Early Contact To Bovine Milk and The Epidemic Rise in Mammary Cancer Incidence & The Search For The Human Mammary Cancer Virus

Early Contact to Bovine Milk and the Epidemic Rise in Mammary Cancer Incidence
&
The search for the Human Mammary Cancer Virus
By Elisabeth Rieping (Stand 2004)
Index
01-Overview
02-Abstract (short)
Short Version (Epidemiology only)
03-“Complete text”: Breast Cancer and Early Contact with Bovine Milk (shorter version, Epidemiology only)
I. Long Version: Early Contact to Bovine Milk and the Epidemic Rise in Mammary Cancer Incidence
0. Introduction
1. Immigrant Data and the Cohort wise Rise in Incidence Data point to the Time of Birth as an Important one for Catching Breast Cancer
2. The Change in Infant Feeding and the Rise in Mammary Cancer Incidence
2.a. More on Change in Infant Food
2.b. Henri Nestlé
3. Risk Factors and their Explanation by Bottle Feeding with Cow's Milk based Products
3.a Weight and Height
3.b Age at Menarche
3.c Wealth and Parental family
3.d Delayed Time of First Full Pregnancy
3.e Urban Residence
3.f i High Birthweight
3.fii Low Birthweight
4. The Geography of Breast Cancer in Comparison to the Availability of Diary Products
5. The Change in Risk Factors for Breast Cancer, if one looks at Breast Cancer Patients only
6. Breast Cancer in Animals
7. Breast Cancer before the introduction of Cow's Milk based Formulas as Infant Food
8. Risks for Breast Cancer may Change
9. Inheritable Breast Cancer (under construction)
10. Breast Cancer and Diabetes Type 1
11. Breast Cancer and Thyroid Disease
II. The search for the Human Mammary Cancer Virus
01-Overview http://web.archive.org/web/*/http://www.erieping.de/overview.htm
04-Introduction: Early Contact to Bovine 1. Immigrant Data and the Cohort wise Rise in Incidence
2.The Change in Infant Feeding and the Rise
Milk and the Epidemic Rise in Breast Data point to the Time of Birth as an Important one for
in Mammary Cancer Incidence
Cancer Catching Breast Cancer
3. Risk Factors and their Explanation by 4. The Geography of Breast Cancer in Comparison to the 5. The Change in Risk Factors for Breast
Early Contact to Bovine Milk and the Epidemic Rise in Mammary Cancer Incidence by Elisabeth Rieping 2
Bottle Feeding with Cow's Milk based Cancer, if one looks at Breast Cancer
Availability of Diary Products
Products Patients only
7. Breast Cancer before the introduction of Cow's
6. Breast Cancer in Animals 8. Risks for Breast Cancer may Change
Milk based Formulas as Infant Food
9. Inheritable Breast Cancer (under 10. Breast Cancer and Diabetes Type 1 (under 11. Breast Cancer and Thyroid
construction) construction) Disease (under construction)
02-Abstract (short) http://web.archive.org/web/*/http://www.erieping.de/bcabstra.htm
Breast Cancer and Early Contact with Bovine Milk

abstract
Last update Elisabeth Rieping 2006/11/08
overview complete text back
Geography
It is shown that breast cancer is uncommon in peoples without diary products. These are Japanese and other East Asian ones,
African peoples in malaria areas and Eskimos. Immigrants show shifts in incidence only if born in the new country.
Risk factors
Obesity early menarche and tallness typical for patients are discussed in connection with over-feeding by the bottle which
seems to hinder the child learning to control its weight. Tallness and early menarche are not explicable by influences exerted
during adult life.
The former expensiveness of artificial feeding explains the tendency of the disease to occur in the wealthy born, well educated
women, who get their first child late.
Time of infection
Cohort analyses, too, show the importance of the time of birth. Rising incidence started with cohorts born after introduction of
bottle feeding in the nineteens century.
Mode of Transmission
Infant food is prone to transmit infections giving rise to later occuring tumors, since viral oncogenesis often affords injection
into new born animals. Heat treatment used to sterilise infant food does not destroy the DNA of RNA tumorviruses integrated
into the DNA of milk lymphocytes.
03-Complete Text (Epidemiology only)
“Complete text”: Breast Cancer and Early Contact with Bovine Milk (shorter version, Epidemiology only)
http://www.erieping.de/bcearcon.htm = wrong link, in fact http://www.erieping.de/bcearcon.htm
Although mammary cancer has been known for centuries and was described even in times of old Greek medicine[i], its incidence has increased
greately during the last hundred years [ii],[iii],[iv],[v].
Considering the major changes which have taken place during this time, one concerning the disease could be the rise in artificial feeding of infants
[vi],[vii],[viii],[ix], and it was thought that women who did not breast-feed their children might be susceptible[x].
However since the analyses of MacMahon in 1970[xi], which were confirmed later many times[xii](review), it is obvious that breast feeding does
not protect women from catching the disease.
In the first animal model, the breast cancer virus was passed on by the milk of the mother to the suckling mouse[xiii].
This example influenced studies on the dangers of breast feeding for daughters of mothers with breast cancer, which failed to show any dangers
[xiv],[xv].
One important thing, the mouse mammary tumor system shows, is that the peroid of susceptibility clings to the time of birth. A time during which
the immune system of the infant is not mature and foreign agents can gain entrance to the organism unregognized. But this hint went unrecognized
by breast cancer epidemiology. In the beginning of tumor virology it was an important finding that it was easy to induce a tumor in a newborn
animal [xvi],[xvii], especially if one used the virus of another species [xviii],[xix],[xx].
Before this was known, the difficulies in building model systems seriously hampered science[xxi].
In the human being, cow’s milk may be an easy vehicle for a milk born virus to enter a newborn infant, especially as viral DNA, being sufficient
for tumor induction, is not destroyed by cooking or pasteurization. In the following analysis I want to show that immigration data and cohort
analyses hint at the time of birth as a period for catching the disease and that the epidemiology of breast cancer is explainable by early contact to
bovine milk which was boosted by a change to bottle feeding after the successful introduction of formulas for infant feeding.
Subsequently I want to outline the connection of milk production and the diary industry to the geographic distribution of breast cancer. This reaches
from Eskimos with neither cattle nor mammary neoplasms, over East Asians having cattle but not using milk products, to countries with easy
access to bovine milk and a high frequency of breast cancer. A connection found in the Western industrial countries and, less well documented,
among East African Nilo Hamitic tribes.
1. IMMIGRANT DATA AND THE COHORT WISE RISE IN INCIDENCE RATES POINT TO THE TIME OF BIRTH AS AN IMPORTANT
ONE FOR CATCHING THE DISEASE
In Japan, were cow’s milk, as well as other diary products were not used as human food before Western habits reached the country, mammary
cancer was an uncommon disease [xxii].
Japanese immigrants to Hawaii an San Francisco were an interesting group to investigate for changes in rates of several types of cancer [xxiii].
While rates for neoplasms of other sites changed to the American number, those for mammary cancer remained ttable for a rather long time, giving
support to speculations of hereditary differences [xxiv].
In the seventies, the first data showing a big rise in site specific incidence rates occuring among American born daughters of Japanese immigrants in
the region of San Francisco were published [xxv],[xxvi].
In Hawaii, where the immigration to the new country had taken place earlier, this change had not been seen [xxiii].
The population of Hawaii, except for its Anglo- American part, consisted mainly of Polynesian, Chinese, Japanese, and later of Phillipine
descendents, which like all East-Asian peoples, did not use milk as human food [xxvii],[xxviii] and it is possible that this commen feature delayed
the change in infant nutrition. Some time before the data on Japanese immigrants were published , Haenszel, who had studied breast cancer
incidence among Polish Americans, in reanalysing his data, found that a rise in incidence rates could only be found in groups with a substantial
American born component [xxix].
These hints to the time of birth as an the decisive one for catching the disease was confirmed by data collected in Iceland, Britan, USA, Finland,
which show that breast cancer incidence varies in a cohort-wise manner ii],[iii],[iv].
If an event affects a cohort, that means people with the same time of birth, it should be something which took place at the time when those persons
were born.
A change in diet, which could be responsible for the rising breast cancer incidence would have to exert its influence at an early time of life of the
affected individual ii] ,[xxx] .
Other factors that may influence breast cancer like radiation or the use of hair dyes would show less variation with the time of birth, as women of
different ages are likely to become radiated or to colour their hair.
That mammary cancer incidence rises in cohort-wise manner in many examined countries stromgly hints to the time of birth as beeing one
important period of susceptibility.
2. CHANGE IN INFANT FEEDING AND THE RISE OF MAMMARY CANCER
The big rise in breast cancer incidnce started with women born at the end of the ninteenth century [ii],[iii],[iv],[v].
At about this time, a change in infant nutrition took place in which the human breast milk was replaced by mixtures of cow’s milk [vi], [vii], [viii],
[ix].
Although known since ancient times, artificial feeding had never been very successful [vii], and as late as in the nineteenth century, artificial feeding
became more popular. The use of cow’s milk lost much of its immediate danger, exerted by contaminating bacteria, when the effect of heat
treatment became known. The importance of hygienic treatment of baby food and the composition of its ingredients were intensively discussed in
the pediatric litarature of that time [vi] .
In Switzerland Nestle began the propagation of the so called formulas[xxxi], and in the United States several companies started similar activities.
Since companies were careful not to compete with the pediatricians but to recommend the use of the formulas only on their advice6 , the artificial
feeding of babies became popular among larger parts of the wealthier population, whose daughters later had greater chances to suffer from
mammary neoplasms. A connection which explains the high incidence of breast cancer in educated women during the start of the epidemic.
3. EPIDEMIOLOGIC FEATURES OF MAMMARY CANCER AND THEIR EXPLANATION AS A FUNCTION OF ARTIFICIAL FEEDING
The epidemiologic data which are connected with breast cancer are overweight, tallness, early menarche, wealth, the delayed age at firth birth e.g.
childlessness, and urban residence [xxxii],[xxxiii],[xxxiv].
Aditionally there are links to Thyroid Disease and Diabetes which will be discussed seperately.
3.a WEIGHT AND HEIGHT
The connection between obesity and breast cancer has been studied extensively and is well established [xxxv],[xxxvi],[xxxvii],[xxxviii],[xxxix],[xl],
[xli],[xlii],[xliii],[xliv],[xlv],[xlvi],[xlvii],[xlviii],[xlix],[l],[li].
On the contrary, the link between overweight and artificial feeding has only in the seventies started to attract the attention of scientists [lii],[liii],
[liv], may be because a big, fat baby was a goal, achieved by loving mothers and pediatrician until recently and not a roblem.
The mode by which bottle feeding induces the development of obesity seems to be the following: The breast fed baby sucks as long as it is hungry
and thereby learns when it is satisfied.
By bottle feeding the mother controls the amount of food the infant has to take in, and, influenced by the former ideal of a big, quickly weight-
gaining baby, she often tries to give the quantity prescribed by pediatricians and infant food industry, weather the child is hungry or not.
In this way she deprives her yougster of learning to control its weight.
Artificially fed children grow quicker than their naturally fed couterparts and they are fatter [lii],[liii],[liv],[lv],[lvi],[lvii],[lviii],[lix],[lx],[lxi],[lxii].
From longitudinal studies, which follow the life of the overfed infant, the adults seem to keep the habit of overeating [lxiii],[lxiv]. That overeating is
a habit that is difficult to change, many people will be able to confirm by their personal experience.
Longitudinal growth data on children who developed obesity during childhood reveal a distinct tendency for height gain to accelarate coincident
with or after the onset of excessive weight gain. The magnitude of the relative height increment is related to the degree of overweight. Overnutrition
accelarates growth, just as undernutrition retards it [lxv].
A further hint to the time during which the diet exerts its influence can be seen in the increased height of breast cancer patients [xxxvii] .
While overrweight could be acquired by overeating as an adult, it is not possible to explain tallness by events taking place lately during individual
life.
3.b AGE AT MENARCHE

Similar to the trend in breastfeeding, the time shift to early menarche started in the nineteenth century [lxiii].
Early menarche is consistently found in breast cancer patients [xl],[lxii],[xliv][xlviii],[lxvi],[lxvii],[lxviii],[lxix],[lxx].[lxxi],[lxxii],[lxxiii],[lxxiv],
[lxxv],[lxxvi] ,[lxxvii].
A feature that is easily explainable as an effect of overweight induced by artificial feeding as menarche dependant on a certain minimal weight.
Obese girls have an earlier menarche than their slim counterparts, a difference that has been found in different societies [lxxviii],[lxxix],[lxxx],
[lxxxi],[lxxxii],[lxxxiii],[lxxxiv],[lxxxv].
Thus, both overweight and early menarche may be a consequence of bottle feeding.
3.c WEALTH
That wealthy women catch breast cancer more frequently [xl],[lxxxvi],[lxxxvii],[lxxxviii],[lxxxix],[xc],[xci],[xcii] is easy to understand if artificial
feeding is related to its induction. Probably the efect would be even bigger if one would look on the wealth of the parental family. Bottle feeding is
more expensive than breast feeding, a point that was more important in the beginning of artificial feeding, but which today can be seen in the third
world [xciii].
3.d DELAYED TIME OF FIRST FULL PREGNANCY

The link between delayed time of first full pregnancy or childlessness and breast cancer has been described for many societies [xl],[xlii],[xliii],
[xliv],[xlv],[lxxxviii],[lxxxix],[xc],[xci],[lxxv],[lxxvi] ,[lxxvii],[xci],[xcii], [xciv], [xcv],[xcvi],[xcvii],[xcviii],[xcix],[c],[ci],[cii],[ciii],[civ] .
The connection between artificial feeding and delayed time of first birth is easily seen to be the same one as that with wealth. If one tries to
understand the factors that influence women to postpone the time of childbearing, one will probably find a prolonged education[cv] .
If breast cancer patients are compared with a control group of the same education the difference in age at first birth vanishes [cvi],[cvii],[cviii] .
A study on risk factors in nurses only showed that there were few births before an age of 20 years which was attributed to the deferal of pregnancy
until completion of training. In this group of women with the same education there was no consistent risk with age at first birth. Nurses having their
first child between 25 and 29 had even less risk than those becoming mother before 20 [cix]. If wealth of the parental family was the closer risk for
catching the disease, this is understandable because it needs financial support to complete education in spite of becoming mother.
Another study comparing two groups at different risk, but of the same educational level, too, did not find differences in reproductive variables [cx].
During the youth of those generations which at the times of the cited studies were afflicted by breast cancer, a good education was confined to the
more affluent parts of the population which could afford it for their daughters. This subgroup is likely to be the same as the one that had the money
for artificial feeding.
Also, prolonged education makes understandable a higher incidence of abortions and the frequent use of contraceptives among patients before their
first pregnacy [xcviii],[xcix],[cxi]. As the time from marriage to first birth does not differ between patients and controls, late first birth does not
seem to reflect medical problems but the decision of the women [cxi] ,[cxii],[cxiii],[cxiv].
3.e URBAN RESIDENCE

