Migraine in women: the role of hormones and their impact on vascular diseases
To help prevent breast cancer, it's important to recognize the links between Knowledge is power, so first up, I want you to understand how cancer and breast cancer Though you can't alter risk factors like your age or parents, simple lifestyle. The pituitary gland secretes factors into the blood that act on the endocrine glands to either increase or decrease hormone production. This is. Hormones are your body's chemical messengers. They affect many processes including mood. Too much or too little of a certain hormone can be serious. IGF -1 (Insulin-Like Growth Factor -1) Test (American Association for Clinical . MedlinePlus links to health information from the National Institutes of.
The endocrine system works in large part by acting on neurons in the brain, which controls the pituitary gland. The pituitary gland secretes factors into the blood that act on the endocrine glands to either increase or decrease hormone production. This is referred to as a feedback loop, and it involves communication from the brain to the pituitary to an endocrine gland and back to the brain.
This system is very important for the activation and control of basic behavioral activities, such as sex; emotion; responses to stress; and eating, drinking, and the regulation of body functions, including growth, reproduction, energy use, and metabolism. The way the brain responds to hormones indicates that the brain is very malleable and capable of responding to environmental signals.
The brain contains receptors for thyroid hormones those produced by the thyroid and the six classes of steroid hormones, which are synthesized from cholesterol — androgens, estrogens, progestins, glucocorticoids, mineralocorticoids, and vitamin D.
The receptors are found in selected populations of neurons in the brain and relevant organs in the body. Thyroid and steroid hormones bind to receptor proteins that in turn bind to DNA and regulate the action of genes.
Hormones | Endocrine Glands | MedlinePlus
This can result in long-lasting changes in cellular structure and function. The brain has receptors for many hormones; for example, the metabolic hormones insulin, insulin-like growth factor, ghrelin, and leptin. These hormones are taken up from the blood and act to affect neuronal activity and certain aspects of neuronal structure. In response to stress and changes in our biological clocks, such as day and night cycles and jet lag, hormones enter the blood and travel to the brain and other organs.
In the brain, hormones alter the production of gene products that participate in synaptic neurotransmission as well as affect the structure of brain cells. As a result, the circuitry of the brain and its capacity for neurotransmission are changed over a course of hours to days.
In this way, the brain adjusts its performance and control of behavior in response to a changing environment. Severe and prolonged stress can impair the ability of the brain to function normally for a period of time, but the brain is also capable of remarkable recovery.
Reproduction in females is a good example of a regular, cyclic process driven by circulating hormones and involving a feedback loop: Studies of this association are part of a larger group of long-term follow-up studies, some of which have demonstrated a well-established protective effect of such hormonal steroids against endometrial, ovarian and colorectal cancer World Health Organization Collaborative Study of Neoplasia and Steroid Contraceptives,; Thomas, ; Grodstein et al.
Use of hormone preparations among menopausal and post-menopausal women is less well documented and more uncertain.
Heterogeneity There are several sources of heterogeneity in exposures and effects. With respect to exposures, hormone types are numerous.
Estrogens can be made bioavailable by sulphurylation in position 3, the conversion of 17d estradiol into 17d ethinyl-estradiol and micronization. They may be delivered through oral, injection, transdermal and transvaginal routes. Progestogen preparations involve a similar variety of administration routes as well as 21 and 19 carbon root molecules that may have different receptor-binding, pharmacokinetic and pharmacodynamic properties. Thus, the various progestogens used in formulations for contraception or menopause hormone treatment may exhibit markedly different effects.
The complexity of the issue is further accentuated by evidence that estrogen—progestogen combinations are associated with greater risk of breast cancer than estrogen alone Colditz et al. With respect to heterogeneity of effects, breast cancer involves different cell types and degrees of cell differentiation, as well as a range of tumour size and clinical extent Stalsberg et al. Hence investigations into a possible association between hormonal steroids and breast cancer entail extraordinary complexities and require consideration of many variables as well as interactive effects.
By the year there will be 1. The population composition will be even more different because the increasing number of elderly persons will be associated with a sharply declining number of children, resulting in a population structure never seen before in history. Estimates and projections of the population structure of the more developed countries are shown in Table IV. In there were more than twice as many children as elderly persons in developed countries, but by projections indicate the reverse, with 2-fold more elderly persons than children.
The maintenance of the functional capacity and humanitarian integrity of the necessary social services in such a society will pose major challenges, and might perhaps even result in immigration from less developed regions in numbers never imagined before. Hormones and breast cancer development Cancer is generally believed to arise when dividing cells undergo mutations and these genetically damaged cells become susceptible to unrestrained division.
Thus, female hormones and other hormones that affect growth of the mammary gland are potential risk factors for breast cancer. In contrast, factors that induce differentiation in the mammary gland, such as pregnancy and lactation, are likely to reduce the risk of breast cancer.
The baseline risk is influenced, however, by higher mammary gland mass and several observations provide indirect evidence of the association between mammary gland mass and breast cancer risk Bernstein and Ross, ; Adami et al.
The studies on hormones in relation to breast cancer are consistent in indicating that virtually every mammotrophic hormone examined is positively associated with breast cancer risk Endogenous Hormones and Breast Cancer Collaborative Group, The list includes total and free estradiol, estrone and estrone sulphate, androstenedione, dehydroepiandrosterone and dehydroepiandrosterone sulphate, testosterone and prolactin.
Factors during adult life Four lines of evidence point to hormones, and particularly sex hormones, as playing a role in the development of breast cancer in the adult woman Adami et al. The first springs from the powerful role that female reproductive factors and, indeed, gender itself, play on breast cancer occurrence.
