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The mortality is a major component of damage caused by COVID-19. The comparative analysis of changes in mortality was carried out on the basis of the ROSSTAT data over 2012-2020 to determine differences in losses of male and female population caused by pandemic in Moscow. It is demonstrated that at close trends in mortality of males and females before pandemic, in 2020 their mortality changed differently. At equal increase of male and female mortality, main contribution into excess mortality (excluding contribution of COVID-19) was made approximately equally by diseases of nervous system and circulatory system in males and diseases of nervous system in females. The male mortality from COVID-19 is 1.9 times higher than female mortality. As a result of younger average age of death the amount of economic losses in terms of years of potential life lost (PYLL) due to premature death of males because of COVID-19 exceeds economic losses due to premature death of females up to 2 times. Although the average age of death of females from all causes decreased by smaller amount, their values of PYLL increased more, mainly due to higher rate of female mortality from disease of nervous system and from mortality related to drug addiction. In Moscow, the highest increase of PYLL is conditioned by dearth related to drug addiction and alcohol consumption. In the structure of this indicator in males they are ranked fourth and fifth. In females, alcohol-related deaths are ranked as sixth and drug-related deaths as eighth. The pandemic, contributing into increase in economic losses, didn't change their leading causes: diseases of circulatory system, external causes and neoplasms in males; neoplasms, diseases of circulatory system and external causes in females. The value of PYLL due to death from COVID-19 takes sixth place in males and fourth place in females.

Accuracy of statistical registration of mortality in Russia, especially in times of crisis, is a pressing and relevant issue; this problem was challenging Moscow in the 2000s: until recently, the capital was a complete outsider in terms of accuracy of statistical registration of mortality. The purpose of the study was to identify peculiar features of evolution and the structure of mortality from an event of undetermined intent among Moscow working-age population in the 2000s against the background of the processes taking place in Russia. The article analyzes mortality from an event of undetermined intent among Moscow population of young and old working age in the 2000s, as well as its nosological aspects in 2011-2018, when certain events of undetermined intent were separated as individual nosological units. A sharp decline in indicators in 1999-2000 and their growth in 2015-2017 have been identified. It is shown that these shifts were due to all leading events of undetermined intent (falls/jumps from a high place, hanging/strangulation/suffocation, medicament, alcohol and drug poisoning as well as specified and unspecified events). As a result, the structure of mortality after 2015 has significantly changed due to a sharp increase in the significance of alcohol, medicament and especially drug poisoning. It should be emphasized that in the 2010s the significance of latent suicide in all age and gender groups of Moscow working-age population is significantly higher than in Russia.

The statistics of causes of death is the informational basis for identifying public health problems. That is why the accurately accounting for mortality from diabetes mellitus, which is a global medical and social problem for society, is important. The study was carried out to analyze the correctness of coding death causes of diabetes mellitus and the frequency of alleged death., Materials and Methods: The Moscow deceased population database of July 2018 - July 2019 was analyzed. Using the decision tables on codes linkages from ICD-10, incorrect codes for underline cause were established for 342 death cases from diabetes mellitus. Among 43044 cases of cardiovascular death the cases of presumed death from diabetes were detected. The analysis was carried out in the Microsoft Access 2007 software., The Results: In 18.4% of cases, the cause of death from diabetes was encoded incorrectly. If a modification of the underline death cause is assumed due to the mention of certain diseases in any line of the Death Certificate, cases of coding for death from diabetes with wrong fourth character are more often detected when mentioning kidney diseases. If modification of the underline cause is provided for cases when information in the Death Certificate indicates that diabetes has caused the development of some diseases then the largest number of cases with incorrect coding was detected when mentioning circulatory diseases. Only in one medical organization the frequency of incorrect coding is 3.4%, in the rest it varies from 15.4% to 52.2%. Among all death causes, diabetes was only 0.41%. If to add cases of presumptive death from diabetes mellitus, then the proportion of diabetes in the structure of death causes will almost triple and reach up to 1.2%., Conclusions: The quality of diagnosis and coding of death causes from diabetes has not improved in recent years. To increase it, it is advisable to organize and establish the institution of coders. It is advisable to indicate the presence of diabetes mellitus in the Death Certificate without fail and use the information from the diabetes register. It is proposed to encode the death cause from diabetes mellitus with multiple complications use line D in the Death Certificate to indicate damage to various organs and systems if it is necessary.

The purpose of this study is to test the prediction of the evolutionary theory of aging that human longevity comes with the cost of impaired reproductive success (higher infertility rates). Our validation study is based on the analysis of particularly reliable genealogical records for European aristocratic families using a logistic regression model with childlessness as a dependent (outcome) variable, and woman's life span, year of birth, age at marriage, husband's age at marriage, and husband's life span as independent (predictor) variables. We found that the woman's exceptional longevity did not increase her chances of being infertile. It appears that the previous reports by other authors of high infertility among long-lived women (up to 50% infertility) are related to incomplete data, that is, births of children not reported. Thus, the concept of the high cost of infertility for human longevity is not supported by the data when these data are carefully cross-checked, cleaned, and reanalyzed.

The evolutionary theory of aging predicts that the equilibrium gene frequency for deleterious mutations should increase with age at onset of mutation action because of weaker (postponed) selection against later-acting mutations. According to this mutation accumulation hypothesis, one would expect the genetic variability for survival (additive genetic variance) to increase with age. The ratio of additive genetic variance to the observed phenotypic variance (the heritability of longevity) can be estimated most reliably as the doubled slope of the regression line for offspring life span on paternal age at death. Thus, if longevity is indeed determined by late-acting deleterious mutations, one would expect this slope to become steeper at higher paternal ages. To test this prediction of evolutionary theory of aging, we computerized and analyzed the most reliable and accurate genealogical data on longevity in European royal and noble families. Offspring longevity for each sex (8409 records for males and 3741 records for females) was considered as a dependent variable in the multiple regression model and as a function of three independent predictors: paternal age at death (for estimation of heritability of life span), paternal age at reproduction (control for parental age effects), and cohort life expectancy (control for cohort and secular trends and fluctuations). We found that the regression slope for offspring longevity as a function of paternal longevity increases with paternal longevity, as predicted by the evolutionary theory of aging and by the mutation accumulation hypothesis in particular.

Since paternal age at reproduction is considered to be the main factor determining human spontaneous mutation rate (Crow, J. (1993) Environ. Mol. Mutagenesis, 21, 122-129), the effect of paternal age on human longevity was studied on 8,518 adult persons (at age 30 and above) from European aristocratic families with well-known genealogy. The daughters born to old fathers (50-59 years) lose about 4.4 years of their life compared to daughters of young fathers (20-29 years) and these losses are highly statistically significant, while sons are not significantly affected. Since only daughters inherit the paternal X chromosome, this sex-specific decrease in daughters' longevity might indicate that human longevity genes (crucial, house-keeping genes) sensitive to mutational load might be located in this chromosome.