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Hypothalamic Amenorrhea Treatment

A lot of you have been asking to read my research paper on HA, so I decided I might as well do a blog post and paste the paper onto my site! The paper could only be 7 pages, so it’s not everything I wanted to say and write, but it covers the main points. At the end I also pasted in my “TOE”, or table of evidence chart, which is a chart of all the research studies broken down for you to read more details about each study! Hope this helps! Feel free to leave comments/ask questions.

Quick tip for those who don’t like reading: If you’re short on time, read the intro and conclusion below and then skip to the TOE chart and read each study if you want more details.

Hypothalamic Amenorrhea

Hypothalamic amenorrhea (HA) is a complex, multifaceted diagnosis that can be difficult to diagnose and treat. The diagnosis of hypothalamic amenorrhea is a diagnosis of exclusion, and there are many interrelating factors, both biological and psychological, that culminate in the development of HA. The hypothalamus produces gonadotropin-releasing hormone (GnRH), while the anterior pituitary releases follicle-stimulating hormone (FSH), which stimulates the secretion of estrogen and the development of ova in women, and luteinizing hormone (LH), which stimulates ovulation (Lewis, et al., 2014, p. 1138). HA is essentially a deficiency in GnRH from the hypothalamus, which results in low levels of estrogen, FSH, and LH and ultimately causes cessation of menstruation.

A multitude of different factors can cause the hypothalamus to produce less GnRH, including physical stress, emotional or perceived stress, malnutrition, anorexia, excessive exercise, and weight loss, among others. Moreover, a disruption in the hypothalamic-pituitary-ovarian axis can lead to amenorrhea. Essentially, any stress perceived by the hypothalamus can cause reproductive function to shut down. Since reproductive function is an essential component of health, many long-term complications can stem from cessation of menstruation due to HA including osteoporosis, infertility, cardiovascular endothelial dysfunction and abnormal lipid profiles, depression, anxiety, and sexual dysfunction (Meczekalski, Katulski, Czyzyk, Prodifgurna-Stopa, & Maciejewska-Jeske, 2014). Consequently, healthcare providers need to be aware of the psychological and biological nature of the disorder and focus their treatment plans on the underlying cause and not solely on the symptoms of the disorder.

Many healthcare providers prescribe oral contraceptives as a temporary solution to HA. While combination oral contraceptives that contain both estrogen and progesterone can restore menses by increasing estrogen levels, and they may protect the patient from osteoporosis, ovulation is not restored. Therefore, combination oral contraceptives are used more as a “Band-Aid” solution to prevent further bone density loss, rather than to fix the root cause of the problem. Many patients are sent home with oral contraceptives but no education on, or consideration of, lifestyle changes that should attend the diagnosis. There is an apparent need for healthcare providers to take a holistic approach, by looking beyond the reproductive system and appreciating the patient as a whole, and the nurse can play an essential role in facilitating recovery through adaptation.

Sister Callista Roy developed the Adaptation Model of Nursing, which is a theoretical framework that further emphasizes the importance of nursing in promoting adaptation. Roy rationalized that adaptation transpires when people respond positively to environmental changes. According to this model, the goal of nursing is to promote client adaptation, and nursing adjusts stimuli that affect adaptation (Polit & Beck, 2017). According to Roy, a person is a bio-psycho-social being, constantly interacting with his or her environment. A person uses biological, psychological, and social coping mechanisms to adapt to changing environments and adaptation is a function of the stimulus to which a person is exposed in the environment (Petiprin, 2016). Nurses must encourage an adjustment of the patient’s stimuli in order to promote recovery. All four of Roy’s adaptive modes— physiologic/physical, role function, interdependence, and self-concept/group identity—are essential components in holistic health and recovery for patients with HA.

The purpose of this literature review is to answer the following question: In females with hypothalamic amenorrhea, are alternative treatment modalities as effective, or more effective, in restoring menses than traditional pharmacologic treatments such as oral contraception? Through a thorough review of the recent literature, this paper seeks to determine alternative treatment modalities to address the root cause of HA and prevent long-term complications from ensuing in female patients diagnosed with HA.

Design and Method

Multiple databases were explored between 1 October 2016 and 9 October 2016. The databases queried included PubMed, Science Direct, and Scopus. The following search terms were used alone or in combination: hypothalamic amenorrhea, alternative treatments, treatments, secondary amenorrhea, resumption of menses, cognitive behavioral therapy, and life style changes. Initially, 6,255 studies were found, but 4,970 studies were excluded for being more than five years old. Of the remaining 1,285 studies, 15 were chosen for further investigation and review. The other 1,270 studies were excluded because they investigated other independent variables that were not of interest in this review, included primary amenorrhea, used conventional treatment modalities, or did not focus on the resumption of menses as the outcome. Nine studies were randomized control trials, one study was a five-year retrospective study, four studies were longitudinal studies, and one study was a randomized, double-blinded, placebo-controlled study. The four most pertinent studies were chosen for inclusion in a review of the literature in order to answer the question under investigation because considered the resumption of menses as an outcome and alternative treatment modalities.

Results and Discussion

In reviewing the literature, a multitude of alternative treatment modalities for HA were presented. The four studies chosen for this investigation focused on one of the following alternative treatment modalities: cognitive behavioral therapy (CBT), interventions designed to increase energy availability (EA), a specific carbohydrate–protein supplement (CHO-PRO), and leptin treatment. HA was defined as cessation of menses for six months or longer in women who had previously had a menstrual cycle. Each of the four studies focused on the outcome of a return of menses.

All four of the studies sought an alternative treatment for HA that was effective in restoring menses. Michopoulos, Mancini, Loucks, and Berga (2013) used a randomized control trial to determine if CBT could improve neuroendocrine, metabolic concomitants, and hypercortisolemia in 17 patients with functional HA. Arends, Cheung, Barrack, and Nattiv (2012) conducted a five-year retrospective study in which 51 female athletes increased their EA by increasing their caloric intake by 250 to 350 kcal/day, and if weight gain was required, a gain of 0.5 to 1 pound per week was recommended. Along the same lines as increased EA, Ciadella-Kam, Guebels, Maddalozzo, and Manore (2014) also employed a dietary intervention of a six-month CHO-PRO supplement (360 kcal/day, 54 g CHO/day, 20 g PRO/day) to treat female athletes with exercise-related menstrual dysfunction (ExMD). Also considering the concept of energy balance (EB) as a solution to HA, Chou, Chamberland, Liu, Matarese, Gao, Stefanakis, and Mantzoros (2011) piloted a randomized, double-blinded, placebo-controlled study in which the role of leptin, a hormone responsible for satiety, was explored. One study was a five-year retrospective study conducted by Arends et al. (2012), and the other three studies were 36 months or less in duration, with the shortest being 20 weeks. While all four studies focused on the resumption of menses (ROM), the size and characteristics of the samples slightly differed between studies.

