Health Psychology Protocol - Essay Example

Table of Contents Introduction 1 Infertility 1 Impact of Infertility 2 Causes 3 Treatments 3 Stress, Smoking and Infertility 4 Materials and Methods 5 Results 7 Discussion 9 Conclusion 10 Reference: 11 Introduction Stress, smoking and infertility hold in themselves a very unique relationship with each other. All three of them are related to each other in a distinctive manner, and have severe affects on one another. Stress holds a great importance in relation to both smoking and infertility. The point to note here is, stress can be a causative agent for smoking, while it remains only a consequence or a psychological effect of infertility, which has been argued in the paper. Smoking is a widespread practice amongst both the youth and adults. Smoking usually takes a position of an obligatory practice of a person by stress, and as a result may become one of the causes of infertility. Infertility, the last and the foremost section of the paper present a general discussion on it, along with its causes, treatments, impacts etc. Infertility Most people grow up believing that having children is a normal and natural part of life. We take for granted that, when the time is right, we'll be able to create the family we want. We don't expect it will be difficult. We don't expect we'll need anyone else's help. For some people, though, creating a family turns out to be a bit more complicated. Impact of Infertility Probably the most common experience for couples when they initially discover they have a fertility problem is shock and disbelief. They might even think the test results are wrong or have been mixed up with someone else's. Most of us grow up with the expectation that, when the time and circumstances are right, we will find the right partner and have children. During adolescence we are constantly taught to be wary of our fertility, to abstain from sex, or to make sure we use contraception. Many of us spend our younger years desperately trying not to get pregnant; worrying that one forgotten pill, one act of unprotected sex, will result in an immediate pregnancy. We grow up believing conception is natural and easy and rarely do we question the fact that it will happen. It is not surprising, therefore, that we are shocked when it doesn't (Stanton, 1991). Men and women both define themselves through their genetic contribution to making a baby, but it is men's only biological contribution, and when they are unable to do this it is not unusual for them to feel an enormous sense of loss, disappointment, frustration or anger (Nachtigall, Becker, & Wozny, 1992). Many men won't want to talk about it either, which may further reinforce their sense of isolation. Society still equates the capacity to father a child with masculinity, and in some cultures this belief is held very strongly. It is not uncommon for men who have problems with their sperm to struggle with issues of identity, masculinity and self-esteem. Many men experience strong feelings of guilt and some even feel that, in a way, they are failing to fulfil their marriage contract. In short, failure to conceive may result in ”depression, anxiety, sexual/relationship difficulties, loss of self-esteem, guilt, frustration, feelings akin to mourning and health problems” (Glover et al., 1996). Causes Infertility or sub-fertility equally affects both men and women. For men it is most commonly due to poor sperm quality or quantity. For women it can be due to a number of factors. The causes of female infertility divide into 42 per cent which is unexplained, 33 per cent which is due to tubal disease, 17 per cent which is due to other medical factors and 8 per cent which is due to endometriosis Treatments Because there are many possible causes of infertility or sub-fertility in both men and women there are also many possible treatments. Few of such treatments have been discussed below: Ovulation induction (hormone treatment) At least 20 per cent of women seeking treatment will have an ovulation problem. Hormone therapy can be used to stimulate ovulation if a woman is not producing eggs regularly. AI (artificial insemination) using the partner's sperm and IUI (intra-uterine insemination) AI may be used to overcome potential problems such as thickening of female mucus, premature ejaculation, impotence or anatomical abnormalities. AI enables the sperm to be inserted directly into the cervix via the vagina. IUI is essentially the same as AI but usually combines ovarian stimulation for the woman and preparation of the semen. Tubal surgery to improve blocked or damaged fallopian tubes Approximately a third of female infertility problems are due to damaged fallopian tubes. Damage may have been the result of previous infection. Depending on the severity of tubal damage surgery may be appropriate and, if successful, fertility may be permanently restored. For some types of tubal damage IVF may be considered (Haynes, & Miller, 2003). Stress, Smoking and Infertility Historically, infertility, particularly "functional" infertility, was attributed to abnormal psychological functioning on the part of one or both members of the couple. Psychogenic infertility was supposed to occur because of unconscious anxiety about sexual feelings, ambivalence toward motherhood, unresolved oedipal conflict, or conflicts of gender identity. Fortunately, advances in reproductive endocrinology and medical technology as well as in psychological research have de-emphasized the significance of psychopathology as the basis of infertility, and modern research shows that there is little evidence to support a role for personality factors or conflicts as a cause of infertility. This perspective