ESTROGENS IN BOVINE MILK: EFFECTS OF MILK SYNTHESIS, PREGNANCY, MASTITIS, AND IMPLICATIONS TO CONSUMERS
Open Access
- Author:
- Zambito, Dana Alyce
- Graduate Program:
- Physiology
- Degree:
- Doctor of Philosophy
- Document Type:
- Dissertation
- Date of Defense:
- July 26, 2007
- Committee Members:
- Ronald Scott Kensinger, Committee Chair/Co-Chair
Daniel R Hagen, Committee Member
Michael Henry Green, Committee Member
Robert F Roberts, Committee Member - Keywords:
- Estrone
Estradiol
Bovine Pregnancy
Milk - Abstract:
- Some individuals have expressed concern about estrogens in food due to their potential to promote growth of estrogen-sensitive cancer cells (breast, ovarian, uterine, and prostate) in humans. Researchers have reported concentrations of estrogens in milk, but few milk samples that contain fat have been analyzed. Furthermore, the mechanisms by which estrogens accumulate in milk are not well-defined. The objectives of this research were to quantify estrone (E1) and 17β-estradiol (E2) concentrations in raw, pasteurized/homogenized, and commercial milk samples and compare the mass consumed in dairy products to 24-h production rates of these hormones in humans. In addition, mechanisms that may contribute to the accumulation of E1 and E2 in milk were investigated. To meet the first objective raw and commercial milk samples were collected and milk composition was recorded. E1 and E2 were quantified by radioimmunoassay after organic solvent extractions and Sephadex LH-20 column chromatography. E2 concentrations in raw whole milk averaged 1.4 ± 0.2 pg/mL from cows of all reproductive stages, and 0.3, 0.9, and 5.0 pg/mL from cows in trimesters 1, 2, and 3 of pregnancy, respectively. E1 concentrations in milk averaged 0.6, 7.9, and 27.1 pg/mL from cows in trimesters 1, 2, and 3 of pregnancy, respectively. Pasteurization/homogenization treatment did not significantly affect E2 concentrations in milk. Concentrations of E1 and E2 in commercial skim, 1%, 2%, and whole milk samples averaged 2.9, 4.2, 5.7, and 7.9 pg E1/mL and 0.4, 0.6, 0.9, and 1.1 pg E2/mL milk, respectively. E1 and E2 concentrations were greater as milk fat increased (butter >> cream > half-and-half > milks). However, type of product (conventional or organic) did not affect E1 and E2 concentrations in these products. It was concluded that the mass of E1 and E2 in a serving of commercial milk was low (0.01%) relative to published estimates of production of estrogens by the ovaries or testis in humans. The predominant factors regulating plasma E1 and E2 concentrations are the production and metabolic clearance rates of E1 and E2 and binding of E1 and E2 to plasma proteins, as opposed to ingestion of E1 and E2 from the diet. Therefore, it is unlikely that the amount of E1 and E2 consumed from milk would lead to adverse health consequences. When investigating mechanisms that may contribute to the accumulation of E1 and E2 in milk, milk E1 and E2 concentrations were highly correlated with their respective concentrations in plasma (r = 0.77 and 0.93). Milk fat and protein percentages were significantly correlated with E1 and E2 concentrations. Additionally, transcripts for an enzyme that can convert E1 to E2 were detected in somatic cells isolated from pregnant cows’ milk, suggesting that cells within the mammary gland may synthesize E2 during pregnancy. Based upon the relationship between plasma and milk concentrations of E1 and E2, this research suggests that passive diffusion from plasma is a significant factor for the accumulation of E1 and E2 in milk. However, fat and protein-mediated mechanisms likely also contribute to the accumulation of E1 and E2 in milk.