All four studies used relatively small sample sizes of 51 females or fewer. Arends et al. (2012) and Ciadella-Kam et al. (2014) both used samples that were composed of female athletes with HA. However, Chou et al. (2011) and Michopoulos et al. (2013) used sample populations of females with HA that were not considered athletes. Pregnancy and oral contraceptive use were both part of the exclusion criteria in all four studies. Despite the difference in whether the females in the studies were considered athletes or not, all of the female participants in the studies did engage in some form of exercise either prior to the study or during the study. Exercise is significant in that it affects one’s overall EB, and a negative EB is a perceived stressor to the hypothalamus. Two of the four studies found that interventions designed to increase EA and improve EB in females with HA were effective in producing ROM.

Arends et al. (2012) found that athletes with ROM had higher absolute and percentage weight gain (mean difference -7.02 + 2.7 p<.05, 95% CI -12.7, -1.3) and experienced a greater change in body mass index during the study period than those without ROM indicating a positive EB. Increasing caloric intake or decreasing exercise expenditure in treating females with HA was determined to be a suitable non-pharmacologic treatment (Arends et al., 2012). Ciadella-Kam et al. (2014) also found that a dietary intervention that improves EA and EB could be considered a suitable non-pharmacologic treatment for ExMD (Ciadella-Kam et al., 2014). EB is, in part, regulated by leptin, which is a hormone secreted from fat cells that signals satiety.

Chou et al. (2011) discovered that seven out of ten subjects who were treated with metreleptin, a synthetic analog of the hormone leptin, resumed menstruation during the course of the study. Two out of nine subjects on a placebo resumed menstruation (p=0.0046). Estradiol and progesterone levels increased substantially in the participants treated with metreleptin (p= 0.0137) as compared with the participants treated with a placebo (p= 0.0342). Essentially, low levels of leptin can cause dysfunction of the neuroendocrine axis (Chou et al., 2011).

Evidently, leptin lowers the stress perceived by the hypothalamus by signaling that the body is in a state of EB. Stress perceived by the hypothalamus can lead to HA, which may be why CBT was also found to be successful in terms of ROM. Women who were randomized to CBT had an ovarian recovery rate of 87% and those women who were randomized to observation had an ovarian recovery rate of 33.3%. CBT was shown to improve neuroendocrine and metabolic concomitants of HA, thereby making CBT an effective treatment for HA (Michopoulos et al., 2013).

Conclusion

All four of the studies under investigation determined an alternative treatment modality to be effective in restoring menses in patients with HA. The common denominator underlying all of the studies seems to be the presence of an energy balance problem that leads the hypothalamus to perceive a stressful environment and therefore shut down reproductive function. CBT was also deemed to be a successful treatment for HA, as it also decreased the stress perceived by the hypothalamus. Therefore, there is a clear and unmistakable connection between perceived stress and HA. Chou et al. (2011) further confirmed that oral contraceptives are not an effective treatment for curing HA. Apart from trying to decrease exercise and/or increase body weight and caloric intake, the mainstay in HA treatment is estrogen replacement, which does not effectively address infertility, other neuroendocrine abnormalities, or bone loss (Chou et al., 2011).

Further studies should be conducted in using larger sample sizes in order to further solidify the role of energy balance and perceived stress in HA. Further research should also use pulsatile hormone assessments to create a better clinical picture of the influence of interventions on hormone levels. In conclusion, using a holistic approach in treating HA patients with alternative treatment modalities that increase energy availability and decrease perceived stress by the hypothalamus is more effective than oral contraceptives in treating the underlying cause of HA. Therefore, healthcare providers and nurses should account for both the biological and psychological aspects of HA during treatment in order to achieve the best outcome.

References

 

Arends, J. C., Cheung, M. Y., Barrack, M. T., & Nattiv, A. (2012). Restoration of menses with

nonpharmacologic therapy in college athletes with menstrual disturbances: a 5-year retrospective study. International Journal of Sport Nutrition and Exercise Metabolism, 2, 98–9108.

 

Chou, S. H., Chamberland, J. P., Liu, X., Matarese, G., Gao, C., Stefanakis, R., …Mantzoros, C.

  1. (2011). Leptin is an effective treatment for hypothalamic amenorrhea. Proceedings of the National Academy of Sciences of the United States of America, 108(16), 6585–6590. http://doi.org/10.1073/pnas.1015674108

 

Cialdella-Kam, L., Guebels, C. P., Maddalozzo, G. F., & Manore, M. M. (2014). Dietary

intervention restored menses in female athletes with exercise-associated menstrual dysfunction with limited impact on bone and muscle health. Nutrients, 6(8), 3018–3039. http://doi.org.proxy1.lib.tju.edu/10.3390/nu6083018

 

Lewis, S. M., Dirksen, S. R., Heitkemper, M. M., Bucher, L., & In Harding, M. (2014). Medical-

surgical nursing: Assessment and management of clinical problems.

 

Meczekalski, B., Katulski, K., Czyzyk, A., Podfigurna-Stopa, A., & Maciejewska-Jeske,

  1. (2014). Functional hypothalamic amenorrhea and its influence on women’s health. Journal of Endocrinological Investigation, 37(11), 1049–1056. http://doi.org/10.1007/s40618-014-0169-3

 

Michopoulos, V., Mancini, F., Loucks, T. L., & Berga, S. L. (2013). Neuroendocrine recovery

initiated by cognitive behavioral therapy in women with functional hypothalamic amenorrhea: A randomized, controlled trial. Fertility and Sterility, 99(7), 2084-2091.e1. doi:http://dx.doi.org.proxy1.lib.tju.edu/10.1016/j.fertnstert.2013.02.036

 

Petiprin, A. (2016). Roy adaptation model. Nursing-Theory. Retrieved from

http://nursing-theory.org/theories-and-models/roy-adaptation-model.php

 

Polit, D. F., & Beck, C. T. (2017). Nursing research: Generating and assessing evidence

for nursing practice (10th ed.). Philadelphia: Wolters Kluwer Health/lippincott Williams & Wilkins.