The last important feature is the overproportional affliction of the urban population, even in high incidence countries [c],[ci],[cii].
In our times, the reasons for that are most easily seen in the developing countries, where new habits like bottle feeding must spread from towns to
the rural area.
Means for artificial feeding, such as bottles, and milk formulas, are supplied by and through the hospitals, and propagated by advertising, which
does not reach the village as quickly as the town. So infections spread by bottlefeeding are more likely to occur more early in urban raised children.
4 . THE GEOGRAPHY OF MAMMARY CANCER IN COMPARISON TO THE AVAILABILITY OF DIARY PRODUCTS

In general , the countries of Western civilisation and high economic standard showed a high incidence rate, except of Japan, where the incidence
was low [xxii], though the country was comparable in standard of living and collecting data.
The other less well known exception probably is the North of Sudan, which, in spite of severe underdevelopment, is said to have a very high
incidence of breast cancer [cxv],[cxvi].
In the following I show that that those differences in breast cancer incidence may be explainable by the availability of dairy products to young
infants. The lowest incidence of breast cancer probably was seen in traditionally living Cancadian Eskimos among which the first case of mammary
carcinoma was described in 1968 [cxvii], although almost 100% were regularly medically checked, including X-ray, because of the high prevalence
of tuberculosis [cxvii] ,[cxviii].
In the report of the International Union Against Cancer, the incidence in five continents were compared for site of occurrence and adjusted to
different standard populaions, African, European and World [cxix].
In that time, Japan, and the Chinese population of Singapore were showing the lowest incidence of developed countries.
Both ethnics did not use cows milk as food [xxvii],[xxviii], neither for infants nor for adults, until Western influence produced a change [cxx].
In the report of the International Union against Cancer only the Chinese of Singapore were included for comparison. But now there are also data
conserning the Indian and the Malaysian population [cxxi].
The Malaysians were not easy to compare as they still prefered their traditioanal medicine. But between Chinese and Indian descendants no
difference in using health facilities were observed. Both groups showed low incidence rates.
But the Indian incidence rate of 30,4 cases per 100.000 was a third higher than the 18.2 found among Chinese population (diagnosed between 1968-
1970).
In comparison to the Chinese kitchen, the Indian one knows many milk dishes which can be verified by every Indian cooking book and it is possible
that the Indian infant has more access to cows milk than a Chinese one, even if both are breast-fed.
The loweset incidence rate were collected from for African regions [cxix].
In Lourenco Marques, today called Mapluto in Mozambiqui, Ibadan in the South of Nigeria, among the Bantu population of Johannesburg, and in
Kyadondo in Uganda, breast cancer was a rare disease. Ibadan in Nigeria lies in the region inhabited by the tsetse fly which forbade the rearing of
Cattle until the invention of insecticides. Milk products were not available.
In Kyadondo incidence rates were further listed for different subgroups of the population [cxxii]. Kyadondo lies around the the Lake Victoria and
was inhabited by immigrants from many parts of Uganda besides the aboriginal Ganda tribe. The Cancer incidence rates for people born in the
region and those of immigrants were compared for the incidence rates of selected sites. There were no substantial differences for both groups
besides breast cancer and leukemias, which were about doubled in the immigrants, which contrasts surprisingly to the highly uniform incidence
rates seen in both groups for the other sites [cxxii] .
The aboriginal Ganda tribe is not used to rearing cattle, as the region aroud Lake Viktoria was spoiled by trypanosoma rhodiense which is passed on
by the tsetse fly. In contrast, the immigrant popuation stems from a number of different tribes, among those Nilo-Hamitic pastoralists.
Trypnosoma rhodiense is not found in all Uganda, and in other parts of the country the rearing of cattle occurs and an immigrant in her infancy
might have had come into contact with cows milk.
There exists some information on the extent of cattle breeding by Bantus in general, suggesting that the habit was acquiered from Nilo Hamitic
tribes not to long ago and that it was not so important for the production of food but for demonstrating wealth and importance of the owner [cxxiii],
[cxxiv].
Women of childbearing age were very restricted in their access to milk and cattle and the production of butter as body lotion being commen among
Nilo Hamitic tribes was not observed [cxxv].
In Contrast to these four African regions, the Sudan is said to have a high frequency of breast cancer [cxxv], [cxxvi].
The Nilo Hamitic tribes living in this region are known for their intensive contact to cattle, and their animals play a major part in the economic life.
Milk products are used as food, medicine, and body lotion, whilst the cows urin serves to clean dishes. Some tribes drink the fresh blood often
mixed with milk. So there may be many chances for a new born infant to get infected by a bovine virus. No incidence rates have been collected, but
ist is intersting that the high incidence of disease is said to stop in the South [cxxv], were the region of the tsetse fly, which restricts the rearing of
cattle, begins.
The age of breast cancer patients in Khartoum is similar to that of patients in developed countries [cxxvii] where older, postmenopausal patients are
predominant. In countries where the eidemic rise in breast cancer incidence has not been observed the rate does not increase with age. Instead the
incidence curve levels off after menopause 88, a phenomenon called Clemmensens hook.
In Ethopia nearly half of the population is said to belong to tribes who although not being Nilo Hamites use similar food [cxxviii].
The women use butter as body lotion soon after birth [cxxviii].
In Addis Abeba the capital of Ethopia among 4640 hospital admission, male and female, there were five breast cancer patients [cxxix].
In the further south lying district Ukambeni in Kenya, a Bantu region, there was no case among 12,475 patients 23% of whom were adult
females[cxxx].
5. THE CHANGE IN RISK FACTORS FOR BREAST CANCER, IF ONE LOOKS ON BREAST CANCER PATIENTS ONLY
Looking for risk factors predisposing women for breast cancer, scientist often compare those with and to others without breast cancer. But if a
researcher would for example look in a mouse to find out what would promote breast cancer development, he would do that with a mouse which by
infection and genetics has at least the possibility to develop the disease. That means he uses infected mice and than test influence of diet, parity or
homonal influences.
In watching a group of breast cancer patients only [cxxxi],[cxxxii] a collective similar to those used in animal experiments was built. Being affected
with breast cancer, they shurely had the possibility of developing the disease. In this groups parity showed to have promoting effect on age of
diagnosis with breast cancer. This resembles the induction of tumors in the mouse infected with the Mouse Mammary Tumor Virus MMTV where
parity promotes tumor development[cxxxiii],[cxxxiv],[cxxxv].
If risk factors are studied by comparing affected and never affected women one possibly compares infected and not infected populations. That may
be the reason that risk factors in man and mouse look so different at the first glance.
6. BREAST CANCER IN ANIMALS
Breast Cancer is very frequent in laboratory rats and mice which are often bred especially to study the disease. So this is a special situation and I
will not include it in the discussion on the epidemiology of breast cancer.
Rabbits are used as lab animals too, but until now I was not able to find anything about breast cancer in the rabbit. In books on rabbit disease
mammary neoplams were not mentioned.
Like in the rabbit there is nothing about breast cancer in the cow. But there is one difference: That cows do not have breast cancer is well known.
If one looks in books on buatric (cow’s) disease, one is surprised about the similarity of the content to books on women’s disease. So the lack of
mammary neoplasms in cows was always found to be surprising.
It is not so surprising if one speculates that the human breast cancer may be a disease which is transmitted by a cow’milk born virus.
As mentioned before, viruses often do not cause dangerous disease in their long term hosts. If they did, this would be deleterious to their host and
deprive the virus of its home and place to multiply.
But if by chance the virus finds entrance to a new species or race to which it is not yet adalpted, the before benigne agent may cause dangerous
disease. That’s what we see now occurring after the infection of humans by the Human Immundefiency Viruses HIV.
In their original simian host the virus cannot become connected with any harm. But in humans, which they infected only recently, they cause deadly
disease in nearly every infected individual.
Cats and dogs very often develop breast cancer [cxxxvi],[cxxxvii].
If it is a cow’s milk born disease this is not surprising as pet animals often serve a an infant substitut and get milk especially if they are young. If one
talks with people breeding this animals they always give the advice that one should not do it, because the animals get diarrhoe and other side effects
problems. Obviously they are well known because feeding pets especially young ones with milk products is not uncommen.
More on animal breast cancer
An animal, to my knowlegde new to the human household, is the hedgehog. In Germany people take little hedgehogs out of the garden because they
want to help it to survive the winter. The think some infant hedgehogs are to small to manage the situation themselves. There are also clubs for this
hedgehog helpers which warn on their homepage to give milk to the animals. Probably because it is done so often. Actually on the first homepage I
saw, besides the warning against using milk as food, I found a picture with a ust rescued baby hedgehog clinging to a typical baby bottle filled with
white stuff looking like milk. Probably because this animal was not perceived as a hedgehog but as a baby hedgehog.
In the light of this new habit I was not surprised to find two papers of mammary carcinoms in hedgehogs[cxxxviii],[cxxxix].
7. BREAST CANCER BEFORE THE INTRODUCTION OF COW’S MILK BASED FORMULAS AS INFANT FOOD
The use of cow’s and other animal’s milk to feed or console human infants is known since ancient times [cxl].
But it was seldom succesfull. In some regions the habit exist to put something like butter in the mouth of the newborn. Often a piece of cloth was
soaked with some fluid like water, beer, wine or milk and honey to give the child something to put in its mouth as we today use a comforter
(pacifier, soother, dummy). In rich families milk and honey were used.
That cow’s milk was an expensive nutrient in many societies may have contributed to the peculiar distribution of breast cancer noted by Ramazzini
around 1700[cxli]. He had observed it’s increased occurrence in nuns.
More than a century later this obsevation became confirmed. In the first epidemiologic study of cancer, published 1844[cxlii], Rigoni-Stern
analysed deaths in Verona between 1760 and 1839. He showed that nuns were five times more likely to develop breast cancer than other women.
Of cause it was thought that their special life style was causative for their disease. But in that time, becoming a nun was a possibility only for a very
select group of the society and had rarely to do with religious feelings. Instead parents tried to put those daughters in a convent who could otherwise
have claimed their part of the families inheritance.
It was necessary to to pay a sometimes very high dowry for the entrance to the convent. So this life was only possible for daughters of rich families.
Girls without dowry could only get a domestic job in a convent. But they could not become a nun.
Although the familiy of the nun had to pay the dowry, the later inheritance could not become claimed. So many rich families chose and could
choose this life for their daughters, when they did not want to divide their fortune. That were possibly the families whoose daughters as infants had
more contact to expensive food like cow’s milk.
So the nuns did not only have a rare life style, but probably a very select parentage and infant nutrition, different from those of most other female
inhabitants of Verona.
8. RISK FACTORS MAY CHANGE
The research on breast cancer produced a vast amount of knowledge on risk factors for the development of disease. I have tried to read this
knowledge to trace the origins of the risks to source of it’s may be infectious origin, as it has been done in aids, where the peculiar epidemology led
the way to the virus.
Although the epidemiology changed as the virus penetrated different populations with their different habits, the concept of virus transmission could
explain the changing affection of populations wether they were promiscous people transmitteing the virus by personal contacts or orphans like in
Romania where the disease long time was confined to children in state own facilities, in which the helpless inhabitants had been vacinated with
unchanged needles.
In this way risk factors for breast cancer will change, too. While for example bottle feeding in the beginning was a habit of wealthy parents, today
many educated mothers fear the risks of early bottle feeding and are no more influenced by the ideal of a big fat baby. They prefer a slim child and
even if they use bottles, fearing later obesity they often don’t use it for overfeeding.
So today the early bottle-fed and quicker weight-gaining infants are more often found in the lower socioeconomic groups [cxliii],[cxliv].
AETIOLOGICAL MECHANISMS WHICH MAY BE IN ACCORDANCE WITH THE ABOVE DESCRIBED ASSOCIATIONS
A possible way of carcinogenesis by early contact with bovine milk could be induction of obesity as outlined in chapter 3.
Other mechanisms of oncogenesis compatible with the outlined hypothesis could involve the induction of tolerance to milk born agents by early oral
contact. Feeding is known to produce tolerance to the given antigen, especillay if the first contact takes place in the neonatal period and it might
render the organism defenceless to a later occuring infectious agents with similar surfaces.
A latent infection by a bovine milk born at the time of birth might be another likely mechanism. This is an interesting possibility as there is a bovine
immundeficiency virus BIV and an oncogenic bovine leukemia virus BLV contained in cow’s milk.
And, of course, there might be other infectous agents in bovine milk, which doing no harm to the cow, are unknown until now.
From the epidemiology one cannot favor one of the possiblities. But knowlegde about BLV, its relative BIV and about the molecular biology of
human breast cancer warrants a close look on this viruses.
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0. Introduction
Although mammary cancer has been known for centuries and was described even in times of old Greek medicine[i], its incidence has increased
greately during the last hundred years [ii],[iii],[iv],[v].
