Also see:
Fat Tissue and Aging – Increased Estrogen
Estrogen Related to Loss of Fat Free Mass with Aging
Maternal Ingestion of Tryptophan and Cancer Risk in Female Offspring
Childhood conditions influence adult progesterone levels
Article on subject:
Obesity and Family Stress Blamed As Girls As Young As Five Reaching Puberty
Quotes by Ray Peat, PhD:
“Several of the things which cause early puberty and high estrogen, also tend to work against progesterone synthesis.”
“Low thyroid function, relative over-feeding, and the presence of unsaturated oils in the diet are known to accelerate sexual maturity. Early sexual maturity has been associated with premature aging and early death. Fish, octopuses, mice, humans, and plants offer examples in which reproductive maturity initiates the aging process. Although it used to be said that “hot tropical” people had early puberty, and “cold northern” types had late puberty, the best available data contradict that opinion. The oldest averages for the occurrence of puberty occur in tropical regions. (Figure 3) Mere calorie restriction can delay puberty (and this usually means a low fat diet, for poor people in the developed countries) as can be seen in data from Appalachia; late puberty, accompanied by very low birth weight for babies, is the typical pattern of poverty. Given enough fat (especially vegetable oil, including that in beans and corn), harsh conditions can probably cause earlier puberty. but I don’t know of any clear evidence on this subject.
…
L. C. Strong, who developed strains of mice with high estrogen and a tendency to die of
mammary cancer, found that early sexual maturity was associated with a shorter life-span. Similar observations have been made in humans.”
Mol Cell Biochem. 1998 Nov;188(1-2):5-12.
Timing of dietary fat exposure and mammary tumorigenesis: role of estrogen receptor and protein kinase C activity.
Hilakivi-Clarke L, Clarke R.
The possible association between a high fat diet and increased breast cancer risk has remained controversial. This largely reflects the conflicting data obtained from migrant, case control and animal studies, which generally support this association, and cohort studies which often fail to show a link between fat and breast cancer. The mammary gland is particularly sensitive to estrogens during fetal development, leading us to hypothesize that dietary fat levels during this period may significantly influence breast cancer risk. Using chemically-induced mammary tumors in rats as our experimental model, we have demonstrated the ability of a maternal diet, high in the polyunsaturated fatty acid (PUFA) linoleic acid, to alter mammary gland differentiation, accelerate the onset of sexual maturation, and increase breast cancer risk. The mammary glands of female rats exposed to a high-fat diet in utero have more of the undifferentiated structures (terminal end buds) and fewer of the differentiated structures (alveolar buds) than the glands of rats exposed to a low-fat diet in utero. Furthermore, these mammary glands contain lower levels of total estrogen receptors and have reduced total protein kinase C activity. These effects appear to be mediated by an increase in the serum estradiol levels of pregnancy, which are elevated at least 30% in pregnant dams fed a high-fat diet. Furthermore, the administration of estradiol to pregnant dams produces effects on mammary gland development, onset of puberty and sensitivity to chemical carcinogenesis comparable to those seen in the offspring of rats fed a high fat diet during pregnancy. Our results, thus, support the hypothesis based on epidemiological data that high maternal estrogen levels increase daughters’ breast cancer risk. The results also suggest that a high-fat diet may be an important factor in increasing pregnancy estrogenic activity.
Proc Natl Acad Sci U S A. 1997 Aug 19;94(17):9372-7.
A maternal diet high in n – 6 polyunsaturated fats alters mammary gland development, puberty onset, and breast cancer risk among female rat offspring.
Hilakivi-Clarke L, Clarke R, Onojafe I, Raygada M, Cho E, Lippman M.
We hypothesized that feeding pregnant rats with a high-fat diet would increase both circulating 17beta-estradiol (E2) levels in the dams and the risk of developing carcinogen-induced mammary tumors among their female offspring. Pregnant rats were fed isocaloric diets containing 12% or 16% (low fat) or 43% or 46% (high fat) of calories from corn oil, which primarily contains the n – 6 polyunsaturated fatty acid (PUFA) linoleic acid, throughout pregnancy. The plasma concentrations of E2 were significantly higher in pregnant females fed a high n – 6 PUFA diet. The female offspring of these rats were fed with a laboratory chow from birth onward, and when exposed to 7,12-dimethylbenz(a)anthracene had a significantly higher mammary tumor incidence (60% vs. 30%) and shorter latency for tumor appearance (11.4 +/- 0.5 weeks vs. 14.2 +/- 0.6 weeks) than the offspring of the low-fat mothers. The high-fat offspring also had puberty onset at a younger age, and their mammary glands contained significantly higher numbers of the epithelial structures that are the targets for malignant transformation. Comparable changes in puberty onset, mammary gland morphology, and tumor incidence were observed in the offspring of rats treated daily with 20 ng of E2 during pregnancy. These data, if extrapolated to humans, may explain the link among diet, early puberty onset, mammary parenchymal patterns, and breast cancer risk, and indicate that an in utero exposure to a diet high in n – 6 PUFA and/or estrogenic stimuli may be critical for affecting breast cancer risk.
Oncol Rep. 1998 May-Jun;5(3):609-16.