 

Appendix A

 

TABLE of EVIDENCE  
Full Citation:

Must use 6th edition APA format

Michopoulos, V., Mancini, F., Loucks, T. L., & Berga, S. L. (2013). Neuroendocrine recovery initiated by cognitive behavioral therapy in women with functional hypothalamic amenorrhea: A randomized, controlled trial. Fertility and Sterility, 99(7), 2084-2091.e1. doi:http://dx.doi.org.proxy1.lib.tju.edu/10.1016/j.fertnstert.2013.02.036
Type of Study Randomized control trial
Research

Question:

(Study aim, purpose or research question(s)

The purpose of the study was to determine if cognitive behavioral therapy (CBT) could improve neuroendocrine, metabolic concomitants, and hypercortisolemia in patients with functional hypothalamic amenorrhea. Cognitive behavioral therapy had been shown in a previous study to restore ovarian function in patients with functional hypothalamic amenorrhea.
Setting/Site

where the research was conducted –country, hospital?

Clinical research center, Magee-Women’s Hospital, at an academic medical university, University of Pittsburgh.

 

Sample

#, characteristics & exclusion criteria

Sample: 17 women.

 

Women included in the study comprised those with an ideal body weight between 90% and 110%. A day-awake, night-rest schedule.

 

Exclusion criteria involved a psychiatric diagnosis, weight loss greater than 10 pounds within the last 5 years, and exercise greater than 10 hours per week that included any type or running more than 10 miles each week. Women with current or past psychiatric disorders were excluded. Women with current or past eating disorders or drug dependence were excluded. Women with syndromal psychiatric conditions were also excluded.

Methods

describe how the study was done

 

Nine women were assigned to observation and 8 women went to CBT. CBT consisted of 16 sessions over 20 weeks. Sessions 1-6 focused on nutrition and exercise habits and attitudes towards both nutrition and exercise. Sessions 7-12 acknowledged maladaptive feelings about stressors, exercise, nutrition, weight, and focused n stress management techniques and healthy attitudes. Sessions 13-16 primed the women for termination of CBT. Weekly blood samples were collected for 4 weeks to determine serum levels of estradiol (E2) and progesterone (P4) in order to evaluate baseline ovarian function before cognitive behavioral therapy (CBT). During the first 6 weeks of the CBT intervention, weekly blood samples of E2 and P4 were collected. The women who participated in the study visited the General Clinical Research Center (GCRC) on two different occasions; once after 4 weeks of the intervention, and a second time after 20 weeks of observation or intervention. During the visits, an indwelling intravenous catheter was inserted and blood samples were collected every 15 minutes for 24 hours. Cortisol, total T4, free T4, thyroid stimulating hormone (TSH), total thyronine (T3), free T3, and leptin were assessed in serum samples. Body mass index (BMI) was also measured. Cortisol was measured every 15 minutes, leptin and TSH were measured hourly, and total T4, free T4, total T3, and free T3 were measured once in a morning blood sample.

 

The functional hypothalamic amenorrhea (FHA) diagnosis was made if the women exhibited persistent amenorrhea during the baseline period of 4 weeks. During the baseline 4-week period, anovulation was present as evidenced by progesterone (P4) levels lower than 1 ng/mL and the initial LH pulse frequency was less than 10 pulses in 24 hours in the first GCRC visit.

 

If there was vaginal bleeding, blood samples were obtained 21 days later to determine E2 and P4 levels. Full ovarian recovery entailed the return of menses and evidence of ovulation, which included E2 levels greater than 100 pg/mL and P4 levels greater than 5 ng/mL. E2 levels greater than 60 pg/mL, and P4 levels less than 5 ng/mL were defined as partial ovarian recovery. E2 less than 60 pg/mL and P4 less than 5 ng/mL were defined as persistent anovulation.

Variables/

Measures:

Identify major IV(s), DV(s)& key operational definitions (describe how variables were measured and include name of tools used)

The independent variable was cognitive behavioral therapy, and the dependent variable was ovarian recovery.

 

CBT consisted of 16 sessions over 20 weeks.

 

Full ovarian recovery entailed the return of menses and evidence of ovulation, which included E2 levels greater than 100 pg/mL and P4 levels greater than 5 ng/mL. E2 levels greater than 60 pg/mL, and P4 levels less than 5 ng/mL were defined as partial ovarian recovery. E2 less than 60 pg/mL and P4 less than 5 ng/mL were defined as persistent anovulation.

Results:

 

Six out of eight women who were randomized to CBT resumed ovulating, one had partial ovarian recovery, and one showed no ovarian recovery. Three out of the nine women who were randomized to observation displayed partial ovarian recovery, and six remained anovulatory. Women in CBT had a higher rate of ovarian recovery than those randomized to observation. Women who were randomized to CBT had an ovarian recovery rate of 87% and those women who were randomized to observation had an ovarian recovery rate of 33.3%. CBT improves neuroendocrine and metabolic concomitants of FHA.
Level of Significance: P < .10 was deemed significant. Women who were randomized to CBT had an ovarian recovery rate of 87% and those women who were randomized to observation had an ovarian recovery rate of 33.3% making Fisher’s exact, P=.05. The odds ratio for ovarian recovery with CBT compared to just observation was 14, with a 95% confidence interval of 1.14-172.6 (P=0.01).
Your Critique:

Limitations

(strengths & weaknesses of the study)

The strengths of the study included having strong defining variables of what women should participate and which should not, and that it was a blind study. The weakness would be that the sample size under study could have been larger, and I would have liked to see the CBT continue for longer than 16 weeks in order to see if the two women with partial ovarian recovery and no ovarian recovery would eventually recover ovarian function.
Suggestions for Further Study The authors of the study suggest using a larger sample size. The authors also wanted to offer CBT to the placebo or observational group of women to see if those subjects regain menses.

 

 

TABLE of EVIDENCE  
Full Citation:

Must use 6th edition APA format

Arends, J. C., Cheung, M. Y., Barrack, M. T., & Nattiv, A. (2012). Restoration of menses with nonpharmacologic therapy in college athletes with menstrual disturbances: a 5-year retrospective study. International Journal of Sport Nutrition and Exercise Metabolism, 2, 98–9108.
Type of Study 5 year retrospective study

 

Research

Question:

(Study aim, purpose or research question(s)

The study aims to examine a large population of female athletes at an NCAA Division I institution over a 5-year period to see how amenorrhea and oligomenorrhea can be managed with purely nonpharmacologic therapies and to determine factors associated with resumption of menses (ROM).

 

The researchers hypothesized that interventions designed to increase energy availability in female athletes with functional hypothalamic amenorrhea (FHA) and oligomenorrhea could serve as effective nonpharmacologic methods to restore normal menstrual function.

 

Setting/Site

where the research was conducted –country, hospital?

A major Division I university, the University of California, Los Angeles (UCLA).