Considering the major changes which have taken place during this time, one concerning the disease could be the rise in artificial feeding of infants
[vi],[vii],[viii],[ix], and it was thought that women who did not breast-feed their children might be susceptible[x].
However, since the analyses of MacMahon in 1970[xi], which were confirmed later many times[xii](review), it is obvious that breast feeding does
not protect women from catching the disease.
In the first animal model, the breast cancer virus was passed on by the milk of the mother to the suckling mouse[xiii]. This example influenced
studies on the dangers of breast feeding for daughters of mothers with breast cancer, which failed to show any dangers [xiv],[xv] [xvi].
One important thing, the mouse mammary tumor system shows, is that the peroid of susceptibility clings to the time of birth. A time during which
the immune system of the infant is not mature and foreign agents can gain entrance to the organism unregognized. But this hint was not taken up by
breast cancer epidemiology.
In the beginning of tumor virology it was an important finding that it was easy to induce a tumor in a newborn animal [xvii],[xviii], especially if one
used the virus of another species [xix],[xx],[xxi].
Before this was known, the difficulties in building model systems seriously hampered science[xxii]. In the human being, cow’s milk may be an easy
vehicle for a milk born virus to enter a newborn infant, especially as viral DNA, being sufficient for tumor induction, is not destroyed by cooking or
pasteurization (more).
In the following analysis I show that immigration data and cohort analyses hint at the time of birth as a period for catching the disease and that the
epidemiology of breast cancer is explainable by early contact to bovine milk, which was boosted by a change to bottle feeding after the successful
introduction of milk – based formulas for infant feeding.
Subsequently I outline the connection of milk production and the diary industry to the geographic distribution of breast cancer. This reaches from
Eskimos with neither cattle nor mammary neoplasms, over East Asians having cattle but not using milk products, to countries with easy access to
bovine milk and a high frequency of breast cancer. A connection found in the Western industrial countries and, less well documented, among East
African Nilo Hamitic tribes.
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13: 689-696,1974.
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54 :402-417, 1980.
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[xi] MacMahon B, Lin TM, Low CR. Lactation and Cancer of the brast. Asummary of an international Study. Bull WHO 42: 185-194, 1970.
[xii] Kalache A, Vessez MP, McPherson K. Lactation and breast cancer. Br Med J: 224-225, 1980.
[xiii] Bittner JJ. Some possible effects of nursing on the mammarz gland tumor incidence in mice. Science 84: 162, 1936.
[xiv] Morgan RW, Vakil DV, Chipman ML. Breast feeding, familiy history and breast disease. Am J Epidemiol 99: 117-122, 1974.
[xv] Tokuhata GK. Morbidity and mortality among offspring of breast cancer mothers. Am J Epidemiol 89: 139-153, 1969.
[xvi] Titus-Ernstoff L, Egan KM, Newcomb PA, Baron JA, Stampfer M, Greenberg ER, Cole BF, Ding J, Willett W, Trichopoulos D. Exposure
to breast milk in infancy and adult breast cancer risk. J Natl Cancer Inst. 1998 Jun 17;90(12):921-4.
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Proc Soc Esp Biol Med 76:27-32, 1951.
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156,1962.
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361-368, 1960.
[xx] Eddy BE, Borman #GS, Berkeley WH, Young RD. Tumors induced in hamsters by injection of Rhesus monkey Kidney cell extracts. Proc
Soc Exp Bio Med 107: 191-197, 1961.
[xxi] Trentin JJ, Yabe Y, Taylor G, the quest for a human cancer virus. Science 137: 835-841, 1962.
[xxii] Tooze J. the molecular biology of tumor viruses. Publisher : Cold Spring Harbour Laboratory, 1973.
1. Immigrant Data and the Cohort Wise Rise in Incidence Rates point to the Time around Birth as an Important one for Catching Breast
Cancer http://web.archive.org/web/*/http://www.erieping.de/cear1.htm
In Japan, where cow’s milk, as well as other diary products were not used as human food before Western habits reached the country, mammary
cancer was an uncommon disease [i].
Japanese immigrants to Hawaii and San Francisco were an interesting group to investigate for changes in rates of several types of cancer [ii].
While rates for neoplasms of other sites changed to the American number, those for mammary cancer remained stable for a rather long time, giving
support to speculations of hereditary differences [iii].
In the seventies of the last century, the first data showing a big rise in site specific incidence rates occuring among American born daughters of
Japanese immigrants in the region of San Francisco were published [iv],[v].
In Hawaii, where the immigration to the new country had taken place earlier, this change had not been seen [ii],[iv].
The population of Hawaii, except for its Anglo - American part, consisted mainly of Polynesian, Chinese, Japanese, and later of Philippine
descendents, which, like all East-Asian peoples, did not use Cow's milk as human food [vi],[vii] and it is possible that this commen feature delayed
the change in infant nutrition.
Some time before the data on Japanese immigrants were published , Haenszel, who had studied breast cancer incidence among Polish Americans,
in reanalysing his data, found that a rise in incidence rates could only be found in groups with a substantial American born component [viii].
These hints to the time of birth as an the decisive one for catching the disease, was confirmed by data collected in Iceland, Britan, USA, Finland,
which show that breast cancer incidence varies in a cohort-wise manner Error: Reference source not found2. The Change in Infant Feeding and
the Rise in Mammary Cancer Incidence http://web.archive.org/web/*/http://www.erieping.de/cear2.htm
The big rise in breast cancer incidence started with women born at the end of the ninteenth century[i],[ii],[iii],[iv].
At about this time, a change in infant nutrition took place in which the human breast milk was replaced by mixtures of cow’s milk [v],[vi],[vii],
[viii].
Although known since ancient times, artificial feeding had never been successful, and as late as in the nineteenth century, artificial feeding became
more popular, the so called “Kindermehl”.
After the death of his sister, who left a some month old child behind, Henri Nestle got interested in developing an artificial food for infants. On the
ad it does not look like a newborn one, was based on cow’s milk but changed in composition to be more similar to human milk. Its use lost much of
its immediate danger, exerted by contaminating bacteria, when the effect of heat treatment became known.
The importance of hygienic treatment of baby food and the composition of its ingredients were intensively discussed in the pediatric litarature of
that time.
In Switzerland Nestle began the propagation of the “Kindermehl” [ix], and in the United States several companies started similar activities. Since
companies were careful not to compete with the pediatricians but to recommend the use of the formulas only on their advice, the artificial feeding of
babies became popular among larger parts of the wealthier population, whose daughters later had greater chances to suffer from mammary
neoplasms.
A connection which explains the high incidence of breast cancer in educated women during the start of the epidemic.
2.a. More on Change in Infant Food http://web.archive.org/web/*/http://www.erieping.de/morcear2.htm
Children of less well off mothers got hand-fed too. But as milk products were expensive, arrowroot and sago were preferred and there was also
patent food made from barley and wheat or potato flour [i].
[i] Lewis M. The problem of infant feeding: the Australian experience from the mid-nineteenth century to the 1920s.
J Hist Med Allied Sci. 1980 Apr;35(2):174-87
2.b. Henri Nestlé
Henri Nestlé was born in Frankfurt in 1814, and moved to Vevey in his twenties, a merchant and small-scale inventor. He slowly gravitated
towards foods and foodstuffs, experimenting with various recipes for baby-food to help mothers who were unable to breastfeed, and eventually
came up with a concoction he called farine lactée, based, as he put it, on “wholesome Swiss milk and a cereal component baked by a special process
of my invention”. In 1867, he fed this to a premature baby boy whose mother was dangerously ill herself; the boy survived, and Nestle's reputation
skyrocketed. The following year he opened an office in London to cope with the quantity of orders, and within five years was exporting to South
America and Australia. In 1874 he sold his company for a million francs
In the time of Nestlé it was a big problem to raise a child when the mother could not do it. The only relatively safe possibility was to engage another
woman for breast-feeding, if the child was sick. For example when it suffered from a congenital syphillis, so that a woman breast-feeding this child
would get infected and develope the disease too, the child had nearly no possibility of survival. In this situation it is imaginable that the new
possibility was seen as a real advantage.
The problems created by Nestles invention which can be seen as a very big intervention in the human ecology, probably were not conceivable by
him. If one is quickly condemning him, I have to think of to other inventions which were more recently introduced in the upbringing of infants and
which may have long term effects, too.
So the buggy and the feeding of water or milk formulars directly after birth to prevent the natural weight lost seen in healthy newborns may have
later appearing consequences which are not much feared now.
3. Risk Factors for Human Breast Cancer http://web.archive.org/web/*/http://www.erieping.de/cear3.htm
The epidemiologic data which are connected with breast cancer are overweight, tallness, early menarche, wealth, the delayed age at firth birth e.g.
childlessness, urban residence [i][i],[ii][ii],[iii][iii],[iv] and prenatal influences like high birth weight.
3.a Weight and Height 3.b Age at Menarche 3.c Wealth and Parental family
3.d Delayed Time of First Full Pregnancy 3.e Urban Residence 3.f i High Birthweight 3.fii Low Birthweight
[i] Kelsey JL. A review of the epidemiology of human breast cancer. Epidemiol Rev 1:74-109, 1979.
[ii] Petrakis NL, Ernster VL, King MC. Breast . In Cancer epidemiolgy and prevention. Editors Schottenfeld D, Fraumeni JF: 855-870, 1982.
[iii] Kalache A. Risk factors for breast cancer. Clinics in Oncology Vol 1 No 3: 661-678, 1982.
[iv] McPherson, K, Steel, CM, & Dixon, JM: Breast cancer-epidemiology, risk factors, and genetics. BMJ 2000, 321:62
3.a. Weight and Height http://web.archive.org/web/*/http://www.erieping.de/3weight.htm
The connection between obesity and breast cancer has been studied in many societies and is well established [i], [ii], [iii], [iv], [v], [vi], [vii], [viii],
[ix], [x], [xi], [xii], [xiii], [xiv], [xv], [xvi], [xvii].
On the contrary, the link between overweight and artificial feeding has only in the seventies started to attract the attention of scientists [xviii], [xix],
[xx].
May be, because until recently raising a big, fat baby was a goal, achieved by many loving mothers and pediatricians, not a problem.
In the beginning of artificial feeding it was probably not anticipated that many overfed baby might keep their eating habits for all their life giving
rise to overweight and its implications.
The mode by which bottle feeding induces the development of obesity seems to be the following: The breast fed baby sucks as long as it is hungry
and thereby learns when it is satisfied.
By bottle feeding the mother controls the amount of food the infant has to take in, and, influenced by the former ideal of a big, quickly weight-
gaining baby, she often tries to give the quantity prescribed by pediatricians and infant food industry, weather the child is hungry or not.
In this way she deprives her yougster of learning to control its weight.
Artificially fed children grow quicker than their naturally fed couterparts and they are fatter [xxi], [xxii], [xxiii], [xxiv], [xxv], [xxvi], [xxvii],
[xxviii], [xxix], [xxx], [xxxi].
From longitudinal studies, which follow the life of the overfed infant, the adults seem to keep the habit of overeating [xxxii],[xxxiii]. That
overeating is a habit that is difficult to change, many people will be able to confirm by their personal experience.
Longitudinal growth data on children who developed obesity during childhood reveal a distinct tendency for height gain to accelarate coincident
with or after the onset of excessive weight gain. The magnitude of the relative height increment is related to the degree of overweight. Overnutrition
accelarates growth, just as undernutrition retards it [xxxiv].
A further hint to the time during which the diet exerts its influence can be seen in the increased height of breast cancer patients [xxxv].
While overweight might be acquired by overeating as an adult, it is not possible to explain tallness by events taking place lately during individual
life.
[i] De Waar F, Baandersvan-Halewijn EA, Huizinga J. The bimodal age distribution of patients with mammary carcinoma. Evidence for the
existence of two types of human breast cancer. Cancer 17: 141-151, 1964.
[ii] De Waard F, Halewijn EAB. A prospective study in general practise on breast cancer risk in postmenopausal women. Int J Cancer 14:153-160,
1974.
[iii] De Waard F, Breast cancer incideence and nutritional status with particular reference to body weight and height. Cancer res 35: 3351-56,
1975.
[iv] MacMAhon B, Formal discussion of “Breast Cancer incidence and nutritional status with particular reference to body weight and height. “
Cncer Res 35: 3357-58, 1975.
[v] Wynder EL, MacCornak F, Hill P. Nutritionand the etiology and prevention of breast cancer. Cancer Det Prev 1: 293-310, 1976.
[vi] Valaaoras VG, MacMahon B, Trichopoulos D,et la. Lactation and reproductive histories of breast cancer patients in greater Athens, 1965-
67. Int J Cancer 4: 350-363, 1969.
[vii] Fasal E, Paffenberger RS. Oral contraceptives as related to cancer and benigne lesions of the breast. J Natl Cancer Inst 55: 767-773, 1975.
[viii] Lin TM, Chen KP, MacMahon B. Epidemiologic Characteristics of cancer Of the Breast in Taiwan. Cancer 27: 1497-1504, 1971.
[ix] Mirra AP, Cole P, MacMahon B. Breast cancer in an area of high parity. Sao Paulo Brazil. Cancer Res 31: 77-83, 1971..
[x] Ravnihar B, MacMahon B, Lindtner J, Epidemiologic features of breast Cancer in Slovenia, 1965-67. Eur J Cancer 7: 295-221, 1971.
[xi] Phillips RL.Role of Life-style and dietary habits in risk of cancer among Seventh- Day Adventists. Cancer Res 35: 3515-3522, 1975
[xii] de Waard F, Cornelis HP, Aoki K, Yoshida M. Breast Cancer incidence according to weight ans Height in two citiies of the Netherlands and
in Aichi Prefecture. Japan Cancer 40: 1269-1275, 1977.
[xiii] Miller A, Kelly A, Choi N. A Study of Diet and breast cancer. Am J Epidemiol 107: 499-509, 1978.
[xiv] Brinton LA Williams RR, Hoover RN, Stegens NL, Feinleib M , Fraumeni JF Jr. Breast cancer risk factors among screening program
participants. J Natl Cancer Inst 62: 37-44. .
[xv] Gray GE, Pike MC, Henderson BE. Breast Cancer incidence and mortality rates in different countries in relation to known risk fctors and
dietary practices. Br J Cancer 39: 1-7, 1979.
[xvi] Lubin J, Burns P, Blot W, Ziegler R, Lees A, Fraumeni J. Dietary factors and breast cancer risk. Int J Cancer 28: 685-689,1981.
