Frank’s essay contains several statements about 5G, its relation to the radiation protection science, and related to this, ICNIRP’s guidance and integrity more generally. ICNIRP considers this to be seriously inaccurate and in need of correction for the sake of both scientific accuracy and development of effective public health policy. However, due to journal word limits we must restrict our response to Frank’s misleading claims about ICNIRP’s integrity (for full response see https://www.icnirp.org/en/activities/news/index.html).

Frank’s essay accuses ICNIRP of unmanaged conflict of interests, and uses this accusation to attempt to throw doubt on ICNIRP’s scientific evaluations. However, ICNIRP has a very rigorous procedure to avoid conflicts of interest (https://www.icnirp.org/en/about-icnirp/commission/index.html), and Frank did not provide any evidence in support of his statement - he merely referred to ‘persistent allegations’ from the Swedish epidemiologist Lennart Hardell. For example, Frank repeats claims made by Hardell that “ICNIRP’s membership includes over-representation of vested interests, especially the giant multinational telecommunications firms who are heavily invested in the roll out of 5G systems internationally”, and no supporting evidence was provided by either author. To be clear, there are no industry representations within ICNIRP; people working for industry are not permitted to be ICNIRP members, and ICNIRP does not receive any funding or in-kind contributions from industry. Moving beyond funding, Frank claims that the “the most damning evidence adduced by Hardell is a table of the cross-appointments held by six members of the WHO Monograph Group, across five major international advisory panels on the health effects of non-ionising radiation”. However, this merely reflects the relatively small EMF research community together with the high public interest that has resulted in many national and international advisory boards. Frank does not tell the reader why this would in any way bias ICNIRP’s work. Thus, the essay’s accusations of industry influence are not only incorrect, but also lack appropriate scientific scholarship.

In conclusion, ICNIRP fully supports and contributes to critical debate related to the 5G rollout, but would like to stress the importance of approaching such debate with appropriate scientific scholarship in order to support effective, evidence-based public health measures that provide appropriate protection to the public. For ICNIRP it is imperative to avoid situations whereby personal interests of its members could affect the independence of ICNIRP’s guidance, and so has strong conflict of interest procedures, including transparent reporting of members’ declarations of interest.

Acknowledgements
Rodney Croft (1), Tania Cestari (2), Nigel Cridland (3), Akimasa Hirata (4), Guglielmo d'Inzeo (5), Anke Huss (6), Ken Karipidis (7), Carmela Marino (8), Sharon Miller (9), Gunnhild Oftedal (10), Tsutomu Okuno (11), Eric van Rongen (12), Martin Röösli (13), Soichi Watanabe (14).

Correspondence to: International Commission on Non-Ionizing Radiation Protection, Dr Gunde Ziegelberger, ICNIRP c/o BfS, Ingolstaedter Landstr. 1, 85764 Oberschleissheim, Germany. info@icnirp.org

Conflicts of Interest
The authors declare no Conflicts of Interest. Further details are available at https://www.icnirp.org/en/about-icnirp/commission/index.html.

References
None

Affiliations of ICNIRP Collaborators
1. ICNIRP and Australian Centre for Electromagnetic Bioeffects Research, Illawarra Health & Medical Research Institute, University of Wollongong, Australia
2. ICNIRP and Hospital de Clínicas de Porto Alegre, Brazil
3. ICNIRP and Public Health England, United Kingdom
4. ICNIRP and Nagoya Institute of Technology, Japan
5. ICNIRP and La Sapienza University Rome, Italy
6. ICNIRP and Institute for Risk Assessment, Utrecht University, The Netherlands
7. ICNIRP and Australian Radiation Protection and Nuclear Safety Agency (ARPANSA), Australia
8. ICNIRP and Agency for New Technologies, Energy and Sustainable Economic Development (ENEA), Italy
9. ICNIRP
10. ICNIRP and Norwegian University of Science and Technology (NTNU), Norway
11. ICNIRP
12. ICNIRP and Health Council, The Netherlands
13. ICNIRP and Swiss Tropical and Public Health Institute, Basel, Switzerland
14. ICNIRP and National Institute of Information and Communications Technology (NICT), Japan