 

Sample

#, characteristics & exclusion criteria

373 female student athletes seen by team physicians over a 5- year period at UCLA. Of those 373, 51 subjects who were a part of a UCLA team for more than 12 months and had menstrual disruptions were reviewed in detail. Exclusionary criteria included pregnancy, eumenorrhea, and current oral-contraceptive use or the use of oral contraceptives within the previous 6 months.

 

373 female athletes participated in the study, but 114 subjects were excluded because of oral-contraceptive use.

 

51 athletes (19.7%) reported menstrual disturbances: 13 with amenorrhea (5.0%) and 38 with oligomenorrhea (14.7%).

 

 

Methods

describe how the study was done

 

All athletes with menstrual disturbances underwent nonpharmacologic intervention. Nonpharmcologic intervention included physician counseling by one of two physicians, increased energy availability by increasing dietary energy intake or decreasing exercise energy expenditure based on each individual’s need. Each athlete also saw a single sport dietitian for further assessment of specific energy needs and for education on how to increase energy availability with a goal to maintain a positive energy balance.

 

Baseline intake, as recorded by a 7-day food diary and evaluated by Nutritionist Pro version 5 (a nutrition software program), was obtained. Total daily energy expenditure was estimated by calculating resting energy expenditure using the Harris-Benedict equation for females and multiplying resting energy expenditure by an activity factor to account for nonexercise activity thermogenesis. An estimate of average daily exercise energy expenditure calculated using activity specific metabolic equivalents from the American College of Sports Medicine was also added into the equation. The activity factor used in the study ranged from 1.2-1.7 and considered activity outside of structured exercise. In order to determine each athlete’s specific intervention, energy availability was also calculated by subtracting exercise energy expenditure from total daily energy intake and adjusted for fat-free mass.

 

Most of the female athletes increased their energy availability by increasing caloric intake by 250-350 kcal/day. If weight gain was required, a gain of 0.5 to 1 pound per week was recommended, but each athlete had an individual plan.

 

Variables of interest included height (cm), weight (kg), age at menarche (years), BMI (kg/m2), hormone levels, energy intake, the presence or absence of disordered eating, and sport type.

 

Baseline measurements were obtained at the initial physical exam when the menstrual disturbances were first reported. Both the type and duration of menstrual disturbances and the duration of resumption of menses (ROM) were recorded. Follow up measurements, weights and laboratory testing, were obtained as close to ROM as possible. The follow up weight measurements ranged from 12 to 25 months.

Variables/

Measures:

Identify major IV(s), DV(s)& key operational definitions (describe how variables were measured and include name of tools used)

The independent variable was an increased dietary intake to increase energy availability individualized for each female (250-350 kcal/day), and the dependent variable was resumption of menses.

Menstrual disturbances were defined as having lack of menarche before age 15, absence of menses for 90 or more consecutive days at the time of the initial evaluation, or menstrual cycles of 36 days or longer in length of time at the initial evaluation.

A rigid definition of cycles of 36 days or less days for 3 months or longer was defined as resumption of menses. This definition was used because it most likely represented hypothalamic recovery, and not simply menstrual bleeding.

Harris-Benedict equation for females was employed to calculate resting energy expenditure and an added activity factor as determined by a dietician was also included in the equation.

Results:

 

Initial weight and BMI were significantly lower in amenorrheic athletes than oligomenorrheic athletes. There was an association between older age of menarche, lower estradiol levels, and a lower number of kilocalories per day consumed in the amenorrheic females, despite lack of statistical significance. Over the 5-year period, 9 of the athletes with amenorrhea or oligomenorrhea at the initial appointment had ROM (17.6%). ROM was seen in 3 of 13 amenorrheic athletes (23.1%) and 6 of 8 oligomenorrheic athletes (15.8%).

 

The mean length of time from the start of nonpharmacologic therapy until resumption of menses in the sample ranged from 8 to 33 months, with mean + standard error of the mean of 15.6 + 2.6 months. The amenorrheic and oligomenorrheic women testified resumption of menses after 17.7 + 4.8 and 14.5 + 3.4 months, respectively.

 

In the remaining athletes, 4 did not have ROM. 5 were lost to follow-up or started oral contraception. Of the oligomenorrheic patients, 12 reported continued oligomenorrhea and 20 started using oral contraceptives or were lost to follow-up.

 

Repeated measures ANOVA showed that athletes who resumed menses had a significant increase in body weight and BMI during the study duration than those who did not resume menses. BMI values at baseline were 20.8 + 0.5 kg/m2 and follow up BMI values were 22.7 + 0.6 kg/m2, p < .005. With no resumption of menses BMI values were initially 20.8 + 0.7 kg/m2 and changed to 21.3 + 0.6 kg/m2 at follow up, p= .14.

Body weight values for ROM at baseline and follow-up were 58.0 + 2.0 kg and 63.3 + 2.3 kg, p<.005, respectively. In no resumption of menses body weight values were 57.7 + 3.2 kg and 59.0 + 3.4 kg, p=.17, at baseline and follow up, respectively.

 

Also, athletes with ROM had higher absolute and percentage weight gain (mean difference -7.02 + 2.7 p<.05, 95% CI -12.7, -1.3) and had a greater change in BMI during the study period than those without ROM.

 

No athlete with weight loss had spontaneous ROM or improved regularity of menses. Percent weight gain emerged as a positive predictor of ROM, OR (95% CI) = 1.25 (1.01, 1.56), p < .05. In the amenorrheic athletes, there was a higher rate of psychologist referral than those without, 66.7% and 0%, respectively (p=0.5).

 

There is evidence for the role of nonpharmacologic interventions, which can include education regarding energy availability by a dietician and a physician with a goal of increased intake or decreased exercise expenditure in treating females with menstrual disturbances.

All except one athlete who had ROM also had a simultaneous weight increase. The athletes who gained 5 pounds or more were twice as likely to resume menstruation than those who had less weight gain.

 

Level of Significance: Statistical significance was set at p < .05. All analyses were performed using the Statistical Package for Social Sciences (SPSS) version 16.0. Weight change (kg): p = .02

Body-mass-index change (kg/m2): p= .02

Weight change (%): p= .02

ROM had higher absolute percentage weight gain: mean difference -7.02 + 2.7 p<.05, 95% CI -12.7, -1.3.

Percent weight gain emerged as a positive predictor of ROM, OR (95% CI) = 1.25 (1.01, 1.56), p < .05.