[xvii] Hiatt RA, Fireman BH. Smoking, Menopause, and Breast Cancer. JNCI 76: 833-838, 1986.
[xviii] Jellifee DB, Jellifee EFP. Fat babies: Perils, Prevalence, and prevention. J Trop Peddiat Env Child Helth 21: 123-159, 1975.
[xix] Taitz LS. Infantile overnutrition among artificially fed infants inthe Sheffield Region. Br. Med J 1: 315-316, 1971.
[xx] Kramer MS. Do breast feeding and the delayed introduction of solid foods protect against subsequent obesity. J pediatr.98: 883-887, 1981.
[xxi] Jellifee DB, Jellifee EFP. Fat babies: Perils, Prevalence, and prevention. J Trop Peddiat Env Child Helth 21: 123-159, 1975.
[xxii] Taitz LS. Infantile overnutrition among artificially fed infants inthe Sheffield Region. Br. Med J 1: 315-316, 1971.
[xxiii] Kramer MS. Do breast feeding and the delayed introduction of solid foods protect against subsequent obesity. J pediatr.98: 883-887, 1981.
[xxiv] Hitchcock NE, Gracey M, Owles EN. Growth of healthy breast fed infants in the first six month. Lancet 2: 64-65, 1981
[xxv] Chandra RK. Breast feeding, grwoth and morbidity. Nutr Res1: 25-31, 1981.
[xxvi] Rowland MGM, Paul AA, Whithead RG. Lactation and infant nutrition. Br. Med Bull 37: 77-82, 1981
[xxvii] Whitehead RG, Paul AA. Infant growth and human milk requirements: A fresh approach. Lancet 2: 161-163, 1981.
[xxviii] Waterlow JC, Ashworth A, Griffith M Faltering in infant growth in less-developed countries Lancet 2: 1176-1177, 1980.
[xxix] Duncan B, Schaefer C, sibley B, Fonseca NM. Reduced growth velocity in exclusively breast- fed infants. Am J Dis Child 138: 309-317,
1984.
[xxx] Tönz O, Schwaninger U, Holzherr E, Schafroth M. Die Säuglingsernährung in der Schweiz, 1978. Schweiz Med WSCHR 100: 937-947, 1980
[xxxi] Hitchcock NE, Gracey M, Gilmour AI. The growth of Breast Fed and Artificially Fed Infants from Birth to Twelve Months. Acta Padiatr
Scand 74: 240-245, 1985.
[xxxii] Tanner JM. Physical growth. In P.M. Mussen (Ed.), Carmichaels Manual of Child Psychology (Vol. 1). New York: Wiley, 1970
[xxxiii] Stini WA. Early nutrition, growth, disease, and human longevity. Nutr. Cancer 1:31-39,1979.
[xxxiv] Forbes GB. Nutrition and growth. J Pediatr 91: 40-42, 1977.
[xxxv] De Waard F, Breast cancer incideence and nutritional status with particular reference to body weight and height. Cancer res 35: 3351-56,
1975.
3.b. Age at Menarche http://web.archive.org/web/*/http://www.erieping.de/3ageatme.htm
Similar to the trend in breastfeeding, the time shift to early menarche started in the nineteenth century[i].
Early menarche is consistently found in breast cancer patients[ii],[iii],[iv],[v],[vi],[vii],[viii],[ix].[x],[xi],[xii],[xiii],[xiv],[xv] ,[xvi].
A feature that is easily explainable as an effect of overweight induced by artificial feeding, as menarche is dependant on a certain minimal weight.
Obese girls have an earlier menarche than their slim counterparts, a difference that has been found in different societies [xvii],[xviii],[xix],[xx],[xxi],
[xxii],[xxiii],[xxiv].
Thus, both overweight and early menarche may be a consequence of bottle feeding.
[i] Tanner JM. Physical growth. In P.M. Mussen (Ed.), Carmichaels Manual of Child Psychology (Vol. 1). New York: Wiley, 1970
[ii] [ii] Valaaoras VG, MacMahon B, Trichopoulos D,et la. Lactation and reproductive histories of breast cancer patients in greater Athens, 1965-
67.Int J Cancer 4: 350-363, 1969.
[iii] Lin TM, Chen KP, MacMahon B. Epidemiologic Characteristics of cancer Of the Breast in Taiwan. Cancer 27: 1497-1504, 1971
[iv] Ravnihar B, MacMahon B, Lindtner J, Epidemiologic features of breast Cancer in Slovenia, 1965-67. Eur J Cancer 7: 295-221, 1971.
[v] Salber EJ, Trichopoulos D, MacMahon B,. Lactation and reproductive histories of breast cancer patients in Boston 1965-1966. J Natl Cancer
Inst, 43: 1013-1024, 1969.
[vi] Shapiro S, Strax P, Venet L, Fink R. The search for Risk factors in breast cancer. Am J Public Health Nations Health 58: 820-835, 1970.
[vii] Henderson BE, Powell D, Rosario I, Keys C, Hanisch R, Young M, Casagrande J, Gerkins V, Pike MC. An epidemioogic study of breast
[viii] Tulinius H, Day NE, Johannesson G, Bjarnason O, Gonzales M. Reproductive factors and risk for breast cancer in Iceland. Int J Cancer 21:
724-730, 1978.
[ix] Thein-Hlang, Thein-Maung-Mint. Risk factors of breast cancer in Burma. Int J Cancer 21: 432-437, 1978.
[x] Talamini R, La Vecchia O, Franceschi S, Colombo F, Decarli A, Granttoni E, Grigoletto E, Tognoni G, Reproductive and hormonal factors and
breast cancer in a northern Italian population. Int J Epidemio 14: 70-74, 1985.
[xi] Yuasa S, MacMahon B. Lactation and reproductive histories of breast cancer patients in Tokyo, Japan. Bull WHO 42: 195-204, 1970.
[xii] Stavracky K, Emmons S. Breast cancer in premenopausal and postmenopausal women. J Natl Cancer Inst 53: 647-654, 1974.
[xiii] Staszewski J. Age at Menarche and breast cancer. J Natl Cancer Inst 47: 935-940, 1971.
[xiv] Lubin Jh, Burns PE, Blot WJ, Lees AW, May C, Morris LE, Fraumeni JF. Risk Factors for Breast Cancer in Women in Northern Alberta,
[xv] Byers T, Graham S, Rzepka T, Marshall J. Lactation and Breast Cancer. Am J Epidemiol 124: 353-358, 1986.
[xvi] McTiernan A, Thomas DB. Evidence for a protective effect of lactation on risk of breast cancer in young women. Am J Epidemoil 124: 353-
358, 1986.
[xvii] Frisch RE, Revelle R. The height and weight of girls and boys at the time of initiation of the adolescent growth spurt in height and weight and
the relationship to menarche. Hum Biol 43: 140-159, 1971.
[xviii] Acheson RM. Marturition of the skeleton. In Human Development. Ed. Faulkner F. Philadelphia, PA, WB Saunders: 465-502, 1966
[xix] Frisch RE. Criticak weight at Menarche, initiation of the adolescent growth spurt, and control of puberty ln: Control of the Onset of Puberty.
Ed Grumbach MM Grave GD, Mayer FE. New York, Wiley 403-423, 1974
[xx] Bruch H. Obesity in childhood. I. Physical growth and development of obese children. Am J Dis Child 58: 457-484, 1939.
[xxi] Forbes GB. Lean body Mass and fat in obese children. Pediatrics 34: 308-314, 1964.
[xxii] Nobecutz P. Obesete et puberte. Presse Med 46: 449-452, 1938.
[xxiii] Quade F, Obese children - Anthropology and Environment. Copenhagen, Danish Science Presse, Ltd, 1955.
[xxiv] Wolff OH. Obesity in childhood. Q J Med 24: 109-123, 1955.
3.c Wealth and the Education of the Fathers of Breast Cancer Patients http://web.archive.org/web/*/http://www.erieping.de/3wealth.htm
That wealthy women catch breast cancer more frequently[i],[ii],[iii],[iv],[v],[vi],[vii],[viii] is easy to understand if artificial feeding is related to its
induction. Probably the effect would be even bigger if one would look on the wealth of the parental family. The Bottle feeding is more expensive
than breast feeding, a point that was more important in the beginning of artificial feeding, but which today can be observed in poor countries [ix].
Besides wealth, the education of the father, too, increases the breast cancer incidence in his daughters, probably for the same reason[x].
[i] Valaaoras VG, MacMahon B, Trichopoulos D,et la. Lactation and reproductive histories of breast cancer patients in greater Athens, 1965-67.
Int J Cancer 4: 350-363, 1969
[ii] Dom HF, Cutler SJ. Morbidity from Cancer in the United States. Public Health Monograph No. 56. Washington, D.C., U.S: Government
Printing Office, 1959.
[iii] Graham S, Levin M, Lilienfeld AM. The economic distribution of cancer of various sites in Buffalo. N.Y., 1948-1952. Cancer 13: 180-191,
1960.
[iv] Clemmensen j. Statistical Studies in the aetiology of malignent neoplasms. In : The Breast, Acta Pathol Microbiol Scand Suppl 174: 1-543,
1965.
[v] Cutler SJ, Young JL (editors). Third National Cancer Survea: Incidence Data. Natl Cancer Inst Monograph No.41. Washington, D.D. , U.S.
Government Printing Office.
[vi] Hiraama T. epideiology of breast cancer with spezial reference to the role of diet. Prev Med /: 173-195, 1978.
[vii] Lowe CR, MacMahon B. Breast Cancer an d reproductive history of woen in South Wales. Lancet 1: 153-157, 1970.
[viii] Soini I Hakama M Inverse Association Between Risk Factors for Benign and Malignent Breast Lesions. Scand J Soc Med /: 79-85, 1979.
[ix] Arbeitsgruppe Dritte Welt Bern. Exportinteressen gegen Muttermilch. Freimut Duve ed.. Rowohlt Verlag, Reinbeck bei Hamburg, 1976.
[x] Titus-Ernstoff L, Egan KM, Newcomb PA, Ding J, Trentham-Dietz A, Greenberg ER, Baron JA, Trichopoulos D, Willett WC. Early life factors
in relation to breast cancer risk in postmenopausal women. Cancer Epidemiol Biomarkers Prev. 2002 Feb;11(2):207-10.
3.d. Delayed Time of First Full Pregnancy http://www.erieping.de/3delayed.htm
The link between delayed time of first full pregnancy or childlessness and breast cancer has been described for many societies [i], [ii], [iii], [iv], [v],
[vi], [vii], [viii], [ix], [x], [xi], [xii], [xiii], [xiv], [xv], [xvi], [xvii], [xviii], [xix], [xx], [xxi], [xxii], [xxiii], [xxiv].
The connection between artificial feeding and delayed time of first birth is easily seen to be the same one as that with wealth. If one tries to
understand the factors that influence women to postpone the time of childbearing, one will probably find a prolonged education[xxv] .
If breast cancer patients are compared with a control group of the same education the difference in age at first birth vanishes [xxvi],[xxvii],[xxviii] .
A study on risk factors in nurses only, showed that there were few births before an age of 20 years. That was attributed to the deferral of pregnancy
until completion of training. In this group of women with the same education there was no consistent risk with age at first birth. Nurses having their
first child between 25 and 29 had even less risk than those becoming mother before 20 [xxix].
If wealth of the parental family was the closer risk for catching the disease, this is understandable because it needs financial support to complete
education in spite of becoming mother.
Another study comparing two groups at different risk, but of the same educational level, too, did not find differences in reproductive
variables [xxx].
During the youth of those generations which at the times of the cited studies were afflicted by breast cancer, a good education was confined to the
more affluent parts of the population which could afford it for their daughters. This subgroup is likely to be the same as the one that had the money
for artificial feeding.
Also, prolonged education makes understandable a higher incidence of abortions and the frequent use of contraceptives among patients before their
first pregnacy[xxxi],[xxxii],,[xxxiii].
As the time from marriage to first birth does not differ between patients and controls, late first birth does not seem to reflect medical problems but
the decision of the women[xxxiv], ,[xxxv],[xxxvi],[xxxvii].
[i] Valaoras VG, MacMahon B, Trichopoulos D,et la. Lactation and reproductive histories of breast cancer patients in greater Athens, 1965-67. Int
J Cancer 4: 350-363, 1969.
[ii] Lin TM, Chen KP, MacMahon B. Epidemiologic Characteristics of cancer Of the Breast in Taiwan. Cancer 27: 1497-1504, 1971.
[iii] Mirra AP, Cole P, MacMahon B. Breast cancer in an area of high parity. Sao Paulo Brazil. Cancer Res 31: 77-83, 1971.
[iv] Ravnihar B, MacMahon B, Lindtner J, Epidemiologic features of breast Cancer in Slovenia, 1965-67. Eur J Cancer 7: 295-221, 1971.
[v] Phillips RL.Role of Life-style and dietary habits in risk of cancer among Seventh- Day Adventists. Cancer Res 35: 3515-3522, 1975.
[vi] Henderson BE, Powell D, Rosario I, Keys C, Hanisch R, Young M, Casagrande J, Gerkins V, Pike MC. An epidemioogic study of breast
[vii] Tulinius H, Day NE, Johannesson G, Bjarnason O, Gonzales M. Reproductive factors and risk for breast cancer in Iceland. Int J Cancer 21:
724-730, 1978.
[viii] Thein-Hlang, Thein-Maung-Mint. Risk factors of breast cancer in Burma. Int J Cancer 21: 432-437, 1978.
[ix] Talamini R, La Vecchia O, Franceschi S, Colombo F, Decarli A, Granttoni E, Grigoletto E, Tognoni G, Reproductive and hormonal factors
and breast cancer in a northern Italian population. Int J Epidemio 14: 70-74, 1985
[x] Lubin Jh, Burns PE, Blot WJ, Lees AW, May C, Morris LE, Fraumeni JF. Risk Factors for Breast Cancer in Women in Northern Alberta,
[xi] McTiernan A, Thomas DB. Evidence for a protective effect of lactation on risk of breast cancer in young women. Am J Epidemoil 124: 353-
358, 1986.
[xii] Lowe CR, MacMahon B. Breast Cancer an d reproductive history of woen in South Wales. Lancet 1: 153-157, 1970.
[xiii] Soini I Hakama M Inverse Association Between Risk Factors for Benign and Malignent Breast Lesions. Scand J Soc Med /: 79-85, 1979.
[xiv] MacMAhon B, Cole P, Lin TM, Lowe CR, Mirra AP, Ravnihar B, Salber EJ, Valaoras VG, Yuasa S. Age at first birth and breast cancer risk.
Bull WHO 43: 209-221, 1970.
[xv] Sartwell PE, Arthes FG, Tonascia JA. Exogenous hormones, Reproductive History, and Breast Cancer . J Natl Cancer Inst 59: 1589-1592,
1977.
[xvi] Craig TJ, Comstock GW, GeiserPB, Epidemiologic comparison of breast cancer patients with early and late onset of malignancy and general
population controls. J.Ntl Cancer Inst 41: 315-329, 1968.
[xvii] Feinleib M. Breast cancer and artificial menopause: A cohort study. J Natl Cancer Inst 41: 315-329, 1968.
[xviii]Paffenbarger RS Jr, Fasal E, Simmons ME, Kampert JB. Cancer risk as related to use of oral contraceptives during fertile years. Cancer 39
(Suppl): 1887-1891, 1977.
[xix] Pike MC, Hendersond BE, Casagrande JT, Rosario I, Gray GE. Oral contraceptives use and early abortion as risk factors for breast cancer
[xx] Hoover R, Gray LA Sr, Cole P, MacMahon B. Menopause estogens and breast cancer. New England J Med 295: 401-405, 1976.
[xxi] Bolt WJ, Fraumeni JF Jr, Stone BJ. Geographic patterns of breast cancer in the United States. J. Natl Cancer Inst 59: 1407-1411, 1977.
[xxii] De Waard F. Recent time trends in breast cancer incidence. Prev Med /; 167-169, 1978.
[xxiii] MacMahon B, Purde M, Cramer D, Hint E. Association of Breast Cancer Risk with Age at First Birth and Subsequent Births: A Study in the
population of the Estonian Republic. JNCI 69: 1035-1038, 1982.
[xxiv] Wysowki DK, Goldberg EL, Comstock GW, Diamond EL. A study of a possible association betweeen breast cancer and glallbladder
disease.Am J Epidemiol 123: 532-543, 1986.
[xxv] Bloom DE, Trussel J. What are the determinants of delayed childbearing and permanent childlessness in the Unites States. Demography 21:
591-611, 1984.
[xxvi] Herity BA, O'Halloran MJ, Bourke GJ, Wilson-Davis K. A study of breast cancer in Irish women. Br J Prev Soc Med 29: 178-181, 1975
[xxvii] Gjorgov AN. Barrier Contraception and Breast Cancer. In : Contributions to Gynecology and Obstetrics. Ed.. Keller PV. Karger Basel 8:
80-84, 1980.
[xxviii] Choi NW, Howe GR, Miller AB, Matthews V, Morgan RW, Munan L, Burch JD, Feather J, Jain M, Kelly A. An epidemiologic study of
breast cancer . Am J Epidemiol 107: 510-521, 1978.
[xxix] Bain C, Willett W, Rosner B, Speizer FE, Belanger C, Hennekens CH. Early age at first birth and decreased risk of breast cancer. Am J
Epidemiol 114: 705-709, 1981.
[xxx] Frisch RE, Wyshak G, Albright NL, Albright TE, Schiff I, Jones KP, Witschi J, Shiang E, Koff E, Marguglio M. Lower prevalence of breast
cancer and cancers of the reproductive system among former college athletes compared to non-athletes. Br J Cancer 52: 885-891, 1985.
[xxxi] Paffenbarger RS Jr, Fasal E, Simmons ME, Kampert JB. Cancer risk as related to use of oral contraceptives during fertile years. Cancer 39
(Suppl): 1887-1891, 1977.