unburdens the couple by relieving them of the additional guilt of thinking that it is their mental stress that may be responsible for their infertility. http://www.infertilitycentral.com/fertility/32-stress-and-infertility.html Considerable scientific research demonstrates smoking has adverse effects on all stages of reproduction, including conception, growth and development in the uterus, miscarriage rates, birth and early childhood development. There is a direct link between the amount you smoke and the negative effects on you and your baby. If you are a heavy smoker you will do more damage than if you are a casual smoker, but all smoking does damage. Nicotine makes the blood vessels in your placenta constrict, which makes it more difficult for oxygen and essential nutrients to get through to your baby. Damage can occur to your baby at any stage during your pregnancy, but smoking in the second and third trimesters—three months and after—carries significant risks for your baby. Even if you don't smoke, but your partner does, you may experience passive smoking, which can also affect foetal development. The effects of smoking, however, are reversible. If you stop smoking before you conceive, you avoid these negative consequences even if you have been smoking for many years. Your baby will benefit from your giving up smoking at any time during the pregnancy or after it is born. Scientific studies over past decades have shown that: In general, smokers suffer from infertility more than non-smokers and can take longer to conceive. Smoking can cause problems with your menstrual cycle that may affect your capacity to conceive. Problems with getting and maintaining an erection are more common in men who smoke. Smoking can reduce testosterone levels in men, which affects the development and quality of sperm. Smoking is associated with higher levels of miscarriage, spontaneous abortions and ectopic pregnancies. Smoking while you are pregnant is associated with premature births and low birth weights. Smoking during pregnancy increases the risk of complications at birth and Sudden Infant Death Syndrome (SIDS). Heavy smokers have a higher chance of having babies with a cleft-palate or hare-lip. Materials and Methods The data for this investigation are originated from the Women's Reproductive Health Study, a possible study of menstrual function as well as early pregnancy loss carried out among 403 premenopausal women, whose data compilation and analytic methods have been explained (Waller et al. 1998; Windham et al. 1999) and are summarized in brief below. Women 18-39 years of age registered in the a Medical Care Program were screened by a short telephone interview to establish eligibility as well as keenness to collect and freeze first morning urine samples on a daily basis for up to six months (Waller et M. 1998). About fifty percent of those entitled agreed to partake. On average, women collected urine on ninety-two percent of suitable study days during 5.6 menstrual cycles. Steroid metabolites were measured each day, and FSH was measured in a separation of 300 cycles after supplementary funding was attained. Participants finished a comprehensive baseline telephone interview that asked regarding reproductive history, demographics, lifestyle factors, as well as various exposures, including past as well as current cigarette smoking. Women filled out diaries everyday during urine collection, recording intercourse, vaginal bleeding, in addition to contraception, as well as the number of cigarettes smoked daily. * Baseline: the E1C baseline assessment worked out as the mean over the initial five days of the cycle. To keep away from including high "spill-over" progesterone values from the preceding luteal phase, the PdG baseline is the least 5-day average taking place before the luteal-phase 5-day maximum. * Daily average: Mean E1C and PdG levels determined over the follicular phase or the luteal phase. * Peak: A 3-day average approximately the utmost E1C or PdG value. For the oestrogen metabolite, the highest value was picked within a 6-day window about the day of ovulation to confine the periovulatory peak. For progesterone, the highest value during the luteal phase was picked. Statistical analysis: many covariates from the baseline interview were observed as possible confounders, comprising reproductive history, demographics, body mass index (BMI), in addition to other way of life factors. Since the primary examination is at the cycle level and a woman's cycles are not free observations, mixed models were used that account for frequent measures for multivariate modelling (Laird and Ware 1982; Zeger and Liang 1986), efficiently increasing the standard error of the estimates. Variables recognized as possible confounders were incorporated in failure models with each covariate separate one at a time to conclude if the relation between smoking and a selected FSH parameter (slope of days -5 to 1) altered. If so, that variable was incorporated in concluding multivariate models. Comparable methods were made use of to construct models for investigating smoking relative to steroid levels. In concluding regression models, the hormone parameters by the amount of non-missing calculations in the appropriate time limit during each cycle were weighted (Windham et al. 2002). As a result, in the absence of missing values, the weight was 1, while the presence of missing values resulted in down-weighting; mean weights for each stricture ranged from 0.76 to 0.90(Lasley, 2005). Results On the whole, participants were largely white (71%), learned, and parous (88%), with an average age of 31 [+ or -] 4.2 years (Waller et al. 1998; Windham et al. 2002). On the baseline