Your Critique:

Limitations

(strengths & weaknesses of the study)

A weakness of the study was that the definition used in the study of resumption of menses consisting of 3 months or longer with cycles shorter than 36 days was a very strict definition. Had the study used a broader definition, there would have been more athletes who experienced resumption of menses. Another weakness of the study was that underlying polycystic ovarian syndrome or subclinical hyperandrogenism was not assessed in all athletes. Another weakness of the study was that sleep patterns, cortisol levels, stress, leptin, and other metabolic hormones were not formally assessed or documented in most of the athletes. Also, the self-report nature of dietary intake may introduce error. A strength of the study was that it had a large sample size.
Suggestions for Further Study The authors suggest that future studies should have a more liberal and conservative definition of resumption of menses to help clarify the length of time for true hypothalamic recovery. The authors also suggest that contributing factors like genetics, neuroendocrine and metabolic factors should be considered in future studies that assess nonpharmacologic interventions of menstrual disturbances in females.

 

TABLE of EVIDENCE  
Full Citation:

Must use 6th edition APA format

Cialdella-Kam, L., Guebels, C. P., Maddalozzo, G. F., & Manore, M. M. (2014). Dietary intervention restored menses in female athletes with exercise-associated menstrual dysfunction with limited impact on bone and muscle health. Nutrients, 6(8), 3018–3039. http://doi.org.proxy1.lib.tju.edu/10.3390/nu6083018

 

Type of Study A longitudinal study
Research

Question:

(Study aim, purpose or research question(s)

The study aimed to determine whether a 6-month carbohydrate-protein (CHO-PRO) supplement (360 kcal/day, 54 g CHO/day, 20 g PRO/day) would improve energy status, improve musculoskeletal health, and restore menses in female athletes with menstrual dysfunction related to exercise or exercise-related menstrual dysfunction (ExMD) associated with energy availability (EA).

 

Setting/Site

where the research was conducted –country, hospital?

USDA National Needs Graduate Fellowship Program, OSU, College of Public Health and Human Sciences.

 

 

Sample

#, characteristics & exclusion criteria

Endurance trained women, 12 amenorrheic/oligomenorrheic [ExMD] were enrolled in the study. 8 of the 12 women completed the study. 4 women dropped out due to personal reasons. A control group with exercise-related menstrual dysfunction (ExMD) was not included due to ethical reasons.

 

Inclusion criteria included equal or greater than 7 hours per week of exercise training for the last 2 years, a VO2max (the maximum amount of oxygen that an athlete can use during intense, maximal exercise effort) greater than 38 mL/kg/min, no oral contraceptives or hormonal replacement therapy use for 6-months, an Eating Disorder Inventory-2 (EDI-2) questionnaire subscale score less than 14, and no self-reported primary amenorrhea or another non-exercise form of amenorrhea. Other types of menstrual dysfunction were eliminated by assessment of luteinizing hormone (LH), prolactin levels, follicular stimulating hormone (FSH), and LH/FSH ratios. All of the participants had to have normal thyroid (T3) levels.

 

Methods

describe how the study was done

 

A baseline questionnaire was employed to assess general health, exercise, and menstrual and dietary history. Mood was also assessed pre and post intervention using a Profile of Mood State (POMS) questionnaire that measures 6 different mood states that include fatigue, anger, vigor, depression, confusion, and anxiety.

 

Females were assigned to either then exercise-related menstrual dysfunction (ExMD) group (n=8) or the eumenorrheic (Eumen) group (n=10) based upon self-reported menstrual history and ovulation status. The participants measured ovulation status daily for 1 month or greater using Clearblue Easy Fertility Monitor. Those who began menstruating during the study intervention were tested for ovulation each month until the end of the study. Blood levels of LH, FSH, prolactin, and LH/FSH ratio were assessed at 0 and 6 months for the ExMD group, but only at 0 months for the Eumen group.

 

Participants did a standardized treadmill VO2max test using indirect calorimetry. Fasting blood was also assessed for iron, vitamin B-12, folate, 25-OH Vitamin D, T3, estradiol, LH, FSH, prolactin, and progesterone. Also, serum osteocalcin, a bone-specific protein of osteoblasts, and procollagen Type I Intact N-Terminal Propeptide, and indicator of newly formed type I collagen, were assessed as a marker of bone formation. Carboxyterminal telopeptide of type I collagen was used as a marker of bone resorption.

 

For 7 consecutive days, participants completed weighed food records, physical activity logs and sported an accelerometer.

 

Running energy expenditure and resting metabolic rate were measured using indirect calorimetry on two separate days within a 7-day period to improve accuracy of energy expenditure (EE). Running energy expenditure was used to estimate each participant’s exercise energy expenditure (EEE) during running. Diet and physical activity were analyzed using a nutrient and activity analysis program (Food Processor SQL). Energy balance (EB) was calculated: EB (kcal/day) = EI-TEE (energy intake – total energy expenditure). Energy availability (EA) (kcal/day) = EI-EEE. Exercise was defined as physical activity greater than 4.0 metabolic equivalents (METs) to eliminate activity of daily living from the EEE calculation.

 

After the baseline assessments, the ExMD group received a 6-month CHO-PRO supplement. The supplement included 325 mL of Gatorade Nutrition Drink (360 kcal/day, 54 g of carbohydrates, 20 g of protein, 8 g of fat, 300 mg of calcium, 100 IU of vitamin D, 0.4 mg of vitamin B6, and 1.2 μg of vitamin B12) to each woman’s daily diet. The participants were to consume the supplement 30 to 60 minutes after exercise or when convenient on non-exercise days. Each participant exercised 6 to 7 days of the week. Researchers met with participants weekly to provide supplements, discuss issues, complete a 24-hour dietary recall, and ensure compliance. The participants were asked if they consumed the supplement as instructed and were to return empty cans to weekly meetings. Another method of assessing compliance included assessing energy status, EI and TEE, at 3 months into the study. There was also a performance, menstrual cycle, and injury diary collected monthly.

Variables/

Measures:

Identify major IV(s), DV(s)& key operational definitions (describe how variables were measured and include name of tools used)

The independent variable was energy intake (+360 kcal/day). The dependent variables included energy balance (EB= Energy intake – total energy expenditure), bone health (normal bone mineral density was defined as a z-score > -1.0), muscle strength and power (measured with the Biodex system 3), and mood state (profile of mood state assessment POMS), and restore reproductive function (resumption of menses as reported).

 

Under-reporters were identified and one Eumen control was excluded from the dietary analysis due to underreporting dietary intake.

 

EB (energy balance) and EA (energy availability) were then calculated as follows: EB (kcal/day) = EI-TEE (energy intake – total energy expenditure); EA (kcal/day) =EI-EEE (energy intake – exercise energy expenditure). Exercise was defined as PA (physical activity) > 4.0 metabolic equivalents (METs) to eliminate activity of daily living.