[xxxii] Pike MC, Hendersond BE, Casagrande JT, Rosario I, Gray GE. Oral contraceptives use and early abortion as risk factors for breast cancer
[xxxiii] McPherson K, Neil A, Vessey MP, Doll R. Oral contraceptives and breast cancer. Lancet 2: 1414, 1983.
[xxxiv] McPherson K, Neil A, Vessey MP, Doll R. Oral contraceptives and breast cancer. Lancet 2: 1414, 1983.
[xxxv] Paffenberger RS, Kampert JB, Chang HG. Characteristics that predict risk of breast cancer before and after the menopause. Am J
Epidemiol 112: 258-268.
[xxxvi] Lilienfeld AM, Coombs J, Bross ID, Chamberlain A.Marital and Reproductive Experience in a Community-Wide Epidemiological Study of
Breast Cancer. The john Hopkins Medical Journal 136: 157-162, 1975.
[xxxvii] Vessey MP, McPherson K, Roberts MM, Neil A, Jones L. Fertility in relation to the risk of breast cancer. Br J Cancer 52: 625-628, 1985.
3.e. Urban Residence http://web.archive.org/web/*/http://www.erieping.de/3uraban.htm
The last important feature is the overproportional affliction of the urban opulation, even in high incidencecountries [i],[ii],[iii].
In our times, the reason for that are most easily seen in the developing countries, where new habits like bottle feeding must spread from towns to the
rural area.
Means for artificial feeding, such as bottles, and milk formulas, are supplied by and through the hospitals, and propagated by advertising, which
does not reach the village as quickly as the town. So infections spread by bottlefeeding are likely to occur more early in urban born infants.
[i] Pike MC, Hendersond BE, Casagrande JT, Rosario I, Gray GE. Oral contraceptives use and early abortion as risk factors for breast cancer in
young women. Br J Cancer 43: 72-78, 1981
[ii] Hoover R, Gray LA Sr, Cole P, MacMahon B. Menopause estogens and breast cancer. New England J Med 295: 401-405, 1976.
[iii] Bolt WJ, Fraumeni JF Jr, Stone BJ. Geographic patterns of breast cancer in the United States. J. Natl Cancer Inst 59: 1407-1411, 1977.
3.f.I. High Birth Weight http://web.archive.org/web/*/http://www.erieping.de/3highbir.htm
That early years of life might be important for developing breast cancer got suspected since age at menarche had been described as an important risk
factor for the disease. Very early even prenatal influences acting during intrauterine life came under suspicion only recently [i],[ii].
Preclampsia/eclampsia, prematurity and birth weight became studied[iii].
High birth weight as a risk factor for breast cancer was seen examining prenatal factors in women born in the Uppsala University Hospital between
1874 and 1954.
Those who according to Swedish Cancer Registry developed breast cancer between 1958 and 1990 were compared with controls selected from
females born by mothers who where admitted directly after the probands to the wards of the Uppsala University Hospital.
The results showed history of preclampsia /eclampsia during pregnancy to be connected with a lower breast cancer rate in the offspring.
Weaker results in the same study showed a positive connection of high birth weight and breast cancer incidence. But this risk factor was confirmed
in several studies [iv],[v],[vi],[vii],[viii],[ix],[x],[xi],[xii],[xiii] in different areas as were USA, Norway, Britain, and Denmark.
The result raises interest in the search for factors which influence birth weight and which might influence breast cancer risk too.
One answer comes from a study with 513 London mothers. The dimensions of babies, their birth weight and head circumference was compared with
the diet of their mothers. Among other nutritients, but not for total intake of energy, the diet of mothers with low birth weight babies was poorer in
dairy products than those of heavier newborns[xiv].
In the East African pastoral tribes which original kept a diet of cow’s blood and cow’s milk, women exclude cow’s milk from their diet during late
pregnancy, because they fear birth complications, if they drink to much milk or milk products. They think that the fetus gets to big for an easy
delivery if the mother includes milk in the diet. Especially the bones of the head are expected to be to mature to allow birth without complication.
So that the head will traumatize the birth channel while passing it.
In this connection one should remember that for example in Germany, where women are encouraged to drink milk and eat milk products during
pregnancy, because this food is thought to be especially healthy, episiotomy is a standard prophylaxis in the majority of deliveries to avoid perineal
laceration.
Of cause, in Western countries the necessity of episiotomy is no problem. And it is not even seen as a birth complication, but as a standard
procedure. For a women in East Africa without access to episiotomy the risks of perineal laceration is one, worth to avoid it by diet restriction.
It is possible that the positiv correlation between higher birth weight and later breast cancer incidence reflects the dairy product intake of the
mothers who give birth to infants with high birth weight and who by this habit of milk consumption offer a route for some milk born factor which is
associated with breast cancer incidence.
Hints that prenatal bovine protein consumption may influence late disease incidence comes from animal models, too. In the last years, initiated by
studies on the risk of Insulin Dependent Diabetes Mellitus IDDM and infant nutrition, especially the some times observed different risk for breast
and bottle-fed infants, it was tried to look at animal models on the influence of infant nutrition and IDDM in animals.
There are two often used models of IDDM . The Non Obese Diabetic Mouse short NOD mouse and the BB rat.
The NOD mouse is an inbred Japanese derived albino mouse. 25 -30% of the female Nod animals develop IDDM between 120 and 200 days of life,
when fed on the laboratory y mouse chow.
This mouse chow contains wheat, barley, meat and bone meal derived from cows, pigs and sheep and includes offal and is also supplemented with
minerals, trace elements and vitamins.[xv]
Meat and bone meal is something which came in connection with the mad cow disease to the knowledge of a bigger audience and what probably
used to enriched the animal diet in a cheap way with animal protein.
If this meat and bone meal in the diet is replaced by a diet free of complete protein which instead contains protein hydrolysate containing only
amino acids, the diabetes prone animals have difficulties to develop the disease.
Concerning the above outlined hypothesis of connections between maternal consumption of milk products, birth weight and cancer risk and early
contact and breast cancer incidence the following is especially interesting. Although the protein free diet exerts its protecting effect, if started just
before weaning[xvi], its influence is bigger if the diet is started by the mother beginning with conception of the tested litters131.
The BB rat another animal prone to develop diabetes was shown to be protected too from developing this disease by the introduction of a
protein free diet shortly after weaning [xvii] .
[i] Epidemiologic evidence of perinatal influence in the etiology of adult cancers. Janerich DT, Hayden CL, Thompson WD, Selenkas SL, Mettlin C.
J Clin epidemiol 1989; 42: 151-7.
[ii] Hypothesis: does breast cancer originate in utero? Trichopoulos D. Lancet. 1990 Apr 1;335(8695):939-40.
[iii] Evidence of prenatal influences on breast cancer risk. Ekbom A, Trichopolous D, Adami H, Hsieh C, Lan S, Lancet 1992, 340:1015-8
[iv] Perinatal factors and the risk of breast cancer.Sanderson M,Williams MA, Malone KE, Epidemiology 1996, 7:34-37 .
[v] Birthweight as a risk factor for breast cancer. Michels KB, Trichopoulos D, Robins JM, Rosner BA, Manson JE, Hunter DJ, Colditz GA,
Hankinson SE, Speizer FE, Willett WE, Lancet 1996, 348:1542-6.
[vi] Birthweight, childhood growth and risk of breast cancer in a British cohort.Stavola BL, Hardy R, Kuh D, Silva IS, Wadsworth M, Swerdlow
AJ.Br J Cancer. 2000 Oct;83(7):964-8.
[vii] Associations of adult measures of childhood growth with breast cancer: findings from the British Women's Heart and Health Study.Lawlor
DA, Okasha M, Gunnell D, Smith GD, Ebrahim S. Br J Cancer. 2003 Jul 7;89(1):81-7.
[viii] Birth characteristics and subsequent risk for breast cancer in very young women.Innes K, Byers T, Schymura M.Am J Epidemiol. 2000 Dec
15;152(12):1121-8.
[ix] Cancer risk in Swedish women: the relation to size at birth. Andersson SW, Bengtsson C, Hallberg L, Lapidus L, Niklasson A, Wallgren A,
Hulthen L.Br J Cancer. 2001 May 4;84(9):1193-8.
[x] Fetal growth and subsequent risk of breast cancer: results from long term follow up of Swedish cohort.McCormack VA, dos Santos Silva I, De
Stavola BL, Mohsen R, Leon DA, Lithell HO.BMJ. 2003 Feb 1;326(7383):248.
[xi] Birth weight as a predictor of breast cancer: a case-control study in Norway.
Vatten LJ, Maehle BO, Lund Nilsen TI, Tretli S, Hsieh CC, Trichopoulos D, Stuver SO. Br J Cancer. 2002 Jan 7;86(1):89-91.
[xii] Birth weight and risk of early-onset breast cancer (Denmark).Mellemkjaer L, Olsen ML, Sorensen HT, Thulstrup AM, Olsen J, Olsen
JH.Cancer Causes Control. 2003 Feb;14(1):61-4.
[xiii] Birth weight and risk of breast cancer in a cohort of 106,504 women.
Int J Cancer. 2003 Dec 20;107(6):997-1000.Ahlgren M, Sorensen T, Wohlfahrt J, Haflidadottir A, Holst C, Melbye M.
[xiv] The association of maternal social class with maternal diet and the dimensions babies in a plopulation of London women. Wynn SW, Wynn
AH, Doyle W, Crawford MA, Nutr Health, 1994, 9:303-15.
[xv] Acombined casein-free-nicotinamide diet prevents diabetes in the NOD mouse with minimum insulinitis. Reddy S, Bibby NJ, Wu D, Swinney C,
Barrow G, Elliot RB, Diabetes Research and Clinical Practise 1995,29: 83-92
[xvi] Dietary Prevention of diabetites in the non-obese diabetic mouse. Elliott RB, Reddy SN, Bibby NJ, Kida K. Diabetologia 1988,31:62-64
[xvii] Dietary Protein: a trigger of insulin-dependent diabetes in the BB rat? ElliottRB, Martin JM, Diabetologia 1984, 26: 297-9
3.f.II. Premature Birth and Low Birth Weight http://web.archive.org/web/*/http://www.erieping.de/3lowbir.htm
The risk of premarture birth was studied in detail for girls born in Stockholm, Sweden from 1925 to 1934. The authors found out what had happened
to this girls after birth: Extremely premature children during this time period were treated in a uniform manner. They stayed at the maternity ward
for about 24 hours, and survivors were then transferred to a pediatric ward, where they were offered nutritional support.
The girls born before the 31st week had a 6.7 fold greater risk of breast cancer and 12.2 fold risk to develope breast cancer before 50 years of
age [i].
The risk of low birth weight sometimes observed in studies of this parameter may have the same reason.
What happens to infants with a low birth weight?
They often get a bottle to improve their nutritional intake. Especially if they are perceived to be to weak for breast feeding what is an active process
affording work of the baby the change to bottle feeding or aditional bottle feeding with milk based formulas is an alternative. Often the newborn
have to stay in the hospital until they have reached a certain minimal weight, while the mother can go home. In this cases, too, the mother is less
present for breast feeding and the chance for the infant to get cow’milk based formulas will be greater.
[i] Risk of Breast Cancer in Prematurely Born Women. Anders Ekbom, Gunnar Erlandsson, Chung-cheng Hsieh, Dimitrios Trichopoulos, Hans-
Olov Adami, Sven Cnattingius J Natl Cancer Inst. 2000 May 17;92(10):840-1
4. Breast Cancer and Early Contact with Bovine Milk: The Geography of Breast Cancer in Comparison to the Availability of Diary
Products http://web.archive.org/web/*/http://www.erieping.de/cear4.htm
In general , the countries of Western civilisation and high economic standard show a high incidence rate, except of Japan, where the incidence was
low [i], although the country was comparable in standard of living and collecting data.
The other less well known exception probably is the North of Sudan, which, in spite of severe underdevelopment, is said to have a very high
incidence of breast cancer [ii],[iii].
In the following I show that those differencesin breast cancer incidence may be explainable by the availability of dairy products to infants.
The lowest incidence of breast cancer probably was seen in traditionally living Cancadian Eskimos among which the first case of mammary
carcinoma was described in 1968 [iv], although almost 100% were regularly medically checked, including X-ray, because of the high prevalence of
tuberculosis [v].
In the report of the International Union Against Cancer, the incidence in five continents were compared for site of occurrence and adjusted to
different standard populaions, African, European and World [vi].
In that time, Japan, and the Chinese population of Singapore were showing the lowest incidence of developed countries.
Both ethnics did not use cows milk as food [vii],[viii], neither for infants nor for adults, until Western influence produced a change [ix].
In the report of the International Union against Cancer only the Chinese of Singapore were included for comparison. But now there are also data
conserning the Indian and the Malaysian population [x].
The malaysians were not easy to compare as they still prefered their traditional medicine. But between Chinese and Indian descendants no
difference in using health facilities were observed. Both groups showed low incidence rates. But the Indian incidence rate of 30,4 cases per 100.000
was a third higher than the 18.2 found among Chinese population (Diagnosed between 1968-1970). In comparison to the Chinese kitchen, the Indian
one knows many milk dishes which can be verified by every Indian cooking book and it is possible that the Indian infant has more access to cows
milk than a Chinese one, even if both are breast-fed.
Similar relations were found when looking for antibodies against MMTV. While there were less than 5% positive sera in Chinese breast cancer
patient. Antibodies could be demonstrated in 37% of Indian breast cancer patients[xi].
From molecular biology there is aditional evidence that there might be an infectious agent in Western population that did not yet infect women who
during infancy lived in an East Asian Country that shielded its population from many foreign influences.
Vietnam is a East Asian country whoose inhabitants traditionally did not use bovine milk as food. And it is one of the regions where Western eating
habits probably were prohibited from spreading in the past. Its inhabitants and refugees did not yet experience the rise in breast cancer
incidence[xii],[xiii], that could be observed in other countries.
Using PCR and primers that amplify gene sequences of MMTV tissue from Caucasian-Australian, Vietnamese-Australian, and Vietnamese women
was tested and it was found that MMTV-like gene sequences were amplified in 19 of 45 (42.2%) archival breast cancer biopsy tissues from
Caucasian-Australian women, but only 1 of 120 (0.8%) and 0 of 41 breast cancer biopsy tissues from Vietnamese and Vietnamese-Australian
women from the first immigrant generation, respectively.
The same sequences were found in only 2 of 111 and 0 of 60 non cancerous breast tissue samples from Australian and Vietnamese women,
respectively. A result that would be in accordance with an exogenous virus which did not yet penetrate all populations[xiv].
The lowest incidence rates were collected from some but not all African regions [xv].
