for adults is as much associated with mortality as is sleeping too short a time i.e. less than about 6 hours.

The purpose of this paper is twofold. Firstly to explore in terms of mortality or especially cancer aetiology if there are links between being sedentary in the wakeful state and spending too long in bed. Further and secondly to establish if the place where exercise is taken is significant. I will show that moving around reduces cancer risk but for far more than just exercise reasons alone.

Being sedentary and Cancer Risk a short review

Sturgeon et al 2017 have showed that Physical activity induced protection against breast cancer risk associated with delayed parity mainly as a result of changes in breast structure and reduced inflammation. Lope at al 2016 showed:

Physical activity protects against pre and postmenopausal breast cancer.

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Physical activity protects against all pathologic breast cancer subtypes.

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Women who comply with international recommendations have lower breast cancer risk.

Borch et al 2017 showed in a nationally representative cohort that 21.9% of endometrial cancers could potentially be avoided if physical activity levels were increased.

Dethlefsen et al 2017 showed cumulative epidemiological evidence shows that regular exercise lowers the risk of developing breast cancer and decreases the risk of disease recurrence. Interestingly they state that the causality underlying this relation has not been fully established.

Colon cancer and breast cancer are among the most commonly diagnosed cancers in the United States, and exercise appears to significantly reduce the risk of both. Physical activity has been linked with a 40 to 50 percent reduction in the risk of developing colon cancer and a 30 to 40 percent reduction in the risk developing breast cancer.2 Risk of other cancers may be reduced by exercise as well, but studies of other cancers have produced less consistent results, see Kari Bohlke, ScD (2006).tv viewing

Johnsson et al (2016) found that occupational sedentariness was associated with increased breast cancer risk, especially in women younger than 55 years. This may be a modifiable risk factor by planning breaks during the working day, adjusted HR 1.20; 95% CI 1.05, 1.37.

Cannioto et al (2017) found using multivariable logistic regression models, we observed significant positive associations between lifetime recreational physical inactivity and renal cancer and bladder cancer risk: odds ratio = 1.77 (95% CI: 1.10–2.85) and odds ratio = 1.73 (95% CI: 1.13–2.63), respectively. Similar associations also persisted among individuals who were not obese for both renal and bladder cancer: odds ratio = 1.75 (95% CI: 1.03–2.98) and odds ratio = 1.70 (95% CI: 1.08–2.69), respectively.

Mendelson et al 2017 present robust associations of BMI with differential DNA methylation at numerous loci in blood cells. BMI-related DNA methylation and gene expression provide mechanistic insights into the relationship between DNA methylation, obesity, and adiposity-related diseases. Gastric cancer ( Pinni et al), Liver Cancer, Hlady et al (2017) and Melanoma (Shen et al) 2017 have all been shown to be associated with global DNA methylation. Mokkarum et al (2017) concluded that exposure to RF radiation emitted by GSM mobile phones can lead to epigenetic detrimental changes in ERα promoter methylation pattern.

Manser et al (2017) conclude that ELF-MF exposure may influence the robustness of histone modification and DNA methylation patterning in the course of the global chromatin reorganization associated with neutrophilic differentiation.

Miousse (2017) reiterates Ionizing radiation (IR) is a ubiquitous environmental stressor with genotoxic and epigenotoxic capabilities. The more we are sedentary the more chance we have been exposed to radon concentrated in our homes or by electric fields from monitors and TV sets for example.

I have showed recently the dangers of TV viewing and separated out the risk factors (ref). Grace (2017) essentially support my findings and show that TV time was associated with increased risk of inflammatory-related mortality. This is consistent with the hypothesis that high TV viewing may be associated with a chronic inflammatory state. In Brazil Turi et al (2017) the higher TV viewing time was associated with a 44.7% increase in all-cause mortality (HR=1.447 [1.019-2.055]), independently of other potential confounders. In conclusion, the findings from this cohort study identified increased risk of mortality among adults with higher TV viewing time, independently of PA and other variables.

Contrary to findings from previous research (based on self-reported physical activity), cancer survivors engaged in more (breast) or equivalent (colon) MVPA compared with adults without cancer. Differences between colon cancer survivors and adults without cancer for light activity and sedentary behaviour highlight the importance of considering the full activity spectrum in the context of cancer control, see Shi et al (2016).

Conclusions in sedentary risks.