 

 

Results:

 

Eumen and ExMD were similar in body composition, VO2max, age, menarcheal age, bone mass density (BMD), and bone mineral content (BMC) at 0 and 6 months. There were trends in increased mean body weight, BMI, and body fat with the intervention, but these observed trends were not significant (p > 0.11).

At 0 and 6 months, EI, EB, and EA were similar between both Eumen and ExMD. A mean weight gain of 1.6 kg was associated with physiological improvements in EI, EB, and EA. 75% of the ExMD women gained weight. There was a 62% positive increase in EB and a 75% increase in EA in the ExMD group.

Both Eumen and ExMD groups had adequate nutrient intake that included adequate protein, fiber, vitamin B12, calcium, iron, phosphorus, and zinc. However, for the ExMD group, there was an inadequate baseline dietary intake in folate at 38%, vitamin b12 at 13%, and vitamin D at 63% with no change post intervention. For the Eumen group, low dietary intakes were seen in folate at 11%, vitamin B12 at 11%, and vitamin D at 56%. One ExMD woman had elevated blood B12 levels due to high supplementation. One participant had iron deficiency anemia (ExMD), and 3 participants had low serum ferritin levels (Eumen: 2; ExMD: 1).

ExMD participants resumed menses and 7 of the 8 participants were ovulating. The mean time to the first period was 2.63 months; there was a range of months from 1 to 7. For those who had amenorrhea for less than one year (n=5), it took 1 to 2 months for menses to resume. For those who had amenorrhea greater than 1 year (n=2) it took 6 months for menses to resume. Serum reproductive hormones and thyroid hormones did not differ between groups nor change with the intervention.

With the intervention, overall mood state did not change. The total mean POMS or domain scores were not different between groups at baseline or at 6 months.

In conclusion, a 6-month intervention of an extra 350 kcal/day resulted in moderate weight gain (1.6 kg) and successfully reversed ExMD. There was also an increase in EI and EA that nearly normalized EB, and concurred with the reversal of ExMD, but these changes were not statistically significant. Since there was no difference between EA and EB between the ExMD group and Eumen group at baseline, its is suggestive that some female athletes may be more sensitive to fluctuations in these variables. A dietary intervention that improves EA and EB, while minimizing fat gain, could be a suitable non-pharmacologic treatment for ExMD.

Level of Significance: A linear regression was used to compare groups and ExMD at pre and post intervention blocking. Adjusted p-values were calculated to control for multiple comparisons at a false discovery rate (FDR) of 5%, and all statistical analysis was done using S-plus (TIBCO). Statistical significance was set at p < 0.05.

 

Your Critique:

Limitations

(strengths & weaknesses of the study)

A weakness of the study was that energy intake fluctuated as athletes moved in and out of their competitive season, which occurred during the 6-month intervention. The sample size was also fairly small. The study also could only evaluate reproductive hormones with the single blood draw at the pre intervention time and post intervention period. Repeated hormonal assessments would have strengthened the study. It was also difficult to get female athletes to commit to such a long study over a 10-month period.

A strength of the study is that the researchers used a very controlled variable of a specific carbohydrate, protein, and fat supplement that all the women consumed.

Suggestions for Further Study The authors suggested using repeated pulsatile hormonal assessments in further studies and also increasing the sample size.

 

 

TABLE of EVIDENCE  
Full Citation:

Must use 6th edition APA format

Chou, S. H., Chamberland, J. P., Liu, X., Matarese, G., Gao, C., Stefanakis, R., …Mantzoros, C. S. (2011). Leptin is an effective treatment for hypothalamic amenorrhea. Proceedings of the National Academy of Sciences of the United States of America, 108(16), 6585–6590. http://doi.org/10.1073/pnas.1015674108

 

Type of Study Randomized, double-blinded, placebo-controlled study
Research

Question:

(Study aim, purpose or research question(s)

The aim of the study was to conclusively prove the role of leptin playing a part in the pathogenesis of hypothalamic amenorrhea (HA). The effects of leptin on reproductive outcomes, neuroendocrine function, and bone metabolism were also assessed.
Setting/Site

where the research was conducted –country, hospital?

General Clinical Research Center (GCRC) of Beth Israel Deaconess Medical Center (BIDMC).

 

 

Sample

#, characteristics & exclusion criteria

20 eligible participants were women between 18 and 35 years old who had had secondary hypothalamic amenorrhea for at least 6 months and coincided with a time of strenuous exercise and/or low body weight. All participants had to be within 15% of ideal body weight, and their weights had to have been stable for at least 6 months at the time of the screening for the study.

 

Women with amenorrhea due to other causes, such as hyperprolactinemia, hypothyroidism, hyperthyroidism, Cushing’s syndrome, congenital adrenal hyperplasia, polycystic ovarian syndrome, or primary ovarian failure, were excluded from the study.

 

Other exclusion criteria included medical conditions such as an active eating disorder, depression, psychiatric disease, drug or tobacco use, malignancies, alcoholism, renal or hepatic disease, myocardial ischemia, gastrointestinal malabsorption, anemia, and diabetes mellitus.

Women who took medications such as glucocorticoids, antiseizure medications, thyroid hormones, or estrogens within 3 months of the screening for the study were also excluded. Any breastfeeding, pregnant, or women who were planning pregnancy were also excluded. Pregnancy tests were performed at the screening and all follow up visits and participants were required to use a double-barrier method or abstain to prevent pregnancy.

Methods

describe how the study was done

 

The participants were randomly assigned in a 1:1 ratio to receive either metreleptin or a placebo. All participants received calcium (600 mg twice daily) and vitamin D (400 international units daily) in supplemental form.

Over the 36-week study timeframe, participants visited the General Clinical Research Center (GCRC) of BIDMC every four weeks for assessments that included blood tests, body composition, resting energy expenditure, and to monitor for potential side effects and review injection technique.

 

Every 12 weeks, the participants were request to keep a 3-day food diary to record all caloric intake for 1 weekend day and 2 weekdays. They were also asked to keep exercise records and to document any menstrual bleeding throughout the study. Participants returned 16 weeks after discontinuing the study medication at week 52 for a follow up visit. All subjects who had a menstrual cycle were to return at day 21 for measurement of serum progesterone and to assess if ovulation had occurred.

 

Metreleptin or a placebo was self-administered by subcutaneous injection once a day between 7 and 11:00 PM for 36 weeks. The dose of metreleptin or placebo was calculated based upon the subject’s weight to achieve physiologic to supraphysiologic leptin levels. The intial dose for all subjects began at 0.08 mg/kg and continued for 12 weeks. Those subjects who did not start menstruating at 12 weeks, had their dose increased to 0.12 mg/kg. Weights were checked at each visit and the treatment doses were adjusted to maintain stable weights. More specifically, if the subject lost greater than 5% of her baseline weight, doses were reduced by 0.04 mg/kg. If body weight decreased to less than 8% of her baseline for more than one visit or to less than 80% of ideal body weight, subjects were withdrawn from the study.

