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A Quest for Sanity

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A Quest for Sanity

By Nick Ford

Originally written: 7//9/11

 

I always like to have a different username wherever I go. I’m not sure exactly sure why per se’ except that I like the feeling that there are many different sides of my personality that I’d like to show off. One of those is the fact that I think a large portion of this world is insane. Listen, I’m not saying everyone around you is getting ready to kill you or something but the fact that some people literally believe things that this authoritarian culture teaches them and that the government instills in them is two things that puzzle and worry me. At the very least the people who rule the society with an iron fist (and it IS an iron fist) are insane  the people in power have so many disincentives to act rationally. They face little to no real scrutiny with a media that can legally lie to a public that is held hostage in cages  and when it gets out of those cages can only go into other prisons to serve their corporate masters. Sure, you could try to start your own business but what are the chances of that working out? Unless it’s a long term idea backed by lots of planning, knowhow and plenty of collective pooling of capital what chance do you have against the currently insulated corporations? You’ll probably be Scratching By and there’s good reason for that. Again, this society is driven by insane people, the people in power in just ordinary organizations have these sorts of drives so can you imagine what the leaders have?

It’s a problem that not only has to do with information, calculation issues applied in different ways than most might think of at first but a problem of sanity. How reasonable is it to really expect that the political leaders will care about you when they claim to be so much higher than you are? When the culture is dominated by subjugation, exclusion and the remnants of things like slavery, apartheid, segregation, what sanity is there? And for more contemporary things the prison system may as well be continuing this. It’s crazy that people think that locking people in cages will make them behave better! Has it ever been such? Haven’t modern prisons only gotten bigger? More financed by the ruling class and CEOS? Less and less used for actually violent people but perhaps removing “undesirables” from “civilized society” and then having them reintroduced and have them become their own worst enemy?

Take the example of the black community, it’s been nothing but ravaged by the state for almost its entire existence.  From the institution of state-sponsored slavery in US to state-sponsored segregation and constantly forcing the blacks to lose any sort of identity. This loss of self translates into chaotic and self-destructive behavior and makes for a heavily dysfunctional society. When libertarians argue that the non-aggression principle and violation of property rights are the only things that matter this is just one of many reasons why such an answer is unacceptable when discussing the prospect for individual liberty. It’s insane that blacks have literally started gangs because of this state and cultural alienation and have killed thousands of members of their own socially constructed race. After all it’s not just the state, the state may aid things like racism, sexism, etc. but these things also exist independently of the state and can be just as dehumanizing with or without it.

I think that the search for actual sanity is the real response we as anarchists should be taking, as a left-libertarian I think this means building the new society, culture and anti-oppression movement (not just state) within this decaying society we are a part of.  Part of finding reason is trying to explain what that exactly is but more importantly showing them how it works. Education is a great tool and it’s one of my preferred tactics (as well as self-educating) but actually going out there building alternatives to the mainstream is something that also should be more focused on by anarchists.

I also think it’s insane to think you’ll win against the state in any meaningful way through violence. They have the guns and you may have guns of your own but unless you come packing some tanks and nukes I think you’ll be a bit outmatched when the iron fist of the state comes down on to you. It might not even take the police just to take you out and it’s not long until another person has been lost to the insanity of the state. I don’t want to see my fellow humans suffering, I don’t want to see them dying for a cause they believe in. I want to see them living for it! I want us all to live for the cause we preach so much in our lives, there’s no reason to starve in a desert if the state gives us some water other than pure insanity. Direct action is great, it can be violent or it can be peaceful but the anarchist should almost always side with the peaceful alternative. This does not mean that I think strict pacifism should be the key thing for the anarchist to keep in mind. Nor do I believe non-cooperation and such are the only ways out. In fact I don’t think there is one way to beat the state. There’s no X on the mark of the state that says, “smash here!” instead it’s up to us to expose the systempunkt’s that the state does have and that we do know about to the best of our ability.

More to the point on violence however, I think if and when the counter and alternative associations, institutions, organizations and so on outnumber the state ones we should certainly start defending ourselves from the police and so on. And even way before that (like now for instance) we should be building mutual aid networks and show solidarity among “anarcho-party lines” (more on that some other time…) to achieve what goals we want to see happen as soon as possible. I think self-defense against cops is required right now on more of an intellectual field than a physical one. You should inform yourself on how to interact with police, what works best for you and what seems to work on best with them. Saying, “fuck you pigs!” over and over might not be the best idea.