In Lourenco Marques, today called Maputo in Mozambique, Ibadan in the South of Nigeria, among the Bantu population of Johannesburg, and in
Kyadondo in Uganda, breast cancer was a rare disease.
Ibadan in Nigeria lies in the region inhabited by the tsetse fly which forbade the rearing of cattle until the invention of insecticides. At that time milk
products were not available.
In Kyadondo incidence rates were further listed for different subgroups of the population. Kyadondo lies around the the Lake Victoria and at the
time of the study was inhabited by immigrants from many parts of Uganda besides the aboriginal Ganda tribe. The incidence rates for people born in
the region and those of immigrants were compared for the incidence rates of selected sites. There were no substantial differences for both groups
besides breast cancer and leukemias, which were about doubled in the immigrants. That contrasted surprisingly to the highly uniform incidence
rates seen in both groups for the other sites. [xvi].
The aboriginal Ganda tribe was not used to rearing cattle, as the region aroud Lake Viktoria was spoiled by trypanosoma rhodiense which is passed
on by the tsetse fly. In contrast, the immigrant popuation stemed from a number of different tribes, among those Nilo-Hamitic pastoralists.
Trypnosoma rhodiense is not found in all Uganda, and in other parts of the country the rearing of cattle occured and an immigrant in her infancy
might have had come into contact with cows milk.
There exists some information on the extent of cattle breeding by Bantus in general, suggesting that the habit was acquiered from Nilo Hamitic
tribes not to long ago and that the new habit was not so important for the production of food but for demonstrating wealth and importance of the
owner [xvii],[xviii].
Women of childbearing age were very restricted in their access to milk and cattle and the production of butter as body lotion being commen among
Nil Hamitic tribes was not observed [xix].
In contrast to these four African regions, the Sudan is said to have had a high frequency of breast cancer [xx],[xxi],[xxii].
The Nilo Hamitic tribes living in this region are known for their intensive contact to cattle, and their animals play a major part in the economic life.
Milk products are used as food, medicine, and body lotion, whilst the cows urin serves to clean dishes. Some tribes drink the fresh blood often
mixed with milk. So there may be many chances for a new born infant to get infected by a bovine virus.
No incidence rates have been collected, but ist is interesting that the high incidence of disease is said to stop in the South[xxiii], the region of the
tsetse fly, which restricts the rearing of cattle.
The age of breast cancer patients in Khartoum is similar to that of patients in developed countries [xxiv] where older, postmenopausal patients are
predominant. In countries where the eidemic rise in breast cancer incidence has not been observed the rate does not increase with age. Instead the
incidence curve levels off after menopause[xxv], a phenomenon called Clemmensens hook.
In Ethopia nearly half of the population is said to belong to tribes who use food similar to those of Nilo-Hamites. The women use butter as body
lotion soon after birth [xxvi].
In Addis Abeba the capital of Ethopia among 4640 hospital admission, male and female, there were five breast cancer patients [xxvii]. In the further
south lying district Ukambeni in Kenya, a Bantu region, there was no case among 12,475 patients 23% of whom were adult females[xxviii].
In studies on antibodies against MMTV reactivity could be demonstrated in 61% of breast cancer patients and in 26.9% of healthy donors of the
region [xxix].
[i] Segi M, Kurihara M, Matsujama T. Cancer Mortality in Japan, 1899-1962. Dep pof Public Health, Tokuho Univers School of Med, Sendai,
Japan
[ii]Burkitt G. Geographical Distribution of Cancer in East Africa. In: Racial and geographical factors in tumor incidence. Ed.: Shivas AA,
[iii] Hickey BB. Malignant Epithelial Tumours in the Sudanese. Ann R Coll 24: 303-322, 1959.
[iv] Schaefer O. Cancer of the Breast and Lactaton. Canad Med Ass J 100: 625-626, 1969.
[v] Schaefer O, Hildes JA, Medd LM, cameron DG. The changing pattern of neoplastic disease in Canadian Eskimos. Canad Med Ass J 112: 1399-
1404, 1975.
[vi] Doll R, Payne P, Waterhouse J. Cancer Incidence in five Continents. Springer Verlag, Berlin Heidelberg New York, 1966.
[vii] Hahn E. Die Haustiere und ihre Beziehungen zur Wirtschaft des Menschen. Leipzig ,1896.
[viii] Sauer CO.Agricultural Origins and Dispersals. Am Geograph Soc, 1952.
[ix] Oiso T. Incidence of stmac cancer and ist ralation to dietary habits and nutrition in Japan between 1900 and 1975. Cancer Res 35: 3254-3258,
1975.
[x] Shanmugaratnam K. Cancer in singapore-Ethnic and dialect group variations in cancer incidence. Singapore Med J 14: 69-81, 1973.
[xi] Day NK, Witkin SS, Sarkar NH, Kinne D, Jussawalla DJ, Levin A, Hsia CC, Geller N, Good RA. Antibodies reactive with murine mammary
tumor virus in sera of patients with breast cancer: geographic and family studies. Proc Natl Acad Sci U S A. 1981 Apr;78(4):2483-7.
[xii] Anh PT, Parkin DM, Hanh NT, Duc NB. Cancer in the population of Hanoi, Vietnam, 1988-1990. Br J Cancer. 1993 Dec;68(6):1236-42.
[xiii] Nguyen MQ, Nguyen CH, Parkin DM. Cancer incidence in Ho Chi Minh City, Viet Nam, 1995-1996. Int J Cancer. 1998 May 18;76(4):472-9..
[xiv] Ford CE, Tran D, Deng Y, Ta VT, Rawlinson WD, Lawson JS. Mouse mammary tumor virus-like gene sequences in breast tumors of
Australian and Vietnamese women. Clin Cancer Res. 2003 Mar;9(3):1118-20.
[xv] Doll R, Payne P, Waterhouse J. Cancer Incidence in five Continents. Springer Verlag, Berlin Heidelberg New York, 1966
[xvi] Davies JNP, Knowelden J, Wlson BA. Incidence rates of cancer in Kyadondo county, Uganda, 1954-1960. J Nat Cancer Inst 35: 798-821,
1965.
[xvii] Baumann H, Thurnwald R, Westermann D, Völkerkunde von Afrika. Essen 1940.
[xviii] Simoons F, The non-milking area of Africa. Anthropos 49: 58-66, 1954.
[xix] Kroll H. die Haustiere der Bantu. Zeitschrift für Ethnologie 60: 170-290, 1928.
[xx] Burkitt G. Geographical Distribution of Cancer in East Africa. In: Racial and geographical factors in tumor incidence. Ed.: Shivas AA,
[xxi] Hickey BB. Malignant Epithelial Tumours in the Sudanese. Ann R Coll 24: 303-322, 1959.
[xxii] Daoud EH, El hassan AM, Zak F, Zakova N. Aspects of Malignant Disease in the Sudan. In Cancer in Africa. Ed.: Clifford P, Lindell CA,
Timm GL, Nairobi, East African Publishing House, 43-50, 1968.
[xxiii] Hickey BB. Malignant Epithelial Tumours in the Sudanese. Ann R Coll 24: 303-322, 1959.
[xxiv] Hamad HMA. A preliminary Report on the Role of Tamoxifen in Advanced Breast Cancer in the Sudan. Arab Med J: 1-3, 1986.
[xxv] Clemmensen j. Statistical Studies in the aetiology of malignent neoplasms. In : The Breast, Acta Pathol Microbiol Scand Suppl 174: 1-543,
1965.
[xxvi] Haberland E. Galla Süd-Äthiopiens. Stuttgart, W.Kohlhammer Verlag, 1963
[xxvii] Lester FT, Tsega E. The Pattern of Adult Medical Admissoins in Addis Abeba, Ethiopia. Aest African Med J 53: 620-634, 1976.
[xxviii] Oomen L. Disease Pattern in Ukambani, Kenya. East African Med J 53341-349, 1976.
[xxix] Day NK, Witkin SS, Sarkar NH, Kinne D, Jussawalla DJ, Levin A, Hsia CC, Geller N, Good RA. Antibodies reactive with murine mammary
tumor virus in sera of patients with breast cancer: geographic and family studies. Proc Natl Acad Sci U S A. 1981 Apr;78(4):2483-7.
5. The Change in Risk Factors for Breast Cancer, if one looks on Breast Cancer Patients only
http://web.archive.org/web/*/http://www.erieping.de/cear5.htm
Looking for risk factors predisposing women for breast cancer, scientist often compare those with to others without breast cancer. But if a
researcher would for example look in a mouse to find out what would promote breast cancer development, he would do that with a mouse which by
infection and genetics has at least the possibility to develop the disease.
That means he uses infected mice and than test influence of diet, parity or hormonal influences.
In watching a group of breast cancer patients only [i],[ii] a collective similar to those used in animal experiments was built. Being affected with
breast cancer, they shurely had the possibility of developing the disease. In this groups parity showed to have promoting effect on age of diagnosis
with breast cancer. This resembles the induction of tumors in the mouse infected with the mouse mammary tumor virus MMTV, where parity
promotes tumor development[iii],[iv],[v].
If risk factors are studied by comparing affected and never affected women one possibly compares infected and not infected populations. That may
be the reason that risk factors in man and mouse look so different at first glance.
[i] Woods KL, Smith SR, Morrison JM: Parity and breast cancer: Evidence of a dual effect Brit Med J 281(6237): 419-421, 1980.
[ii] Wang DY, Rubens RD, Allen DS, Milllis RR, Bullbrook RD, Chaudary MA, Hayward JL. Influence of reproductive history on age at diagnosis
of breast cancer and prognosis. Int J Cancer 36: 427-432, 1985.
[iii] Nie R van. In: Mammary Tumors in the Mouse. Ed.: Hilgers J, Sluyser M, 202-266, 1981.
[iv] Dao TL, Sunderland H, Mammary carcinogenesis by 2-methylcholanthrene. I. Hormonal aspects in tumor induction and growth. J Natl Cancer
Inst 23: 567-585, 1959.
[v] McCormick GM, Moon RC. Effect of pregnancy and lactation on growth of mammary tumours induced by 7,12 DMBA. Br J Cancer 19:160-
166, 1965.
6. Breast Cancer in Animals http://web.archive.org/web/*/http://www.erieping.de/cear6.htm
While in wild animals breast cancer seems to be a rare disease, it is not uncommon in zoo and domestic animals. Especially cats and dogs very often
develop breast cancer [i],[ii].
If it is a cow’s milk born disease this is not surprising as pet animals often serve a infant substituts and get milk, especially if they are young. If one
talks with people breeding this animals they always give the advice that one should not do it, because the animals get diarrhoe and other problems.
Obviously
Abbildungen fehlen Milk adapted for raising young cats.
known, because feeding pets, especially young ones, with milk products is common. Zoo animals too, are often raised with cow’s milk mixtures,
if their captured mothers do not show appropiate behavior to the infant and there is is no other way to bring it up.
Another animal developing breast cancer seems to be mus domesticus, the house mouse which likes human food and waste and tries to get it,
without being domesticated. On the other hand there is an animal known to lack breast cancer. It is the cow. If one looks in books on buatric
(cow’s) disease, the similarity of the content to books on women’s disease is obvious. So the lack of mammary neoplasms in cows was always
found to be surprising.
It is not so surprising if one speculates that the human breast cancer may be a disease which is transmitted by a cow’milk born virus.
Milk for raising infant dogs
As mentioned before, viruses often do not cause dangerous disease in their long term hosts. If they did, this would be deleterious to themselves
depriving the virus of its home and place to multiply. So evolution works in favor of a benign outcome of infections.
But if by chance the virus finds entrance to a new species or race to which it is not yet adapted, the before benign agent may cause dangerous
disease. That’s what we see now occurring after the infection of humans by the Human Immundefiency Viruses HIV.
In their original simian host this virus cannot become connected with any harm. But in humans, which they infected only recently, they cause deadly
disease in nearly every infected individual.
An animal, to my knowlegde new to the human household, is the hedgehog. People take little hedgehogs out of the garden because they want to
help it to survive the winter. The rational behind is the thought that some infant hedgehogs are to small to manage the situation themselves. There
are also clubs for this hedgehog helpers which warn on their homepage to give milk to the animals. Probably because it is done so often. Actually,
on the first homepage of hedgehog helpers I visited, besides the warning against using milk as food, I saw a picture with a just rescued baby
hedgehog clinging to a typical baby bottle filled with white stuff looking like milk. Probably because this animal was not perceived as a hedgehog
but as a baby hedgehog
In the light of this new habit I was not surprised to find two papers on mammary carcinomas in hedgehogs[iii],[iv].
An infant animal raised by humans probably not with milk of its own species. In this way it may catch new, latent diseases. The animals raised here
in Kenya are raised in captivity because their mothers are dead. It is planned that they go back to wilderness as adults. By this way they may
introduce a hole bunch of bovine and human infectious agents to the wild elefant population.
[i] Casey HW, Giles RC, Kwapien RP. Mammary neoplasia in animals: pathologic aspects and the effects of contraceptive steroids. Recent Results
Cancer Res 66: 129-60.
[ii] Novasad CA Principles of treatment for mammary gland tumors. Clin Tech Small Anim Pract 18 : 107-9, 2003
[iii] Raymond JT, GernerM. Mammary gland tumors in captive African hedgehogs. J Wildl Dis 36: 405-8.
[iv] Wellehan JF, Southhorn E, Smith DA, Taylor WM. Surgical removal of a mammary adenocarcinoma and a granulos cell tumor in an African
pygmy hedgehog.
7. Breast Cancer before Introduction of Cow's Milk based Formulas as Infant Food
http://web.archive.org/web/*/http://www.erieping.de/cear7.htm
The use of cow’s and other animal’s milk to feed or console human infants is known since ancient times [i].
But it was seldom succesfull. In some regions there is a habit to put something like butter in the mouth of the newborn. Often a piece of cloth was
soaked with some fluid like water, beer, wine or milk and honey to give the child something to put in its mouth as we today use a comforter
(pacifier, soother, dummy). In rich families milk and honey were used.
That cow’s milk was an expensive nutrient in many societies may have contributed to the peculiar distribution of breast cancer noted by Ramazzini
around 1700[ii]. He had observed it’s increased occurrence in nuns. In the first epidemiologic study of cancer, published 1844[iii]
Rigoni-Stern had analysed deaths in Verona between 1760 an1839. He showed that nuns were five times more likely to develop breast cancer than
other women. Of cause it was thought that their special life style was causative for their disease. But in that time, becoming a nun was a possibility
only for a very select group of the society and had rarely to do with religious feelings. Instead parents tried to put those daughters in a convent who
could otherwise have claimed their part of the families inheritance. Of cause a dowry had to be paid for the entrance to the convent. So this life was
only possible for daughters of rich families. Girls without dowry could only get a domestic job in a convent. But without a dowry they could not
become a nun. Although the familiy of the nun had to pay a considerable sum, the later inheritance had not to be paid. So many rich families chose
this life style for their daughters, if they did not want to divide their fortune. In this rich families the daughters as infants probably had more contact
to expensive food like cow’s milk.
So the nuns did not only have a rare life style, but a very select parentage, different from those of most other female inhabitants of Verona.
[i] Brüning H. Künstliche Säuglingsernährung. Enke Verlag, Stuttgart 1908