 

Fasting blood samples were also collected at each visit to measure free leptin, leptin, antileptin antibodies, luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone, estradiol, testosterone, inhibin B, thyroid-stimulating hormone (TSH), free thyroxine (fT4), free triidothryonine (fT3), cortisol, insulin-like growth factor-1 (IGF1), IGF binding protein 3 (IGFBP-3), prolactin, osteocalcin, bone-specific alkaline phosphatase, osteoprotegerin, and C-telopeptides of type 1 collagen (CTX).

 

Bone density and body composition were also measured using dual-energy X-ray absorptiometry (DEXA) (Hologic QDR-4500; Hologic) in whole body array mode at baseline and every 12 weeks after an overnight stay at the GCRC.

Variables/

Measures:

Identify major IV(s), DV(s)& key operational definitions (describe how variables were measured and include name of tools used)

The independent variable included metreleptin or matching placebo. The dependent variables included recovery of menstruation, free T3, IGF1:IGFBP-3 ratio, cortisol, and bone density. Hormone levels were measured using immunoassays.
Results:

 

Except for one participant who was removed form the study because of weight loss, all participants maintained stable weight throughout the study with dosing adjustments. Four of the participants required a decrease in dosage due to weight loss. The metreleptin treated group had a progressive loss of total body fat mass measured by dual energy X-ray absorptiometry (DEXA) scan. There was a mean loss of 2.02 kg of fat in the metreleptin group as compared to the placebo treated group (P =0.023 for total body fat mass and P= 0.014 for total body fat percentage). The difference in fat mass occurred at week 24 of the study and was controlled for with appropriate adjustments of the metreleptin dosage. Those treated with metreleptin regained their fat mass to levels of their baseline by week 16 after the study ended. There was not a significant difference in resting energy expenditure between the placebo group and metreleptin group. There was a greater respiratory quotient increase in the metreleptin group (P=0.047), which may suggest that there was greater carbohydrate oxidation in the metreleptin group. There was no significant difference in reported caloric intake between the two groups from the beginning to the end of the study.

The metreleptin-treated group had serum total leptin level increase considerably after 4 weeks of metreleptin administration (25.99 ± 5.43 ng/mL compared with 3.54 ± 0.59 ng/mL for placebo; P < 0.0001) and the levels continued to rise throughout the study. The treatment dose of four participants in the metreleptin-treated group was increased at 12 weeks to 0.12 mg/kg of metreleptin due to lack of menstruation. Two participants required dosing to be lowered back down to 0.08 mg/kg due to weight loss, and back down to 0.04 mg/kg because of weight loss at week 16.

The mean leptin level in the metreleptin treated group decreased 12 weeks after discontinuing the treatment to 8.64 ± 3.92 ng/mL at week 52, which was a level that was not significantly different from the placebo group (P = 0.054). The control group did not have any significant changes in leptin levels throughout the study.

7 of 10 subjects who were treated with metreleptin developed menstruation during the course of the study. 2 of 9 subjects on placebo developed menstruation (P=0.0046). Menstruation came at various stages of metreleptin therapy. Menstruation appearance ranged from 4 weeks to 32 weeks after initiation of treatment. On average, menstruation occurred earlier in subjects treated with metreleptin. All who menstruated had irregular cycles but cycles that were sustained. Menstruating subjects had their progesterone levels measured at day 21 of their cycle. Four of the subjects who were menstruating were determined to be ovulatory. Ovulation was defined as a serum progesterone level greater than 10 ng/mL at the midluteal phase. One subject who resumed menses after 8 weeks of metreleptin became pregnant at week 24. Of 5 participants who regained menses, three continued to have menses until the week 52 follow up visit.

Estradiol and progesterone levels increased considerably in the participants treated with metreleptin (P= 0.0137) as compared with the participants treated with placebo (P = 0.0342).

Low levels of leptin can cause the dysfunction of neuroendocrine axes and bone metabolism associated with HA. Treatment with metreleptin in may be a safe, effective therapeutic option. Apart from trying to decrease exercise and/or increase body weight and caloric intake, the mainstay treatment for HA is estrogen replacement, which does not effectively address infertility, other neuroendocrine abnormalities, nor bone loss.

Level of Significance: P < 0.05 (two-tailed) was considered statistically significant for all analyses.

7 of 10 subjects who were treated with metreleptin developed menstruation during the course of the study. 2 of 9 subjects on placebo developed menstruation (P=0.0046).

 

Estradiol and progesterone levels increased considerably in the participants treated with metreleptin (P= 0.0137) as compared with the participants treated with placebo (P = 0.0342).

 

Your Critique:

Limitations

(strengths & weaknesses of the study)

A weakness of the study is that it could have been longer to see if menses resumed, and the sample size of the study could have been larger. A strength of the study is that other variables were controlled for by using a double blind, placebo-controlled methodology.
Suggestions for Further Study The authors write that longer studies are in process to determine the effect of metreleptin therapy on bone mineral density, and larger studies are needed to determine the safety and efficacy of metreleptin as a treatment for this condition.

 

 

Chocolate Protein Zucchini Bread Recipe

Hello beautiful people🙂

I know I said I would post this recipe yesterday, but I had a random change of plans and ended up not being able to post! I ended up going to Atlantic City with some of my friends from the gym to the Europa fitness expo and fitness show!

I had a great time and got lots of free samples to try out! I’ll keep you guys posted on how the different brands stack up😉

Now, on to the main event, the recipe!

I randomly threw this recipe together the other night. I had a lot of extra zucchini laying around that needed to be used up.

I happen to own a really cool food processor, Magimix by Robot coupe, that has an attachment that easily shreds any veggie I throw into it. It’s an amazing. I got mine at William and Sonoma!