survey, 9.2% of women accounted being existing regular smokers, and the daily diaries pointed out that ten percent smoked a standard of 1 cigarettes/day, with 5% smoking less often. Smokers did not fluctuate much from those in the general study apart from they were even less expected to have a college degree. Non-smokers in the separation were less expected to be Hispanic and more expected to be older than were all non-smokers. The allocation of cycle description (long follicular phase, short cycle, etc.) was alike in the subset and on the whole, the study and the relationship of shorter cycle length with smoking was also examined [crude risk ratio = 2.1; 95% confidence time (CI), 1.1-4.0]. The urinary FSH levels reveal the increase during the luteal-follicular transition, with the highest levels taking place untimely in the follicular phase at days 3-5 and then yet again just about ovulation. Smokers have a propensity to have elevated daily FSH levels than non-smokers throughout the luteal-follicular phase transition stage. Steady with that, mean FSH parameters in temperate to heavy smokers ([more than or equal to] 10 cigarettes/day) matched up to with non-smokers were statistically considerably augmented for all 7 of the original time windows observed. Light smokers had levels more comparable to non-smokers or very to some extent lower. Smokers did have a propensity to attain the midcycle peak FSH level > 1 day earlier than did non-smokers, with a middle value among light smokers, but this was less strong after alteration. Generally, when including the woman with the elevated FSH values, the average FSH levels during the cycle transition were considerably high by 52-57% in moderate smokers, while excluding her, the means were elevated about thirty to thirty-five percent. The steroid metabolites were observed in separate models that comprised of race, age, pregnancy history, score (exercise levels), education, metabolic correspondence, in addition to caffeine intake. The baseline altitudes of both steroid hormones were high among the heaviest smokers in multivariate models, but not statistically considerably: almost 40% for PdG and 22% for E1C. These elevations were important at the temperate smoking cut point ([more than or up to] 10 cigarettes/day), where there is more power; the mean baseline E1C was high greater than 25% ([beta] = 6.3; 95% CI, 0.40-12.3), and baseline PdG was increased around thirty-five percent ([beta] = 0.20; 95% CI, 0.03-0.38), compared with non-smokers (Lasley, 2005). Discussion The present analysis demonstrated that temperate to heavy smokers had high baseline (for instance, early follicular phase) levels of the steroid metabolites as well as heavy smokers had fairly dampened progesterone metabolite levels during the luteal phase. Further, the mean urinary FSH levels during the instance of the luteal-follicular phase transition were elevated among moderate to heavy smokers than among non-smokers. Some of the disease samples examined with smoking may in fact reflect increases in androgens or progesterone. A few studies have accounted that smoking increases adrenal activity, with increase in adrenal androgens seen chiefly among postmenopausal smokers (Baron et al. 1995; Friedman et al. 1987; Key et al. 1991; Khaw et al. 1988). Zumoff et al. (1990) calculated serum levels at multiple points during the cycle and accounted high serum progesterone levels during the early follicular phase among smokers, when most progesterone is of adrenocortical source. This is steady with the finding of high baseline progesterone levels among heavier smokers. There are a number of limits of the current study that must be measured. Women who obeyed with the labor-intensive urine collection procedure might not be completely generalizable, and the eligibility standard would be liable to eliminate women with chronic menstrual cycle disorder. The FSH subset must leave out most women exposed to ecological tobacco smoke from non-smokers based on the cotinine level standard used (< 0.5 ng/mL), however they would be incorporated in steroid hormone analyses (Lasley, 2005). Conclusion In conclusion, the current data are steady and present first time the effect of smoking on steroid as well as gonado-tropin patterns across cycles. This advance allows the assessment of the reliability of the HPO alliance during the full period of follicular recruitment as well as maturation rather than merely analyzing hormone patterns all through the individual menstrual cycles. For the reason that progesterone modulates FSH in the endocrine reaction loop, the lower progesterone metabolite levels in smokers at some stage in the luteal phase are constant with reduced entrainment of FSH during the luteal-follicular stage transition, leading to the altitudes noted. The decrease of the follicular stage may be a direct result of the augmented FSH, constant with other findings (Cramer et al. 1994; De Souza et al. 1998). The augment in FSH may speed up the recruitment as well as growth of follicles, moving ovulation in advance. Short follicular stage has been related with reduced productiveness rates in some studies (Check et al. 1992; Fukuda et al. 2001; Kolstad et al. 1999; Liss et al. 2002). This prototype of higher FSH levels in addition to shorter cycles in smokers is also steady with the observation that smokers have a propensity to experience earlier menopause (Cooper et al. 1999; Midgette and Baron 1990). Therefore, the reduced progesterone as well as perturbation of FSH proposes both a target in addition to one mechanism by which cigarette smoke may modify ovarian function and decrease female fertility. 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