[ii]Mustacchi P Ramazzini and Rigoi Stern on Parity and Breast Cancer. Clinical impressinons and statistical corroboration. Arch Intern Med
1961 108: 639-642
[iii] Rigoni-Stern DA: Fatti staistici relativi alli malatie cancerose. Gior Servire Prop Path Terap 2: 507-517, 1842 cited after Shimkin MB. Some
historical Landmarks in Cancer Epidemioogy. In: Cancer Epidemiology and Prevention ed. Schottenfeld D, Elsevier, 1982.
Also in: Mustacchi P Ramazzini and Rigoi Stern on Parity and Breast Cancer. Clinical impressinons and statistical corroboration. Ach Intern Med
1961 108: 639-642
and in
Scott J, Bailar JC 3rd. Rigoni-Stern and medical statistics. A nineteenth century approach to cancer research. J Hist Med Allied Sci 24: 65-
75,1969.
8. Risks for Breast Cancer may Change http://web.archive.org/web/*/http://www.erieping.de/cear8.htm
The research on breast cancer produced a vast amount of knowledge on risk factors for the development of disease.
I have tried to read this knowledge to trace the origins of the risks to the source of it’s may be infectious origin, as it has been with aids, where the
peculiar epidemology led the way to the virus.
Although the epidemiology changed as the virus penetrated different populations with their different habits, the concept of virus transmission could
explain the changing affection of populations wether they were promiscous people or orphans like in Romania where the disease long time was
confined to children in state own facilities, in which this children had been vacinated with unchanged needles.
In this way risk factors for breast cancer will change, too. While for example bottle feeding in the beginning was a habit of wealthy parents, today
many educated mothers fear the risks of early bottle feeding and are no more influenced by the ideal of a big fat baby. They prefer a slim child and
even if they use bottles, fearing later obesity they often don’t use it for overfeeding. So, today bottle-fed and quicker weight-gaining infants are
more often found in the lower socioeconomic groups [i],[ii]and it is possible that the groups preferentially affected by breast cancer change in a
similar way.
[i] Hitchcock NE, Coy JF.Infant-feeding practices in Western Australia and Tasmania: a joint survey, 1984-1985. Med J Aust.148:114-7, 1988.
[ii] Hitchcock NE, Coy JF. The growth of healthy Australian infants in relation to infant feeding and social group. Med J Aust 1989 : 306-308,
310-311.
9. Inheritable Breast Cancer (missing)
10. Breast Cancer and Diabetes Type 1 (missing)
11. Breast Cancer and Thyroid Disease http://web.archive.org/web/*/http://www.erieping.de/ciod.htm
The link between breast cancer and thyroid disease has induced many studies out of which the following picture emerges:
Prospective follow-ups of patients with thyroid disease show that they seem to be no more prone to develop mammary carcinoma than the average
person[i],[ii],[iii],[iv].
On the other hand, breast cancer patients have a high incidence of goitre[v],[vi],[vii] a condition reflecting the compensation of iodine deficiency,
which does not have to be associated with abnormal hormone concentration. In regions with high iodine supply, for example in the Germany of
today, where the foood is enriched with iodine, and where is enough iodine for the thyroid and for the cells of breast cancer and its metastases, no
goitre will develop. But in Turkey the development of goitre is still found today[viii].
The reason for the iodine uptake can be seen in the task of the breast to supply the child with iodine[ix] during lactation. The lactating breast shows
a 20 to 30 fold accumulation of iodine compared to blood [x],[xi].
In breast cancer cells this function seems to be active independent of lactation. For mouse mammary tumor cells it was shown that the iodine uptake
could be further stimulated by estrogens, differing from the uptake by thyroid cells depending on thyroid stimulating hormone TSH[xii].
This difference in regulation is now looked for to enable therapy of human breast cancer without removing the thyroid[xiii] ,[xiv].
There is also histological evidence for a nodular formation in thyroid organs accompanied by hyperthrophy of pituary TSH producing cells[xv],
probably developing in response to the activity of iodine trapping tumor cells.
Because of the excellent results of treatment of the differentiated thyroid carcinoma with radioactive iodine[xvi], a similar treatment of breast
carcinoma should be worth testing.
Especially in patients showing development of goitre, as this condition hints not only to the survival of active tumor cells, what is reflected in the
shorter survival time of these patients[xvii], but also to an accumulation of iodine by the metastatic cells, this should be promising. The appearance
of antibodies against thyreoglobulin or transperoxidase which occur during lactation and breast cancer can be seen as a sign of an active iodine
accumulation by the breast too.
The enzymes which do the uptake of iodine, the sodium/iodide symporter called NIS, have been isolated and shown to be active in the healthy
lactating gland and in mammary tumors. More than 80% of isolated of human breast cancer samples expressed the symporter compared to none of
the normal nonlactating samples from reductive mammoplasties[xviii].
Since it is known for longer time that breast tissue may take up iodine, the risk of breast cancer was feared for women being treated with radioactive
iodine 131 for hyperthyroidism. But the results of a risk evaluation showed that the risk was not elevated but reduced after the treatment.
The relative risk for breast cancer in patients with hyperthyroidism treated with radioactive iodine was 0.7 compared to those treated
surgically [xix]. That could mean that small developing breast cancers had been killed as a side effect of the iodine 131 therapy aimed at treating
the hyperthyroidism.
[i] Wynder EL, Bross IJ, Hirayama T. A study of the epidemiology of cancer of the breast. Cancer. 1960 May-Jun;13:559-601.
[ii] Levy J, Levy JA, Role of the hypometabolic state in breast cancer. Am Pract Digest Treat 1951; 522-526.
[iii] Schottenfield D, The relationship of breast cancer to thyroid disease. J Chron Dis 1968; 21: 303-313.
[iv] Hedley AJ, Jones SJ, Spiegelhalter DJ, Clements P, Bewsher PD, Simpson JG, Weir RD. Breast cancer in thyroid disease: fact or fallacy?
Lancet. 1981 Jan 17;1(8212):131-3.
[v] Dassaive P, Observations cliniques en faveur de L’existence de ralations entre la fonction thyroidienne et le compartment de cancer
heterologues. Acta Chir Belge1956 ; 55 :25-49.
[vi] Humphrey LJ, Swerdlow M, The relationship of breast disease to thyroid disease. Cancer 1964; 17: 1170-1176.
[vii] Backwinkel K, Jackson AS. Some features of breast cancer and thyroid deficiency. Cancer 1964; 17: 1174-1176.
[viii] Turken O, NarIn Y, DemIrbas S, Onde ME, Sayan O, KandemIr EG, YaylacI M, Ozturk A. Breast cancer in association with thyroid
disorders. Breast Cancer Res. 2003;5(5):R110-3
[ix] Eskin BA, Parker J, Bassett JG, George DL. Human breast uptake of radioactive iodine. Obstet Gynaecol 1974, 44: 398-402.
[x] Brown-Grant K. The iodide concentrationg mechanismof the mammary gland. J Physiol (lond) 1975;
135: 644-654.
[xi] Brown-Grant K. Extrathyroidal iodide concentration mechanisms. Physiol Rev 1961; 41:189-213.
[xii] Thorpe SM. Increased uptake of iodide by hormone-responsive compared to hormone-independent mammary tumours in GR mice. Int J
Cancer 1976; 18:345-350.
[xiii]Upadhyay G, Singh R, Agarwal G, Mishra SK, Pal L, Pradhan PK, Das BK, Godbole MM. Functional expression of sodium iodide symporter
(NIS) in human breast cancer tissue. Breast Cancer Res Treat. 2003 Jan;77(2):157-65.
[xiv] Wapnir IL, Goris M, Yudd A, Dohan O, Adelman D, Nowels K, Carrasco N. The Na+/I- symporter mediates iodide uptake in breast cancer
metastases and can be selectively down-regulated in the thyroid. Clin Cancer Res. 2004 Jul 1;10(13):4294-302.
[xv] Somers SC Endocrine abnormalities in woman with breasst cancer. Lab Invest 1955; 4: 160-174.
[xvi] Buckwalter JA, Thomas GG. Selection of surgical treatment for well differentiated thyroid carcinomas. Ann Surg 1972; 176: 565.
[xvii] Moossa AR, Price-Evans DA, Brewer AC, Thyroid status and breast cancer: A new appraisal. Ann R Coll Surg Engl 1973; 53: 178-188.
[xviii] Tazebay UH, Wapnir IL, Levy O, Dohan O, Zuckier LS, Zhao QH, Deng HF, Amenta PS, Fineberg S, Pestell RG, Carrasco N. The mammary
gland iodide transporter is expressed during lactation and in breast cancer. Nat Med. 2000 Aug;6(8):871-8.
[xix] Hoffman DA, McConahey WM. Breast Cancer Following Iodine-131 Therapy for Hyperthyroidism. JNCI 1983; 70: 63-67.
II. THE SEARCH FOR THE HUMAN MAMMARY TUMOR VIRUS http://web.archive.org/web/*/http://www.erieping.de/bcvirus.htm
Since it became known that the breast cancer of the mouse is transmitted by a virus, scientists had tried to discover a similar agent responsible for
the disease in women.
Of cause, the standard procedure to find a transmissible agent, a transfection experiment to an other person for ethical reasons was not done.
But it was tried to transmit the human breast cancer to mice. In the animals infected with human breast cancer material the incidence in mammary
tumors raised only slightly from less then 1% to 3%. Instead an increased incidence of lymphoma could become demonstrated after inoculation with
human mammary cancer extracts[i]. More recently, the frequent development of murine T-cell lymphomas after implantation of human
inflammatory breast cancer cells in nude mice was demonstrated[ii]. Two experiments that hint to a transmissible agent inside breast cancer
material.
It has also been looked for immunological cross reactions with the mouse mammary tumour virus MMTV antigens in material of human breast
carcinoma lines [iii], pleural effusion fluids from patients [iv], in cancer tissue[v], and in human milk [vi]. And it was looked for nucleic acids
similar to those of MMTV [vii], [viii]. But early experiments might have been confounded by endogenous viruses.
Then, monocytes from breast cancer patients were discovered to form giant cells [ix]. As giant cell formation may be a sign of viral infection, it was
tried to find retroviral particles and to test them for reverse transcriptase activitity.
After cultivating mononuclear cells for some days particles could be harvested from 97% of all breast cancer patients and from about 11% of
healthy controls. Possibly women, who were carriers, but who did not yet had developed cancer.
The reverse transcriptases of the retroviruses work best with magnesium ions while cellular enzymes prefer manganese ions. The enzyme of the
particles from cultivated monocytes of breast cancer cells preferred magnesium ions. The particles were described to be slightly smaller than
MMTV. Its size was described to be more similar to that of Human Immundeficiency Virus HIV [x].
Two groups tried to confirm the work, but failed in different ways. One could not cultivate the monocytes in a way to produce multinuclear giant
cells. Neither did they find reverse transcriptase activity[xi]. The test done with the same primer that had been used in the original work showed no
reverse transcrpitase activity with the examined material from cultivated monocytes of human breast cancer cells. It neither showed significant
activity with HIV-1 nor with HTLV1 used as positiv controls. Why not was not elucidated.
Contrary to this results, the other group found a lot of multinuclear giant cell formation. But they found them not only in cultured monocytes from
breast cancer patients but as well in those of control subjects with no or with benign breast disease[xii].
Fortunately this publication was very detailed. And one change in the design of their study in comparison to the original work was the use of a
different tissue culture medium. They had taken pooled female AB serum. Al-Sumidaie and his colleges had used calves serum. Unpooled serum
derived from one animal is much less likely to be contaminated.
In the original study it was shown that the retrovirus like particles could be cultivated from cells of nearly all breast cancer patients and from the
blood of about 10% of controls, possibly women who were already infected, but who did not yet have a tumor big enough to be clinically
detectable.
Pooled human serum might contain material from this virus carriers.
Very interesting was an additional result from this study. In spite of giant cell formation a reverse transcriptase activity could not be demonstrated.
The crude supernatant from the mononuclear cell cultures even blocked the activity of MMTV reverse transcriptase which had been used as a
positive control.
As the originally described particles could be observed only after several days of cultivation in non human serum conditioned tissue culture
medium, it is possible, that by growing the cells with the help of pooled human serum the virus production or release to the medium was inhibited or
their activity like that of the MMTV particles became blocked.
It is known that some retroviruses seem to escape eradiction by producing little virus in vivo[xiii].
In her recent review on a possible retroviral etiology of human breast cancer [xiv] the author, probably stimulated by her experience with bone
disease [xv], [xvi], but also by examples of other animal [xvii],[xviii] and human retroviruses[xix] pointed out that blood mononuclear cells should
be examined first, when searching for a human breast cancer virus and that a possibly causative retrovirus must not be MMTV or a very close
relative.
Unlike MMTV which ist difficult to be seen as an agent getting entrance to the human food chain or another way of transmittance, bovine leukemia
virus BLV is a virus contained in milk used for human nutrition especially for nutrition of human and pet animal infants in Western, but today also
in non -Western societies. It had been suspicious since it was known. But with old methods antibodies against it could not be found in human sera.
This has changed however[xx]. Using immunoblotting to test the sera of 257 humans for antibodies of four isotypes (IgG1, IgM, IgA, and IgG4) to
the BLV capsid antigen (p24), at least one antibody isotype reactive with BLV was detected in 74% of the human sera tested. The specificity of the
reactivity was strongly suggested by competition studies and by ruling out cross-reacting antibodies to other chronic human viruses.
I was also looked for changes BLV might induce in bovine mammary tissue. Changed growth properties of bovine mammary epithelial cells lines
containing BLV DNA were found. The cell line showed reduced population-doubling time, higher saturation density, and increased longevity,
features that are typical for tumor cells[xxi]. That BLV could produce such changes in bovine mammary cells inspired a search for BLV DNA in
human breast cancer.
DNA of BLV was found in tissue of breast cancer patients. The study is going on[xxii].
A search for traces of BLV but also for other bovine born agents in cultivated mononuclear cells of breast cancer patients might thus be fruitful.
Two known candidates propagating in cattle are the Bovine Immunedeficiency Virus BIV which is said to be quite similar to Human Immune
deficiency Virus HIV-1 and the Bovine Respiratory Syncytical Virus BRSV. And there may be other bovine retroviruses which if not causing
disease in their natural host may have gone unrecognised until today.
On the other hand, the argument that MMTV ist is not a likely candidate for entering the human food chain does not rule out its involvement.
Although it is not very likely that the virus jumped from mouse to man, it is possible that both species became infected by the same food.
It was shown that the highest incidence of human breast cancer world wide occurs in countries where mus domesticus is the resident native or
introduced species of house mouse[xxiii].
Mus domesticus, also and better known as house mouse, is very interested in human food and it is not unlikly that it got infected by human food or
waste. That mice like man are probably new victims of a putative breast cancer inducing virus is likely because they develop mammary tumors so
easily.
In species harbouring a virus since ancient times it is unlikely that it still induces harmful disease. So while HIV – 1 could cause millions of deaths
in its new human host, its ancestors simian immundeficiency viruses found in numerous African species could not become linked to diease
symptoms. That mice develop mammary tumors so easily makes it likely that they contacted the MMTV ancestors not to long ago.
Similar interesting is the observation of a 44% reduction in the incidence of breast cancer in women fully immunosuppressed following organ
transplantation .This was discussed in connection with observations that some kinds of immunsupression reduced the incidence of mammary tumors
in mice infected with MMTV, too[xxiv].
As mentioned above, retroviral DNA similar to MMTV DNA had been described in material from breast cancer patients before. But is was difficult
to distinguish it from endogenous sequences similar to retroviral DNA occuring in the human genome.
Recently DNA sequences related to the env region of the MMTV genome became isolated from human breast cancer[xxv]. They were specific for
cancer cells and not found in genetic material from probably healthy breast tissue obtained from reduction mammoplasty [xxvi]. They were neither
present in healthy breast tissue of the same patient. That speaks for an exogenous origin of the material.
MMTV like LTR and LTR env gene sequences were found too in human breast cancer cells but not in healthy tissue[xxvii]. They contained the
DNA for the glucocorticoid resposive elements GRE and the superantigen SAG.
That MMTV contains sequences coding for a superantigen is well known and the role the superantigen plays in the disease developement is very
well documented. So finding sequences conding for a superantigen reminds of MMTV.
But the Human Immundeficiency Virus HIV-1, too, containes sequences coding for an superantigen[xxviii].
Another group could, too, could demonstrate MMTV-like env gene sequences in human breast cancer DNA and in a T-Cell lymphoma of a breast
cancer patient[xxix].
The last result is interesting because in many inbred strains of mice, both breast cancer and T-cell lymphoma are caused by MMTV [xxx],[xxxi],
[xxxii].
To induce a lymphoma instead of a mammary tumor in the mouse changes in the long terminal repeats LTRs seem to have had occurred constituing
of about 400 nucleotide deletions and occasional substitutions resulting in unique tandem repeats. Viruses with this changes in its LTRs cause
lymphomas but no mammary tumors 4 to 11 months after inoculation[xxxiii].
As mentioned above, tumors induced by breast cancer material in mice were mainlyy lymphomas, too.
Very recently it was shown that progression from normal breast pathology to breast cancer is associated with increased prevalence of MMTV like
sequences in women and in men[xxxiv].
A new argument against the involvement of MMTV in human breast cancer is the lack of a suitable receptor for MMTV in human cells [xxxv]. The
human transferrin receptor 1, whoose mouse homolog is the entry receptor for MMTV, does not work with MMTV [xxxvi].
But it is interesting that individuals being homozygous for certain mutations of the transferrin receptor 1 gene in combination with a variant of the
hemochromatosis gene have an increased susceptibility to breast cancer[xxxvii].
The transferrin receptor 1 delivers iron-bound transferrin to cells. It is a membran-spanning glycoprotein with a short cytoplasmic domain. At
neutral ph it has a high affinity for iron loaded transferrin. After binding transferrin it traffics to the early acidic endosome where it releases the iron.
Then it goes back to the cell surface, where it releases the transferrin. Peptides or particles that bind at other sites of the tranferrin receptor 1 cause it
to be endocytosed and trafficed to the acidic endosome, too.
That mutations in the transferrin receptor change the susceptibility to breast cancer can thus be seen as an argument for the possibility of a viral
etiology of the disease, which does not have to be MMTV, but may be a relative better adapted to the human homolog of the trasferrin receptor1
which seem to differs for less than 15 base pairs from it’s mouse counterpart [xxxvi] .
Going back to the epidemiology of human breast cancer there might be another possibility for a foreign virus to change it host range . As milk
products used for infant nutrition are cooked, it is unlikely that the infection takes place by virus particles containing not very stable RNA, but as a
transfection by heat stable proviral DNA contained for example in the DNA of milk lymphocytes seems possible. By passaging through this DNA
infected cells host range variants might develope which are able to infect other human cells.
Experimentally host range variants of MMTVs were developed by serial virus passage in feline, human, rat, and canine cells. This MMTV variants
retained the ability to replicate well in the cells of its new species[xxxviii].
On the protein level, material cross reacting with retroviral envelope antigens, which was not present in normal cells, was found, too. This antigens
cross reacted with antibodies against human immundeficiency virus type 1 HIV-1[xxxix]. But they were not identical to HIV-1 proteins. Infection
with HIV-1 was excluded by lack of reactivity to HIV-1 p24 another protein of HIV-1.
HIV-1 is related to human t-cell lymphothrophic virus HTLV-1 and its close relative BLV, the up to now best candidate for a Human Mammary
Tumor Virus HMTV. But HIV-1 seems to be even more closly related to the above mentioned BIV.
MMTV, HIV-1 are well examined viruses. Both are transmitted by milk and have structures coding for superantigens. HTLV-1 causing human
disease also gets examined.
From the closely related bovine viruses only BLV is better known. BIV, BRSV and other bovine viruses are not. That breast cancer contains
material that can elicit lymphoma like MMTV, HTLV-1 and BLV and that it may contain exogenous DNA related to MMTV and its superantigen
coding sequences and exogenous proteins that cross react with HIV-1 hints to a may be still unkown, closely related virus which considering the
epidemiology might be of bovine origin.
That the DNA of BLV is found in the DNA of breast cancer tissue, makes this virus the most likely candidate. Especially because the appearance of
this virus in breast cancer tissue may explain the peculiar epidemiology of human and animal breast cancer, too, as already proposed in 1986 [xl].
Since an increase in mammary tumors in breast fed daughters from breast cancer patients has never been observed [xli],[xlii] ,[xliii], the putative
virus is not very likely to produce infective particles in human epithelial breast tissue which can become transmitted by milk.
So it may be easier to isolate it from cultivated monocytes of breast cancer patients, as has been done before [x].
[i] Basombrio M. A., Mayer A. M. S., Rivell C. An increased incidence of lymphoma in mice inoculated with human breast cancer extracts. Arch.
Geschwulstforsch., 47: 679-684, 1977
[ii] Wakasugi H., Koyama K., Gyotoku M., Yoshimoto M., Hirohashi S., Sugimura T., Terada M. Frequent development of murine T-cell
lymphomas with TcR/+, cd4/8- phenotype after implantation of human inflammatory breast cancer cells in BALB/c nude mice. Jpn. J. Cancer Res.,
86: 1086-1096, 1995.
[iii] Keydar I, Ohno T, Nayak R, Sweet R, Simoni F, Weiss F, Karby S, Mesa-Tejada R, Spiegelman S. Properties of retrovirus-like particles
produced by a human breast carcinoma cell line: immunological relationship with mouse mammary tumor virus proteins. Proc Natl Acad Sci U S
A. 1984 Jul;81(13):4188-92
[iv] Soule HR, Linder E, Edgington TS. Membrane 126-kilodalton phosphoglycoprotein associated with human carcinomas identified by a
hybridoma antibody to mammary carcinoma cells.Proc Natl Acad Sci U S A. 1983 Mar;80(5):1332-6..
[v] Chopra HC, Feller WF. Viruslike particles in human breast cancer. Tex Rep Biol Med. 1969 Winter;27(4):945-53
[vi] Moore DH, Charney J, Kramarsky B, Lasfargues EY, Sarkar NH, Brennan MJ, Burrows JH, Sirsat SM, Paymaster JC, Vaidya AB. Search for a
human breast cancer virus. Nature. 1971 Feb 26;229(5287):611-4.
[vii] Szakacs JG, Moscinski LC. Sequence homology of deoxyribonucleic acid to mouse mammary tumor virus genome in human breast tumors.
Ann Clin Lab Sci. 1991 Nov-Dec;21(6):402-12.
[viii] Andersson ML, Medstrand P, Yin H, Blomberg J. Differential expression of human endogenous retroviral sequences similar to mouse
mammary tumor virus in normal peripheral blood mononuclear cells. Aids Res Human Retroviruses 1996 12: 833-40.
[ix] Al-Sumidaie AM, Leinster SJ, Jenkins SA Transformation of blood monocytes to giant cells in vitro from patients with breast cancer. Br J Surg.
1986 Oct;73(10):839-42.
[x] Al-Sumidaie AM, Leinster SJ, Hart CA, Green CD, McCarthy K. Particles with properties of retroviruses in monocytes from patients with
breast cancer. Lancet. 1988 Jan 2-9;1(8575-6):5-9.
[xi] Hallam N, McAlpine L, Puszczynska E, Bayliss G. Absence of reverse transcriptase activity in monocyte cultures from patients with breast
cancer. Lancet. 1990 Oct 27;336(8722):1079.
[xii] Kahl LP, Carroll AR, Rhodes P, Wood J, Read NG. En evaluation of the putative human mammary tumorvirus associated with peripheral
blood monocytes. Br J Cancer 1991, 63:534-540.
[xiii] Merezak C, Pierreux C, Adam E, Lemaigre F, Rousseau GG, Calomme C, Van Lint C, Christophe D, Kerkhofs P, Burny A, Kettmann R,
Willems L. Suboptimal enhancer sequences are required for efficient bovine leukemia virus propagation in vivo: implications for viral latency. J
Virol. 2001 Aug;75(15):6977-88.
[xiv] Labat ML Possible retroviral etiology of human breast cancer. Biomed Pharmacother. 1998;52(1):6-12.
[xv] Labat ML A new approach to the study of the origin of genetic diseases: retroviral etiology of osteopetrosis. Biomed Pharmacother.
1991;45(1):23-7.
[xvi] Labat ML. Retroviruses and bone diseases. Clin Orthop. 1996 May;(326):287-309.
[xvii] Burny A, Bruck C, Chantrenne H, Cleuter Y, Dekegel D, Ghysdael J, et al. Bovine Leukemia Virus : Molecular Biology and epidemiology. In
Klein G. ed. Viral Oncology New York : Raven Press 1980: 231-89
[xviii] Miller JM, Miller MD, Olson C, Gilette KG, Virus-like particles in phythemagglutin.stimulated lymphocyte cultures with references to
bovine Lymphosarcoma. J Natl Cancer Inst 1969, 43: 1459-62.
[xix] Poiesz BJ, Ruscetti FW, Gazdar AF, Bunn PA, Minna JD, Gallo RC. Detection and isolation of type C retrovirus particles from fresh and
cultured lymphocytes of a patient with cutaneous T-cell lymphoma. Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9.
[xx] Buehring GC, Philpott SM, Choi KY A reverse transcriptase assay for detection of the bovine leukemia virus. Am J Vet Res.
1977 Nov;38(11):1739-44. Humans have antibodies reactive with Bovine leukemia virus. AIDS Res Hum Retroviruses. 2003
Dec;19(12):1105-13
[xxi] Motton DD, Buehring GC. Bovine leukemia virus alters growth properties and casein synthesis in mammary epithelial cells. J
Dairy Sci. 2003 Sep;86(9):2826-38.
[xxii] Buehring GC. Bovine Leukemia Virus Infection and Human Breast Cancer Risk.
http://www.cbcrp.org/research/PageGrant.asp?grant_id=1815 or http://www.erieping.de/Buehring.htm
[xxiii] Stewart TH, Sage RD, Stewart AF, Cameron DW. Breast cancer incidence highest in the range of one species of house
mouse, Mus domesticus. Br J Cancer. 2000 Jan;82(2):446-51
[xxiv] Stewart et al (1995) Lancet 346: 796-798
[xxv] Wang Y, Holland JF, Bleiweiss IJ, Melana S, Liu X, Pelisson I, Cantarella A, Stellrecht K, Mani S, Pogo BG. Detection of
mammary tumor virus env gene-like sequences in human breast cancer. Cancer Res. 1995 Nov 15;55(22):5173-9.
[xxvi] Wang Y, Melana SM, Baker B, Bleiweiss I, Fernandez-Cobo M, Mandeli JF, Holland JF, Pogo BG. High prevalence of
MMTV-like env gene sequences in gestational breast cancer. Med Oncol. 2003;20(3):233-6
[xxvii] Wang Y, Pelisson I, Melana SM, Holland JF, Pogo BG. Detection of MMTV-like LTR and LTR-env gene sequences in
human breast cancer. Int J Oncol. 2001 May;18(5):1041-4
[xxviii] Townsley-Fuchs J, Neshat MS, Margolin DH, Braun J, Goodglick L. HIV-1 gp120: a novel viral B cell superantigen. Int
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[xxix] Etkind P, Du J, Khan A, Pillitteri J, Wiernik PH. Mouse mammary tumor virus-like ENV gene sequences in human breast
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[xxx] Michalides R., Wagenaar E., Hilkins J., Hilgers J., Goner B., Hynes N. E. Acquisition of proviral DNA of mouse mammary
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[xxxi] Dekaban G. A., Ball J. K. Integration of type B retroviral DNA in virus-induced primary murine thymic lymphomas. J.
Virol., 52: 784-792, 1984
[xxxii] Dudley J., Arfsten A., Hsu C-H. L., Kosak C., Risser R. Molecular cloning and characterization of mouse mammary tumor
proviruses from T-cell lymphoma. J. Virol., 57: 385-388, 1986
[xxxiii] Yanagawa S, Kakimi K, Tanaka H, Murakami A, Nakagawa Y, Kubo Y, Yamada Y, Hiai H, Kuribayashi K, Masuda T, et al.
Mouse mammary tumor virus with rearranged long terminal repeats causes murine lymphomas. J Virol. 1993 Jan;67(1):112-8.
[xxxiv] Ford CE, Faedo M, Crouch R, Lawson JS, Rawlinson WD. Progression from normal breast pathology to breast cancer is
associated with increasing prevalence of mouse mammary tumor virus-like sequences in men and women. Cancer Res. 2004 Jul
15;64(14):4755-9.
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explicitly under www.erieping.de
[xli]Morgan RW, Vakil DV, Chipman ML. Breast feeding, familiy history and breast disease. Am J Epidemiol 99: 117-122, 1974.
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Early Contact To Bovine Milk and The Epidemic Rise in Mammary Cancer Incidence & The Search For The Human Mammary Cancer Virus