1. Sedentary lifestyle leads to obesity hence increased global DNA methylation, inflammation and cancer. https://www.ncbi.nlm.nih.gov/pubmed/24935969

2. However, in the modern environment there are confounding factors.

3. For instance, it is more risky to be sedentary and a TV viewer, due to concentration of radon (ref) , atmospheric pollutants (ref) and light at night exposure. http://drchrisbarnes.co.uk/TVCAN.htm

4. It is more risky to be sedentary in radio frequency fields of certain frequencies (http://drchrisbarnes.co.uk/Freqsol01.htm) and at certain distances from transmitting antennas (http://drchrisbarnes.co.uk/More%20egg%20than%20chicken.html).

5. Such environmental changes over the past 5-6 decades probably help explain the explosion in cancer rates, including melanoma, which apart from those in the minority with a certain phenotype and extremely fair non-tanning skin is not predominantly an issue to do with the sun.

6. Exercise, particularly green exercise is extremely good for us but here I have shown this is not simply due to a matter of weight loss reducing risk. It also removes us from sources of internal pollution and disrupts the possibility of time and position coherent wave interaction in ubiquitous ever present RF fields.

7. Outdoor exercise also provides sun exposure / vitamin D3 which further helps reduces most cancer risks.

Sleep time and Cancer Risks a short review.

Devore et al (2017 ) produced the following results and conclusions.

Results: Higher urinary melatonin levels were suggestively associated with a lower overall risk of breast cancer (multivariable-adjusted RR = 0.78; 95% CI = 0.61–0.99, comparing quartile 4 vs. quartile 1; Ptrend = 0.08); this association was similar for invasive vs. in situ tumors (Pheterogeneity = 0.12). There was no evidence that associations differed according to MT1R status of the tumor (e.g., Pheterogeneity for overall breast cancer = 0.88).

Conclusions: Higher urinary melatonin levels were associated with reduced breast cancer risk in this cohort of postmenopausal women, and the association was not modified by MT1R subtype.

Wu ET AL (2008) showed that Melatonin levels were 42% higher in those with 9+ versus those with ≤6 h of sleep. Conclusion: Sleep duration may influence breast cancer risk, possibly via its effect on melatonin levels. Blask 2008 concluded that the mutual reinforcement of interacting circadian rhythms of melatonin production, the sleep/wake cycle and immune function may indicate a new role for undisturbed, high quality sleep, and perhaps even more importantly, uninterrupted darkness, as a previously unappreciated endogenous mechanism of cancer prevention. The data of Tamarkin (1982) suggest data suggest that low nocturnal melatonin concentrations may indicate the presence of oestrogen receptor positive breast cancer and could conceivably have etiologic significance.

Theoretically then one should expect the longer the sleep duration the less the odds of cancer, particularly hormone related cancers. In practice and especially in the majority of later studies a somewhat unexpected result is found wherein there is a J or U shaped relationship between sleep time and cancer risk, general mortality risk, type II diabetes risk and the like.

Lui et al 2016 considered sleep duration and risk of all-cause mortality using a flexible, non-linear, meta-regression of 40 prospective cohort studies enrolling an enormous 2,200,425 participants with 271,507 deaths. They deduced that approximately 27–37% of the general population experience prolonged sleep duration and 12–16% report shortened sleep duration. However, prolonged or shortened sleep duration may be associated with serious health problems. Lowest risk was associated with 8h sleep increasing risk was reported for less sleep down to 4h and significantly increased risk for extended sleep up to 12h. Their conclusions are essentially similar to the much earlier work of Kripke et al (1979) where prospective epidemiologic data of the American Cancer Society disclosed that reported usual sleep durations among groups who complained of insomnia and sleeping pill use "often" overlapped with those of groups who had no complaints. Reports of insomnia were not consistently associated with increased mortality when several factors were controlled; however, men who reported usually sleeping less than four hours were 2.80 times as likely to have died within six years as men who reported 7.0 to 7.9 hours of sleep. The ratio for women was 1.4.8. Men and women who reported sleeping ten hours or more had about 1.8 times the mortality of those who reported 7.0 to 7.9 hours of sleep. Those who reported using sleeping pills "often" had 1.5 times the mortality of those who "never" used sleeping pills.