Maternal genistein exposure mimics the effects of estrogen on mammary gland development in female mouse offspring.
Hilakivi-Clarke L, Cho E, Clarke R.
Human and animal data indicate that a high maternal estrogen exposure during pregnancy increases breast cancer risk among daughters. This may reflect an increase in the epithelial structures that are the sites for malignant transformation, i.e., terminal end buds (TEBs), and a reduction in epithelial differentiation in the mammary gland. Some phytoestrogens, such as genistein which is a major component in soy-based foods, and zearalenone, a mycotoxin found in agricultural products, have estrogenic effects on the reproductive system, breast and brain. The present study examined whether in utero exposure to genistein or zearalenone influences mammary gland development. Pregnant mice were injected daily with i) 20 ng estradiol (E2); ii) 20 microg genistein; iii) 2 microg zearalenone; iv) 2 microg tamoxifen (TAM), a partial estrogen receptor agonist; or v) oil-vehicle between days 15 and 20 of gestation. E2, genistein, zearalenone, and tamoxifen all increased the density of TEBs in the mammary glands. Genistein reduced, and zearalenone increased, epithelial differentiation. Zearalenone also increased epithelial density, when compared with the vehicle-controls. None of the treatments had permanent effects on circulating E2 levels. Maternal exposure to E2 accelerated body weight gain, physical maturation (eyelid opening), and puberty onset (vaginal opening) in the female offspring. Genistein and tamoxifen had similar effects on puberty onset than E2. Zearalenone caused persistent cornification of the estrus smears. These findings indicate that maternal exposure to physiological doses of genistein mimics the effects of E2 on the mammary gland and reproductive systems in the offspring. Thus, our results suggest that genistein acts as an estrogen in utero, and may increase the incidence of mammary tumors if given through a pregnant mother. The estrogenic effects of zearalenone on the mammary gland, in contrast, are probably counteracted by the permanent changes in estrus cycling.
The population trends toward greater obesity and earlier puberty, both of which are associated with a higher risk of breast cancer, suggest that the war against cancer is far from over. In the 19th century when the incidence of breast cancer was much lower than it is now, puberty usually occurred around the age of 17. In countries with a low incidence of breast cancer, puberty still occurs in the middle to late teens. People who are now 100 generally had puberty years later than girls do now. The biological changes now seen in children in the U.S. suggest that the incidence of degenerative diseases of all sorts is likely to increase as these children grow up. -Ray Peat, PhD
Ethn Dis. 1999 Spring-Summer;9(2):181-9.
Secular trend of earlier onset of menarche with increasing obesity in black and white girls: the Bogalusa Heart Study.
Wattigney WA, Srinivasan SR, Chen W, Greenlund KJ, Berenson GS.
Secular trends in onset of menarche and obesity were examined 14 years apart in two biracial (black-white) cohorts of girls aged 8 to 17 under study for cardiovascular risk. The first cohort (N=1,190, 64% white) was examined in 1978-1979, the second (N=1,164, 57% white) in 1992-1994. The second cohort was heavier in terms of body weight and Rohrer index (weight/height3) than the first (P<0.001), except among black girls aged 12 to 13 years. Subscapular skinfold thickness increased in the second cohort of all ages (P<0.0001), while increases in triceps skinfold were less marked. The onset of menarche occurred at an earlier age in the second cohort compared with the first cohort (P<0.0001), both in black girls (11.4+/-1.3 vs 12.3+/-1.4 years) and white girls (11.5+/-1.3 vs 12.3+/-1.3 years). Furthermore, twice as many girls in the second cohort had reached menarche by ages younger than 12 years (P<0.001). All of these obesity measures were significantly associated with the age of menarche in both cohorts (P<0.001) adjusting for height, race and age at examination. These results suggest that this secular trend toward increasing frequency of early onset of menarche may be the result of increasing obesity noted in girls of both races. Since increases in body fatness and related early onset of menarche are risk factors for disorders in adult life including cardiovascular disease and breast cancer, the secular trend in the increasing incidence of obesity throughout the United States is becoming a major public health problem.
Curr Opin Obstet Gynecol. 2006 Oct;18(5):487-91.
Pubertal development in girls: secular trends.
Kaplowitz P.
PURPOSE OF REVIEW:
To provide an overview of recent studies from the US and other parts of the world that provide conflicting data as to whether there has been a secular trend for earlier onset of puberty and menarche from about 1960 to the present.
RECENT FINDINGS:
Studies from the US suggest a decrease in the age of onset of puberty over the past 40 years of between 0.5 and 1.0 years, with black girls maturing 0.5 to 1 year earlier than white girls. There has been a smaller decrease in the mean age at menarche, on the order of 0.2 years. Northern European countries have not reported such a trend, but several other countries have. The most likely explanation for this trend is an increase in the prevalence of obesity in children.
SUMMARY:
In light of the above trends, the view that onset of any pubertal changes prior to age 8 years requires an extensive evaluation should be reevaluated. The majority of such early-maturing girls are normal girls at the early end of the age distribution for pubertal onset. As much attention should be paid to the rate of progression of pubertal findings as to their age of appearance.