I think the internet is a fantastic tool to combat the state’s insanity. Besides just being a general catalyst for more organizations to spawn within the statist constructs and gradually get more and more ground it’s wonderful to have a convenient way to show solidarity. Things like Anonymous, Wikileaks, Anti-Sec and more have come together on just trying to keep government under control; now as anarchists we know this is folly. But they seem to be learning this as well as times goes on and perhaps eventually they’ll come around to our position. Until then we’ve got our media centers, we’ve got our alliances set up  and we’ve got a growing movement that is aiming to educate students and there’s so much more going on. But we’re going to need ALL of this and more if we’re going to want to battle the insanity of the state and move towards a more sane society and culture.

Another reason why I’m harping on the sanity aspect of this whole thing is that the state, more than anything else is a mental construct more than a physical one. No, I’m not running the tired line that “government doesn’t exist!”. Instead I’m suggesting that we can and should think of government as an organization that claims a monopoly on violence in a given territorial area and manifests through the other monopolies this so called “protector of people” forms. The police, the courts, the teachers and so on are all manifestations of the state and it’s intrusion in society. But what I mean to suggest is that there is both an internal state and an external state, one that is manifesting in the ways I’ve suggested already but another that’s internalized. From this I think I can safely say that if the state somehow went away tomorrow people would just create another one. They wouldn’t want anarchism; they certainly haven’t embraced the ideas! And that’s the thing; the state inside of them so to speak convinces of them that the insanity they keep buying.

This isn’t to insult people who believe in the state, you believing in insanity isn’t going to make me stop me from treating you as a fellow member of the oppressed class or a fellow human being. It’s not going to make me call you insane night and day. It’s not going to make me “de-foo” you like some anarchists have suggested. Nor is it going to make me hate you, I’d find it a waste of time to hate you or anyone really anyways. No, instead what I’m suggesting is that this culture, this government has convinced you of insanity and that you believe it. If anything my real indictment lies with those who not only believe these but act on them and make it more possible to oppress people in large countable ways. That they keep people unemployed, scratching by, dying, hardly living, employed in jobs they hate, buying things they don’t need (materialism) and becoming disenfranchised with this beautiful world.

I’m not here to be overly cynical or overly optimistic but realistic. Anarchism won’t happen in our lifetimes despite what any organization tells us that but that doesn’t mean it’ll never happen or that such a goal isn’t worthy of pursing. The empire is crumbling with debt, wars; failing currency, blatantly corrupt leaders, and an authoritarian culture. With all of this it’s only a matter of time before things fall apart. And we as the anarchists have to be there with as many alternatives in hand and say,

 

“Look at what this insanity has wrought! Look at what it has given you! I suggest you try something new, try something sane, and try anarchism!

Time trends and sex patterns in Hodgkin’s disease incidence in Canada, 1970-1995

Canadian Journal of Public Health May 1, 2000 | Shiliang Liu; Robert Semenciw; Chris Waters; Shi Wu Wen; Yang Mao ABSTRACT Purpose: To examine time trends and sex patterns in Hodgkin’s disease incidence in Canada, from 1970 through 1995.

Method.. In addition to analyses of the secular trends and sex ratio in incidence rates, ageperiod-cohort models were fitted to estimate the effects on the trends. Age-specific male/female incidence rate ratios were examined for the disease and for its two major histologic subtypes.

Results: The overall age-adjusted incidence rate of Hodgkin’s disease decreased significantly in males (3.5 per 100,000 in 1970-71 to 2.8 in 1994-95) but only slightly in Females 2.4 per 100,000 co 2.3). There was a significant increase in the incidence among females aged 10-29 and among males aged 10-24, but a dramatic decrease among older ages. Age-period-cohort modelling showed that birth cohort and period effects were responsible for the observed trends in males and females, respectively.

Conclusion: The risk factors responsible for Hodgkin’s disease are different in Females and males. Reproductive factors are likely to be associated with the occurrence of the disease in young women.

ABREGE But : Examiner les tendances temporelles et les repartitions par sexe de (incidence de la maladie de Hodgkin au Canada, de 1970 a 1995.

Methode: En plus des analyses des tendances ‘a long terme et du sex-ratio duns les faux d’incidence, des modules utilisant des cohortes fondees sur les periodes de la vie ont ete integres pour estimer les efFets sur les tendances. Les ratios d’incidence hommes/femmes pour des grouper d’age determines ont ete examines pour la maladie de Hodgkin et pour dews grands soul-types histologiques.