Wong et al (2017) showed that compared with sleeping 8 hours/day on average, ≤7 hours/day was associated with significantly increased HRs ranging from 1.39 to 1.58 in ages ≥41 years in men, and 1.29 to 2.47 in ages ≥51 years in women. Furthermore, sleeping ≥10 hours/day was associated with significantly increased HRs ranging from 2.44 to 3.27 in ages ≥41 year in men, and 1.31 to 2.45 in ages ≤60 years in women. Greater and less than 8 hours/day of sleep in various age-periods may be associated with elevated risk of lung cancer mortality in Xuanwei, China. Cancer Prev Res; 1–9.

Yaggi et al (2006) showed that Men reporting short sleep duration (≤5 and 6 h of sleep per night) were twice as likely to develop diabetes, and men reporting long sleep duration (>8 h of sleep per night) were more than three times as likely to develop diabetes over the period of follow-up. Elevated risks remained essentially unchanged after adjustment for age, hypertension, smoking status, self-rated health status, education, and waist circumference (RR 1.95 [95% CI 0.95–4.01] for ≤5 h and 3.12 [1.53–6.37] for >8 h). RRs were altered considerably for the two extreme sleep groups when adjusted for testosterone (1.51 [0.71–3.19] for ≤5 h and 2.81 [1.34–5.90] for >8 h), suggesting that the effects of sleep on diabetes could be mediated via changes in endogenous testosterone levels.

Patel et al ( ) has suggested depression and low socioeconomic status are strong candidates for producing the statistical association between long sleep and mortality, either as confounders or as causal intermediates. Their conclusion is also that future causal research on the effects of long sleep should include a detailed assessment of psychiatric disease and socioeconomic status. Both factors have also been associated with obesity/large BMI and to reiterate, Mendelson et al 2017 present robust associations of BMI with differential DNA methylation at numerous loci in blood cells. And of course global DNA methylation is also associated with ageing and cancer.

We can this begin to see the link between cancer and sedentary life style and cancer and excess sleep. All the more reason not to keep still!

The question arises, however, could there be another confounding factor related to increased cancer risk with time spent in bed? Hallberg and Johansson (2010) in their paper ‘Sleep on the right side—Get cancer on the left?’ explain the prevalence of left sided melanoma in parts of the body never exposed to the sun and explain the prevalence of left sided breast cancer in both men and women in terms of the effects of 90MHz RF fields from FM broadcasting and their interaction with mattress springs and the body.

Conclusions in sleep time effects

1. Cancer risk increases at below 7-8 h sleep due to low melatonin.

2. Cancer risk increases over 8 h sleep for multiple reasons including inactivity/high BMI and RF field exposure.

Further discussion: move around to cut cancer risk the connection with RF FIELDS and quantum biology.

Sedentary occupations and excessive sleep both increase cancer risk due inter alia to bio –soliton interaction with RF fields. Such interaction can only maximise in an adverse manner over sufficient coherence time and at certain frequencies and modulation frequencies. Information is carried by the modulation in a radio wave and according to my previous calculations I would expect energy dumping into biological tissue i.e. humans in houses at key distances from transmitters according to the electromagnetic Aharonov-Bohm effect (Puthoff 1998 and Fang et al 2013). Thus it is crucial not to stay at home all day if one lives at such a key distance. Even in today’s equal society there are still marginally more stay at home women. Guo et al (2004) calculate the lifetime cancer risk to be maximum for stay at home women/housewives on the basis of VOC exposure but I would argue that RF radiation is a strongly confounding factor. Although specifically for lung cancer, every 10 μg/m3 increase in PM1 is associated with 45 % increased risk, see Mu et al (2013).

In quantum biologically, interaction frequency and energy matching and space-time coherence is critical. This explains why for example occasional exposure to very high level RF fields do not have the same biological effect as longer term exposure to weak time varying fields. For instance the body/brain is tuned to the tiny energy fields associated with Schumann resonance. I have discussed exact interaction frequencies elsewhere and a detailed understanding of these is not required here.

Overall the key to staying safer and minimising risk is movement, having multiple work and sleep locations and lots of green exercise. Various antioxidants have been reckoned to reduce the effects of RF radiation but the only very common compounds known to reduce global DNA methylation are vitamin C and Turmeric both of which I recommend.

Final conclusions

Exercise, especially green or outdoor (walking, running or cycling) exercise, has been shown by others to be the finest way to cut one’s cancer risk but shown to be confounded here are some quite unexpected reasons for its efficacy. It removes us from household radon, VOC’S and coherent RF fields. All of which we are exposed to while sitting sedentary or spending too much time in bed.