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Early Contact to Bovine Milk and the Epidemic Rise in Mammary Cancer Incidence

The search for the Human Mammary Cancer Virus

By Elisabeth Rieping (Stand 2004)

02-Abstract (short) http://web.archive.org/web/*/http://www.erieping.de/bcabstra.htm

Breast Cancer and Early Contact with Bovine Milk

2. CHANGE IN INFANT FEEDING AND THE RISE OF MAMMARY CANCER

3.b AGE AT MENARCHE

3.d DELAYED TIME OF FIRST FULL PREGNANCY

3.e URBAN RESIDENCE

4 . THE GEOGRAPHY OF MAMMARY CANCER IN COMPARISON TO THE AVAILABILITY OF DIARY PRODUCTS

6. BREAST CANCER IN ANIMALS

More on animal breast cancer

8. RISK FACTORS MAY CHANGE

2.a. More on Change in Infant Food http://web.archive.org/web/*/http://www.erieping.de/morcear2.htm

3. Risk Factors for Human Breast Cancer http://web.archive.org/web/*/http://www.erieping.de/cear3.htm

3.a. Weight and Height http://web.archive.org/web/*/http://www.erieping.de/3weight.htm

3.b. Age at Menarche http://web.archive.org/web/*/http://www.erieping.de/3ageatme.htm

3.d. Delayed Time of First Full Pregnancy http://www.erieping.de/3delayed.htm

3.e. Urban Residence http://web.archive.org/web/*/http://www.erieping.de/3uraban.htm

3.f.I. High Birth Weight http://web.archive.org/web/*/http://www.erieping.de/3highbir.htm

Preclampsia/eclampsia, prematurity and birth weight became studied[iii].

3.f.II. Premature Birth and Low Birth Weight http://web.archive.org/web/*/http://www.erieping.de/3lowbir.htm

Abbildungen fehlen Milk adapted for raising young cats.

Milk for raising infant dogs

[i] Brüning H. Künstliche Säuglingsernährung. Enke Verlag, Stuttgart 1908

8. Risks for Breast Cancer may Change http://web.archive.org/web/*/http://www.erieping.de/cear8.htm

9. Inheritable Breast Cancer (missing)

10. Breast Cancer and Diabetes Type 1 (missing)

[xxiv] Stewart et al (1995) Lancet 346: 796-798

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