Resultats : Le taux global d’incidence de la maladie de Hodgkin ajuste en fonction de Page a baisse sensiblement chez les hommes (de 3,5 at 2,$ pour 100 000 hommes entre 1970-71 et 1994-95) mail il a peu change pour les femmes (de 2,4 a 2,3 pour 100 000 femmes). On a observe une augmentation notable de (incidence parmi les personnel de sexe feminin de 10 at 29 ans et parmi les personnel de sexe masculin de 10 a 24 ans, mail un flechislement marque parmi les grouper plus ages. Les modeles fonder sur les cohortes par periodes de la vie demontraient que les effets des cohortes de naissance et les effets des periodes de la vie etaient responsables des tendances observes chez les personnel d’un sexe comme de l’autre.

Conclusion: Les facteurs de risque responsables de la maladie de Hodgkin sent differents chez les femmes et chez les hommes. tl est probable que des facteurs lies a la reproduction ont un rapport avec (occurrence de la maladie chez Les jeunes de sexe feminin.

Hodgkin’s disease is a relatively uncommon malignancy, representing less than 1.0% of all cancer;1,2 however, it is one of the most common forms of malignancy affecting young adults. An unusual bimodal age-specific incidence curve with peak occurrence at age 20 to 29 years and at age 75 to 84 years supports the “twodisease hypothesis” of Hodgkin’s disease causation.2-5 Epidemiologic studies have identified several factors that increase the risk of developing Hodgkin’s disease, including age (young adult), race (Caucasian), family history of Hodgkin’s disease, and occupational exposure to wood and some chemicals.3,5,6 Research has also focussed on specific viruses in the pathogenesis of Hodgkin’s disease.7-9 Molecular genetic studies have found evidence of the Epstein-Barr virus (EBV) genome in malignant cells of approximately half of Hodgkin’s disease patients.3,5,8 Nevertheless, the understanding of the etiology of this lymphoma is incomplete.

A few studies have shown that reproductive factors may play a role in the pathogenesis of Hodgkin’s lymphoma, but no association has been established.4,10,11 In this paper, Canadian cancer registry data were used to examine time trends and gender differences in Hodgkin’s disease incidence, with a focus on generating etiologic hypotheses.

METHODS Data on the incidence of Hodgkin’s disease were obtained from the National Cancer Incidence Reporting System (NCIRS) of Statistics Canada, which began collecting data from provincial and territorial cancer registries in 1969. Data for 1992 to 1995 were obtained from the Canadian Cancer Registry (CCR) which replaced the NCIRS in 1992. Data for the province of Quebec were excluded from this analysis because improved reporting procedures were not implemented in Quebec until 1981. In general, cancer registry data included in this study are comparable and reliable. The information regarding the CCR and the quality of Canadian cancer incidence data has been well documented.12,13 Annual population estimates were obtained from the Demography Division of Statistics Canada.

Information on histologic classification of Hodgkin’s disease was not consistently recorded by all provinces and territories in Canada until 1983, although Ontario, Saskatchewan and British Colombia collected such data for previous decades. The combined population of these three provinces accounts for about 60% of the Canadian population. Although several systems of classification and coding for primary site have been used by the registries during the decades of cancer registration, all the records were recoded according to the International Classification of Disease for Oncology (ICD-O). Hodgkin’s disease is coded as ICD-O codes 9650-9667. this web site hodgkin s disease

We contrasted average 3-year age-specific rates by sex for the period 1970-72 with races for 1993-95. The secular trends in age-adjusted incidence rates as well as male/female rate ratios were modelled using linear regression based on the logarithm of the annual rates.14 The average annual percent change (AAPC) in Hodgkin’s disease incidence was derived from the expression [exp (beta)-1]x100, where beta is the regression coefficient. The age-adjusted rates were calculated using direct standardization with the World Standard Population serving as the standard.15 Male/female incidence rate ratios by age group for all cases of Hodgkin’s disease and for the two main histologic subtypes – nodular sclerosis and mixed cellularity – were calculated using the most recent 5 years of data, i.e., from 1991 to 1995. Nodular sclerosis (ICD-O 96639667) and mixed cellularity (ICD-O 9652) encompass more than 75% of all Hodgkin’s disease cases in those five years. Based on our preliminary analysis, we focussed our analysis on two particular age groups: one showing increasing incidence (ages 10-24 years among males and 10-29 years among females), and the other decreasing incidence over the study period (ages 2584 years among males and 30-84 years among females). Analysis integrating age at diagnosis, time period of diagnosis and birth cohort were then performed for the two age groups by sex. Age at diagnosis was grouped into 5year intervals. The entire period of diagnosis was divided into four 5-year intervals from 1970 through 1989 and two 3-year intervals from 1990 through 1995. Corresponding to these age intervals and time periods, the appropriate number of birth cohorts were derived. The effects of age, time period and birth cohort on Hodgkin’s disease incidence were then estimated separately for each sex and the particular age group.