Breast cancer risk is increased, for example, in women with earlier menarche and later menopause. The second line of evidence relies on experimental animal data indicating that estrogen and progesterone promote some types of mammary tumours. The third line of evidence derives from studies indicating that exogenous estrogens and progesterone in hormonal contraceptives and menopause hormone treatment regimens increase breast cancer risk, whereas tamoxifen reduces this risk.
The fourth line of evidence involves analytic epidemiological studies, particularly cohort investigations, that implicate various hormones and expression of hormone receptors in the risk of breast cancer Endogenous Hormones and Breast Cancer Collaborative Group, Studies of endogenous hormones may be more directly relevant to the pathogenesis of breast cancer than studies of exogenous hormones. Nevertheless, hormonal exposure evidence is stronger for post-menopausal women, possibly because in pre-menopausal women, cyclic variation of hormones during the menstrual cycle increases exposure misclassification Bernstein and Ross, ; Endogenous Hormones and Breast Cancer Collaborative Group, ; Hankinson and Hunter, The pattern of positive associations could, of course, simply reflect powerful mutual confounding that is difficult to disentangle through statistical procedures.
The reported, though not yet established, positive association of insulin-like growth factor I with breast cancer risk among pre-menopausal women is compatible with such a hypothesis, except that the possible association is manifested at an earlier stage in life.
Factors acting during intrauterine life The hypothesis that breast cancer development may have intrauterine component causes is based on a number of generally accepted assumptions. Mammary gland cells in utero are not terminally differentiated; factors that increase the risk of cancer during adult life, as exogenous and endogenous estrogens do for breast cancer, may have similar effects when they act in utero; estrogens and other hormones with growth-enhancing properties are abundant during pregnancy; and adult life exposures do not fully explain the substantial variability of breast cancer occurrence between and within populations.
Potischman and Troisi concluded that the collective evidence is consistent with the hypothesis that prenatal exposures, notably pregnancy estrogens, are associated with adult life breast cancer risk. More consistent is the evidence concerning the positive association between birthweight and breast cancer risk in the offspring Ahlgren et al.
It should be noted that a link between perinatal factors and breast cancer risk in the offspring does not necessarily or exclusively incriminate pregnancy estrogens, despite the role of the latter as an important determinant of several of these factors, including birthweight. The effects of hormonal influences in fetal and adult life are consistent with the hypothesis that breast cancer develops when cells undergo a series of mutations that cause damage to genes involved in the control of cell division El-Ashry and Lippman, The genetic damage may inactivate repressor genes or activate proto-oncogenes, leading to structural changes and excessive proliferation.
Also, estrogen may be associated with the initiation of breast cancer through oncogenic actions of the aromatase gene Clemon and Goss, Both estrogen and progesterone accelerate the rate of breast epithelial cell division, thereby increasing the risk of critical mutational changes Anderson et al.
Increasing cell synthesis also may enhance the survival of genetically damaged cells, leading to promotion of breast cancer, or increase the growth of pre-clinical tumours, leading to earlier diagnosis. Hormones may have an influence at any time during the 15—19 years from mutation to clinical diagnosis of breast cancer Cutuli et al. Thus female hormones may increase breast cancer risk by increasing the number of cell divisions and the likelihood of mutational damage, or after the genetic damage has occurred by promoting the survival and growth of the pre-clinical cancer.
Breast cancer risk in relation to childbearing and breastfeeding Although childbearing protects against later development of breast cancer, it has been difficult to isolate the impact, if any, of breastfeeding because it is closely related to other aspects of childbearing.
For example, women breastfeed only after they have had a livebirth, and the earlier they commence childbearing, the more children they tend to have and the longer their lifetime duration of breastfeeding.
The Collaborative Group on Hormonal Factors in Breast Cancer published findings from a collaborative reanalysis of data from 47 epidemiological studies conducted in 30 countries which examined the role of both childbearing and breastfeeding on breast cancer risk.
This summary of the current evidence on the relative contributions of childbearing and breastfeeding on breast cancer risk is based on the collaborative report The Collaborative Group on Hormonal Factors in Breast Cancer, The relative contributions of childbearing and breastfeeding to breast cancer risk Although parity has long been known to protect against breast cancer risk, at least in the long term, the interdependence of key indices of childbearing, such as parity, timing of births and breastfeeding, make it difficult to disentangle which factors have an independent effect on breast cancer risk.
For this reason, it is sensible to estimate first the effect of childbearing in the absence of breastfeeding, and then the additional effect of breastfeeding among parous women by adjusting for childbearing history. Among women who have never breastfed, the risk of breast cancer increases in linear fashion with the age at first birth.
The effect of breastfeeding on breast cancer risk among all parous women, after adjustment for childbearing history, is a further risk reduction beyond that due to childbearing.
The decline in breast cancer risk correlates inversely with increasing total duration of breastfeeding, with a 4. Moreover, the RR declines by 3.
Hormones: Communication between the Brain and the Body
The relationship with number of children breastfed appears to be secondary to that with total duration of breastfeeding since the effect of total duration of breastfeeding persists after adjustment for number of children breastfed but the reverse does not hold.
The effect of breastfeeding on breast cancer risk does not appear to be modified by any other reproductive factors such as age at first birth or parity. Nor is there any evidence to suggest that the decline in risk with total duration of breastfeeding differs according to a range of other characteristics including age, family history, menopausal status and ethnic origin.
Impact on different populations Worldwide epidemiological evidence suggests that breastfeeding has an additional protective effect on breast cancer risk over and above that afforded by childbearing. These associations are significant and are seen consistently in data from developed and developing countries, in women of different ages and ethnic origins having various childbearing and other characteristics.
It is estimated that the cumulative incidence of breast cancer observed in developed countries around would be more than halved 2.