The question “Why does Russia have such high cardiovascular (CV) mortality rates?”1 can be answered by a pathologist who practiced during the Soviet time.2 Since then, the quality of post mortem examinations has decreased especially during the 1990s: autopsies were sometimes made perfunctorily. The deterioration in anatomic pathology and the health care in general during the 1990s coincided with the increase in the registered CV mortality. A tendency to over-diagnose CV diseases is generally known to exist also for people dying at home and not undergoing autopsy. If a cause of death is not entirely clear, it has been usual to write on a death certificate: “Ischemic heart disease with cardiac insufficiency” or a similar formulation.2 Concerning the relatively high CV mortality in Russia, it should be commented that irregular treatment of hypertension,3 diabetes and other chronic diseases continues to be a problem. Considering the above, the differences between Norwegian and Russian cohorts1 can be better understood. The levels of serum lipids were comparable between Russia and Norway being slightly higher in the latter possibly due to better nutrition. Interestingly, N-terminal pro-b-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hs-cTnT), and high-sensitivity C-reactive protein (hsCRP) were higher in Russia.1 It can be reasonably assumed that average levels of these markers inversely correlate with a nation’s health reflected by the life expectancy at birth. Indeed, elevated C-reactive protein is known to be associated with various inflammatory conditions. The natriuretic peptide (NP) plays an important role by opposing the vasoconstriction and sodium retention. A plasma NP elevation was found in essential hypertension, decreasing with effective antihypertensive therapy.4 Hs-cTnT is a biomarker for myocardial damage; but other conditions are also associated with its enhanced level: diabetes, COPD, decreased renal function, anaemia etc.5 The insufficient access to modern healthcare,1 higher consumption of alcohol and cigarettes in Russia vs. Norway (the data can be found in Wikipedia), as well as relatively poor quality of alcohol sold in Russia,6 have probably contributed to a higher morbidity. In conclusion, the valuable results by Dr. Iakunchykova and co-workers1 should motivate further search for associations between NT-proBNP, hs-cTnT and other markers with various pathological conditions.
REFERENCES
1. Iakunchykova O, Averina M, Wilsgaard T, et al. Why does Russia have such high cardiovascular mortality rates? Comparisons of blood–based biomarkers with Norway implicate non-ischaemic cardiac damage. J Epidemiol Community Health 2020;74:698–704.
2. Jargin SV. Cardiovascular mortality trends in Russia: possible mechanisms. Nat Rev Cardiol 2015;12:740.
3. Roberts B, Stickley A, Balabanova D, et al. The persistence of irregular treatment of hypertension in the former Soviet Union. J Epidemiol Community Health 2012;66:1079–82.
4. Hu W, Zhou PH, Zhang XB, Xu CG, Wang W. Plasma concentrations of adrenomedullin and natriuretic peptides in patients with essential hypertension. Exp Ther Med 2015;9:1901–908.
5. Wu W, Li DX, Wang Q, et al. Relationship between high-sensitivity cardiac troponin T and the prognosis of elderly inpatients with non-acute coronary syndromes. Clin Interv Aging 2018;13:1091–8.
6. Jargin SV. Vodka vs. Fortified Wine in Russia: Retrospective View. Alcohol Alcohol 2015;50:624–5.

We read with great interest the report from Hamer and colleagues that examined the hypothesis that associations between television (TV) viewing and mortality from heart disease (HD) are due to confounding (1). They employed a negative control approach (2) and report evidence of associations between TV viewing and HD mortality (HR=1.09 [1.06, 1.12] per 1 hr/day increase in TV) and accidental deaths (the negative control outcome; HR=1.06 [0.98, 1.15]) after adjusting for age, sex, smoking, education, and prevalent HD (1)

The positive association between TV and accidental deaths was interpreted as evidence that the TV-HD mortality association was due to confounding. Although key study limitations were noted including a small number of accidental deaths and limited adjustment for confounding, the authors concluded that “observed associations between TV and HD are likely to be driven by confounding”. Although we agree that confounding is a worrisome threat to the internal validity of epidemiologic studies, we believe that the conclusion in the Hamer report is overstated.

A critical additional strategy to understand bias due to confounding, one that was not employed in the current study, is to examine relevant results from published studies conducted in different study populations using different methods. (2) We previously reported results in two studies that examined associations for accidental deaths and HD mortality with TV viewing (3) and leisure-time sitting (predominantly TV viewing) (4), but these findings were not cited in the Hamer report. Our studies each examined 3-5 times more accidental deaths than the Hamer report, and adjusted for a much larger number of confounding factors. (3,4) We found significant positive associations with TV-HD mortality, but no evidence of association between accidental deaths and greater TV time (HR=1.01 [0.62, 1.64]; 7+ vs. < 1 hr/day) (3) or leisure-time sitting (HR=0.91 [0.76, 1.10]; 6+ vs. < 3 hr/d). (4) In context of the negative control outcome framework, our results provide no evidence that previously observed HD associations, or associations with several other causes of death, were due only to confounding. (3,4)

Many studies have reported positive associations between disease/mortality outcomes and TV, a prevalent leisure-time behavior that, as Hamer and colleagues note, is likely to displace time spent in more healthful physically active pursuits. We strongly support efforts to better understand these relationships, including careful consideration of bias and threats to validity. As we do so, it is critical that we consider the broad range of information available before drawing strong conclusions based on a single study.