Age-period-cohort models were fitted with the standard Poisson assumption.16,17′ To test the effect of period and cohort individually after controlling for the effect of age, respective two-factor models were compared to the full model. Parameters of the models were estimated by means of the maximum likelihood method with SAS procedure GENMOD (release 6.12, SAS Institute Inc., Cary, NC 1996). The goodness of fit of models was evaluated using the deviance (defined to be twice the dif ference between the maximum achievable log likelihood and the log likelihood at the maximum likelihood estimates of the regression parameters) and specific effects (such as cohort and period effects) were tested by comparing the difference in deviance between the respective models.

RESULTS A substantial change in age-specific rates of Hodgkin’s disease was seen over the two periods 1970-72 and 1993-95. Two incidence peaks were seen across the age range among both males and females: the first in young adults, and another in older persons. An apparent increase in the rates was observed in age 10-14 years through age 20-24 years, and age 10-14 years through age 25-29 years, respectively, in males and females. A substantial decrease over time was seen among those aged 25 years and older (Figures 1 and 2). The overall ageadjusted incidence rate decreased significantly in males (AAPC = -0.83%, p < 0.01), from 3.50 per 100,000 in 1970-71 to 2.80 per 100,000 in 1994-95, but changed very slightly in females (AAPC = 0.15%, p > 0.05), from 2.37 per 100,000 to 2.31 per 100,000 over the same period. The male/female age-adjusted incidence rate ratio decreased from 1.48 in 1970-71 to 1.21 in 1994-95 (AAPC = -1.00%, p c 0.01, Table I).

Based on data for 1991-95, the rate ratio varied substantially by age group for all cases of Hodgkin’s disease and for its two main histologic subtypes: nodular sclerosis and mixed cellularity. For all cases, two age groups of young females (15-19 and 20-24 years) experienced higher incidence rates than males of the same age. There was almost no difference in the overall rate ratio for nodular sclerosis, i.e., 0.98, but the overall incidence of the mixed cellularity type of Hodgkin’s disease was 2.1 times higher among males than females (Table II). Age-specific rates of the two subtypes of Hodgkin’s disease ratio varied significantly by sex. In their reproductive years (15-19 through 40-44 years), women experienced higher or similar incidence rates of nodular sclerosis, although incidence rates for Hodgkin’s disease of the mixed cellularity type was much higher in men than women in almost all age groups. In older age groups, the difference in incidence rates by gender were almost comparable for the two subtypes of Hodgkin’s disease.

Table III shows the effects of age at diagnosis, time period of diagnosis and birth cohort on the incidence of Hodgkin’s disease by sex and particular age group. Among males for both age groups, the agecohort model significantly improved the explanatory power of the age-period model, indicating that birth cohort was a more important determinant of Hodgkin’s disease incidence than time period. Among females, the age-period model was better than the age-cohort model, suggesting that the trends in Hodgkin’s disease incidence in females (either age IO-29 years or age 30-84 years) were more likely to have been associated with specific events in calender time.

DISCUSSION Our analysis shows that the incidence of Hodgkin’s disease has increased among adolescents and young adults, but decreased sharply among older persons between 1970 and 1995. The trends dif fered substantially between males and females in terms of age-specific rates and age-period-cohort effects. Substantial sex differences in age-specific incidence of Hodgkin’s disease and its two main subtypes, nodular sclerosis and mixed cellularity, were also observed in recent data (1991-1995). Our data suggest that significant changes in time trends and gender patterns of incidence of Hodgkin’s disease have occurred over the last three decades. The observed age-specific incidence patterns among females support the hypothesis that reproductive factors play a role in the development of Hodgkin’s disease.

Currently identified risk factors, such as EBV infection, human immunodeficiency virus (HIV) infection, and improved standard of living or economic status are not likely explanations for the observed trends and major sex difference in the incidence of Hodgkin’s disease and its two main subtypes in Canada. Over the last decade, the relationship between EBV and Hodgkin’s disease has been examined extensively.3,7-9 Molecular evidence has suggested that EBV plays a role in the development of Hodgkin’s disease, but with a limited direct correlation, because EBV is detectable in only 18-49% of cases. More importantly, the presence of the EBV genome is primarily associated with the mixed cellularity histologic type.3,8 Our results show that a significant increase is mainly from the nodular sclerosis subtype of Hodgkin’s disease, which is more frequently observed in young women than in men (Table II). This finding contradicts the hypothesis of EBV infection. On the other hand, although a few occupations have been reported to be associated with Hodgkin’s disease, attributable risks are too low to explain a major sex difference.3,4,10 Hodgkin’s disease also has not been associated with smoking or other high-risk behaviours more prevalent in men. Thus, to date, identified exogenous exposure does not explain the age-dependent gender variations in the incidence of this cancer.

Our analysis by age, period and birth cohort shows different effects in males and females: temporal changes in Hodgkin’s disease among males followed a birth cohort pattern while period efFects were underlying the trends observed among females. Birth cohort effects imply a change in disease incidence for individuals born at a particular time secondary to particular levels of exposure to a specific risk factor.18,19 Period effects occur when disease risk is altered for all individuals alive at a particular point in time, regardless of age. For instance, pollution of the air or water supply at a particular time will produce a similar change in disease risk for everyone in the population. Generally speaking, diagnostic and registration practices are major contributors to period effects.18,19 Our analysis shows that period effects underlie the incidence trends in Hodgkin’s disease among females. The absence of period effects among males suggests that changes in diagnosis and registration did not play a major role in the trends observed in Hodgkin’s disease incidence. Further, previous studies have shown relatively little diagnostic error and misclassification of Hodgkin’s disease.20 We believe that the period effects observed in Hodgkin’s disease incidence among young women represent a true change and this finding provides a clue to etiology.

Some indirect evidence has suggested that reproductive factors, or sex hormones, may play a role in the etiology of Hodgkin’s disease.4,10,11 If true, reproductive factors may underlie the change in Hodgkin’s disease incidence which is partially responsible for the observed sex ratio in nodular sclerosis of Hodgkin’s disease. Some epidemiologic studies have shown a reduced risk of Hodgkin’s disease associated with marriage, higher parity, and young age at first full-term pregnancy less than 30 years. We thus speculate that the increasing frequency of young women with low fertility rate, low parity, later marriage and later age at first pregnancy may also have contributed to the observed increase in Hodgkin’s disease incidence (i.e., nodular sclerosis) in young adult women in Canada.2′ For instance, live births to women aged 20-24 years and aged 25-29 years declined substantially in Canada, from 108.8 per 1,000 and 128.3 per 1,000 in 1974 to 72.2 per 1,000 and 114.0 per 1,000 in 1994, respectively.21 Glaser” suggested that hormonal factors play a role in the pathogenesis of Hodgkin’s disease, which may operate through an effect on the immune system. Other studies have also suggested that the role of sex hormones and other hormonerelated factors such as oral contraceptives needs further investigation.4,22,23 In summary, the understanding of the cause of Hodgkin’s disease remains elusive. The main etiologic candidate, EBV, has been detected in only a proportion of cases, and there is lack of evidence of other co-factors. Our data show that Hodgkin’s disease incidence increased in young women while decreasing significantly in older persons. A major sex difference was observed in the age-specific incidence rates of Hodgkin’s disease and its main subtypes. Prior viral infection seems an unlikely explanation for observed temporal patterns of the disease. Our data suggest that elevated incidence rates of Hodgkin’s disease in young women may be associated with childbearing-related reproductive factors. website hodgkin s disease

ACKNOWLEDGEMENTS Data were provided to Health Canada from the Canadian Cancer Registry, formerly the National Cancer Incidence Reporting System, at Statistics Canada. The cooperation of the provincial and territorial cancer registries that supply the data to Statistics Canada is gratefully acknowledged.

[Reference] REFERENCES [Reference] 1. National Cancer Institute of Canada (NCIC). Canadian Cancer Statistics 1998. Toronto: NCIC, 1997; 13-25.