References

1. Hamer M, Ding D, Chau J, Duncan MJ, Stamatakis E. Association between TV viewing and heart disease mortality: observational study using negative control outcome. Journal of Epidemiology and Community Health. 2020:jech-2019-212739.
2. Pearce N, Vandenbroucke JP, Lawlor DA. Causal Inference in Environmental Epidemiology: Old and New Approaches. Epidemiology. 2019;30(3):311-316.
3. Keadle SK, Moore SC, Sampson JN, Xiao Q, Albanes D, Matthews CE. Causes of Death Associated With Prolonged TV Viewing: NIH-AARP Diet and Health Study. American Journal of Preventive Medicine. 2015;49(6):811-821.
4. Patel AV, Maliniak ML, Rees-Punia E, Matthews CE, Gapstur SM. Prolonged Leisure Time Spent Sitting in Relation to Cause-Specific Mortality in a Large US Cohort. American Journal of Epidemiology. 2018;187(10):2151-2158.

Dear Editor,
The authors of “Effects of physical activity calorie equivalent food labelling to reduce food selection and consumption: systematic review and meta-analysis of randomized controlled studies” make a strong claim that PACE food labeling can increase consumer consciousness of calorie consumption and therefore caloric reduction, but perhaps this concept deters true understanding of "healthful eating" and may have larger health implications for those with disordered eating.
There is a growing knowledge that that not all calories are created equal. Different foods may not only have different effects on hunger and satiety but also insulin production, gut microbiome interactions, and de novo lipogenesis in the liver (1). While not all consumers need this level of understanding, but without a basic acknowledgement of food’s qualities- like fats, fiber, sugar, ect- the consumer is lead to believe that calories are the most important determinant in what makes food “healthful.” With PACE food labeling, a consumer is led to believe that an ice cream cone and a handful of nuts, both of which could amount to 200 calories, are “equal.” However, in this comparison, only the nuts are possibly advantageous to people with diabetes and cardiovascular disease (2).
Stripping foods down to solely their caloric energy through PACE food labeling could inadvertently foster unhealthy relationships with food. As stated in the article, PACE labeling could be used to “help the public understand what a calorie means and therefore more able to decide whether the calories are ‘worth it.’” Through directing consumers to regard food as just calories to burn off through exercise, instead of fuel for a person’s body, perhaps consumers will come to regard food as punishment instead of its role as nourishment. Those who could be most affected from this way of thinking are the 30 million individuals living in the US with eating disorders (3,4). While obesity does affect more individuals than eating disorders, this is a population of individuals that should be considered when suggesting policymakers to consider implementation of this labeling system. Eating disorders are characterized by a pervasive thought pattern concerning both weight and food so implementing a labeling system that emphasizes food purging through the form of exercise can be detrimental to the mental health of these unique populations (5). Eating disorders have the highest mortality rate of any mental illness and 1 in 5 anorexia deaths are by suicide (6,7). Not only could PACE food labeling adversely affect those with eating disorders, but through fostering unhealthful relationships with food, they could potentially exacerbate the issue. On the other hand, reducing the risk and/or actual prevalence of obesity and all its related ailments, including psychological stress, is a worthy endeavor.
In conclusion, while the authors of this article review a novel and potentially helpful way to combat the growing obesity epidemic, further studies need to be done to compare PACE against current public health education programs and to investigate potential harm to those with eating disorders prior to policy making.
1) Mozaffarian, D.(2017). Foods, obesity, and diabetes—are all calories created equal?, Nutrition Reviews, Issue Suppl_1 Volume 75, Pages 19–31
2) Allen, L. (2008). Priority Areas for Research on the Intake, Composition, and Health Effects of Tree Nuts and Peanuts, The Journal of Nutrition, Volume 138, Issue 9, Pages 1763S–1765S
3) Hudson, J. I., Hiripi, E., Pope, H. G., & Kessler, R. C. (2007). The prevalence and correlates of eating disorders in the national comorbidity survey replication. Biological Psychiatry, 61(3), 348–358.
4) Le Grange, D., Swanson, S. A., Crow, S. J., & Merikangas, K. R. (2012). Eating disorder not otherwise specified presentation in the US population. International Journal of Eating Disorders, 45(5), 711-718.
5) Dell'Osso, L., Abelli, M., Carpita, B., Pini, S., Castellini, G., Carmassi, C., & Ricca, V. (2016). Historical evolution of the concept of anorexia nervosa and relationships with orthorexia nervosa, autism, and obsessive-compulsive spectrum. Neuropsychiatric disease and treatment, 12, 1651–1660.
6) Smink, F. E., van Hoeken, D., & Hoek, H. W. (2012). Epidemiology of eating disorders: Incidence, prevalence and mortality rates. Current Psychiatry Reports,14, 406-414.
7) Arcelus, J., Mitchell, A. J., Wales, J., & Nielsen, S. (2011). Mortality rates in patients with anorexia nervosa and other eating disorders: a meta-analysis of 36 studies. Archives of General Psychiatry, 68, 724-731.