2. Coleman MP, Esteve J, Damiecki P, et al. Trends in cancer incidence and mortality. Lyon: International Agency for Research on Cancer, 1993 (IARC Sci Publ no. 121):673-704.

3. Mueller NE. Hodgkin’s disease. In: Peckham M, Pinedo H, Veronesi U (Eds.), Oxford Textbook of Oncology Vol. 2, Oxford: Oxford University Press. 1995;893-919.

[Reference] 4. Chen YT, Zheng T, Chou MC, et al. The increase of Hodgkin’s disease incidence among young adults: Experience in Connecticut, 19351992. Cancer 1997;79:2209-18.

5. Glaser SL. Recent incidence and secular trends in Hodgkin’s disease and its histologic subtypes. J Chron Dis 1986;39:789-98.

6. Spitz MR, Sider JG, Johnson CC, et al. Ethnic patterns of Hodgkin’s disease incidence among children and adolescents in the United States, 1973-82. JNatl Cancer Inst 1986;76:235-39.

7. Jarrett RF, Gallagher RF, Jones DB, et al. Detection of Epstein-Barr virus genomes in Hodgkin’s disease: Relation to age. J Chron Dis 1986;39:789-98.

[Reference] 8. Glaser SL, Lin RJ, Stewart SL, et al. Epstein-Barr virus-associated Hodgkin’s disease: Epidemiologic characteristics in international data.IntJ Cancer 1997;70:375-82.

9. Rabkin CS, Biggar RJ, Baptiste MS, et al. Cancer incidence trends in women at high risk of human immunodeficiency virus (HIS infection. Int J Cancer 1993;55:208-12.

10. Jarrett RF. Hodgkin’s disease. Bailliere’s Clin Haematol 1992;5:57-79.

11. Glaser SL. Reproductive factors in Hodgkin’s disease in women: A review. Am J Epidermal 1994;139:237-46.

[Reference] 12. Band PR, Gaudette L> Hill GB, et al. The making of the Canadian cancer registry: Cancer incidence in Canada and its regions, 1969 to 1988. Ottawa: Canadian Council of Cancer Registries, 1993;16-21.

13. Gaudette L, Lee L. Cancer incidence in Canada, 1969-1993. Ottawa: Ministry of Industry (catalogue 82-566-XPB), 1997;xiv-xvii.

14. Kleinbaum DG, Kupper LL, Muller KE. Dummy variables in regression. In: Applied Regression Analysis and Other Multivariable Methods. Boston: PWS-KENT Publishing Company, 1988;271-72.

15. Parkin DM, Muir CS> Whelan SL, et al. (Eds.) Cancer Incidence in Five Continents. Vol. VI.

[Reference] Lyon: International Agency for Research on Cancer, 1992 (IARC Sci Publ no.120):865-70.

16. Clayton D, Schifflers E. Models for temporal variation in cancer rates, I; Age-period and agecohort models. Star Med 1987;6:449-67.

17. Clayton D, Schifflers E. Models for temporal variation in cancer rates, II: Age-period-cohort models. Stat Med 1987;6:469-81.

18. Holford TR. Understanding the effects of age, period, and cohort on incidence and mortality races. Annu Rev Public Health 1991;12:425-57.

19. Holford TR. Analysing the effects of age, period, and cohort. Stat Meth Med Res 1992;1:317-37.

[Reference] 20. Glaser SL, Swartz WG. Time trends in Hodgkin’s disease incidence: The role of diagnostic accuracy. Cancer 1990;66:2196-204.

21. Ford D, Nault F. Changing fertility patterns, 1974 to 1994. Health Rep 1996;8:39-46.

22. Miller AB, Barclay THC, Choi NW, et al. A study of cancer, parity and age at first pregnancy. J Chron Dis 1980;33:595-605.

23. Olsson H, Olsson ML, Ranstam J. Late age at first full-term pregnancy as a risk Factor for women with malignant lymphoma. Neoplasma 1990;37:185-91.

[Reference] Received: August 16, 1999 Accepted: December 100, 1999 [Author Affiliation] Shiliang Liu, MB, PhD, Robert Semenciw, MSc, Chris Waters, BSc, Shi Weu Wen, MB, PhD, Yang Mao, PhD [Author Affiliation] Laboratory Centre for Disease Control, Health Canada, Ottawa, Ontario Shiliang Liu; Robert Semenciw; Chris Waters; Shi Wu Wen; Yang Mao

SearchingForSanityA Quest for Sanity

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