This recipe makes a large loaf, but I had already eaten most of it before this picture was taken ! Couldn't help myself ;)

This recipe makes a large loaf, but I had already eaten most of it before this picture was taken ! Couldn’t help myself😉

Chocolate Protein Zucchini Bread Recipe

  • 2.00 scoop (42g), Protein Powder – Vanilla –I used Jamie Eason Lean Body for Her Chocolate protein.
  • 102.00 gram, Egg Whites
  • 1.50 Tbsp (15g), Unsweetened Carob Chips
  • 150.00 g, Squash, summer, zucchini, includes skin, raw
  • 1.00 oz, Love raw foods coconut flour
  • teaspoon baking powder
  • 1/4 teaspoon of salt
  • teaspoon vanilla extract
  • 4 tbsp water

Directions:

Preheat oven to 350 F. Grate the zucchini or shred it. Mix all of the above ingredients together in a large bowl, except for the carob chips or chocolate chips. Slowly add the water to get a good consistency to the batter. You want it to be on the thicker side, but definitely pliable. Mix in carob chips or chocolate chips. Pour into a parchment lined loaf pan and bake at 350 F for 30-40 minutes or until it doesn’t look giggly anymore!

Macros:

Screen Shot 2015-08-30 at 1.20.07 PM

I topped mine with Fluff butter from D’s naturals and Bare Butter!

Topped with Bare Butter cookie dough butter , cinnamon and siggi's vanilla yogurt!

Topped with Bare Butter cookie dough butter , cinnamon and siggi’s vanilla yogurt!

Topped with D's Naturals fluff butter and green valley's kefir!

Topped with D’s Naturals fluff butter and green valley’s kefir!

My Experience with Fitness Competitions

Why I’ve decided to not compete in fitness competitions:

Hey guys, long time no post!

I’m not usually one to put my personal business out for everyone to read, but I feel like this is something I have to share.

I’ve recently competed in the bikini division of an NPC fitness competition. This was my third competition. I honestly decided not to compete after the second competition, but I had made friends with these great girls at my gym who talked me into one last competition before I go into an accelerated nurse practitioner program in the fall.

I knew before going into the competition prep that it’s not really healthy. I knew that I did not enjoy prepping for competitions. I knew that I did not need to lose weight or fat (I was at a healthy weight BMI for my height). However, I wanted to be there for my friends, and I figured one last competition wouldn’t hurt.

I did a 14 week prep, which, in retrospect, was way too much for me. I did not have that much to lose to begin with, and I lost a lot of weight really fast. I would classify myself as a bit of a perfectionist. I tend to take whatever I do to extremes. It is something I am working on changing.

I started off at about 122 pounds and quickly dropped down to about 116 in the matter of a few short weeks. Then, I was stuck at 116 for a few weeks, but suddenly my weight plummeted down to 110 rather quickly. I had not changed my diet or exercise so I was highly surprised by this sudden drop.

Toward the end of prep, I was pretty exhausted and run down. I had no energy to do much of anything besides workout and cook food. I also had a week where I was just so depleted and “depressed”. I was just sad. I could not cheer up for the life of me. Nothing was exciting or fun or interesting.

I was feeling this way towards the last 3 weeks of the prep, but I did not want to stop because I had already ordered my suit and bought new heels and the whole nine yards. Looking back, I probably should have just stopped prepping and focus more on the pressing health issues at hand, but I did not want to be a “quitter”.

What also made things even more difficult to back out of the competition was that a huge group of people from my gym were coming to watch the show and cheer us all on. I knew I would feel guilty or like a loser if I just quit with only three weeks left of the 14 week prep.

So, I pushed through and some how made it through the last 3 weeks. Competition day came, I did fairly well. I placed 4th in my division. When it was all over, I looked at my little plastic trophy and all I could think was “wow, this totally was not worth it at all”. All of the social events I gave up, all of the pain I pushed myself through, all of the dieting I did, all of the cardio and weight lifting and days of complete depletion — and all for what? Some recognition by random judges? All to say, “I did it!, I competed and placed!” . All to say I was able to push myself to my lowest weight yet? To be able to write on my instagram, “qualified npc bikini competitor!” ?

I understand that people love competing, and I am not knocking or belittling anyone who competes. It’s a great thing to have goals and to accomplish those goals.

However, for me, I found competing to be unfulfilling and disappointing.

And the darker side:

3 weeks post competition, and I am at my lowest weight ever. I am 106 pounds and the body fat machine at the gym won’t even register my percentage. It says “error”.

This is extremely unhealthy, especially for the female body. We need fat to function, reproduce, protect our organs, conserve body heat, and much more! I’ve cut back immensely on my workouts. I’ve upped my caloric intake, but I just continue to drop.

I have noticed some disordered tendencies in my eating too. Without meaning to, I pick diet foods. I still count what I eat and weigh and measure. I try a bit of some food, decide it’s not worth the calories, and throw it out. I am really struggling to just let myself go and eat whatever. It’s hard to get out of the “prep mentality”.

I am making huge strides to change my mentality, because at this point, it’s affecting my long-term health.

Low levels of body fat and hormone levels lead to osteoporosis later in life. I do not want to be hunched over and immobile later in life. I do not want to become permanently infertile. I want the option to be able to have children in the future. I do not want my long-term health to suffer for short-term bodily aesthetics.

So, I am working out less! I’m following an online program to cut back my workouts. I am slowly ratcheting down the length of my workouts.

I am allowing myself to indulge more.

I am probably going to start minnie maud protocols to restore my health.

I am making myself go out to eat at least twice per week to places I would have forbidden in the past.

I am challenging myself to eat “bad” foods.

I am filling my mind with positive and uplifting information.

I am reading my Bible and remembering that only God can judge me. It is a great reminder that we are more than our bodies, that our souls are what matter. Nourishing your soul can make all the difference.

Competing has really brought out a super perfectionist side of myself, a side of myself that I do not like. It is so unhealthy. I’ve never had such disordered thoughts before. All I can do is hold myself accountable to changing and setting a good example for everyone else thinking of competing or struggling with getting back to “normal” post competition.

There are so many bigger and better things I’d rather put my resources towards than worrying about what to eat or how my body looks. I have big goals in life that I plan on accomplishing, and I will not allow this small bump in the road to hold me back from my full potential.

Has anyone else experienced this? Please leave tips/advice/stories below!

God Bless!

Danielle

Soft Pretzel Chocolate Chip Banana Protein Cookies; Paleo, Gluten Free

Guess who’s back, back, back?! Back again.. lol jk.

I’ve got quite the recipe for you lovely ladies and gents!😉

Introducing… SOFT PRETZEL CHOCOLATE CHIP PROTEIN COOKIES !

IMG_5366-2

These are salty and sweet with a hint of banana flavor. They are gluten free and Paleo! I’ve recently discovered that I do not do well with eggs. So, no more eggs for me😦 … They were my favorite breakfast food. I ate at least 3-4 a day, maybe that’s why I developed an intolerance!! Too much of anything is not good!

RECIPE:

  • 1/4 cup almond flour (I use Bob’s Red Mill)
  • 2 scoops whey protein (I use grass-fed vanilla whey)
  • 2 TBSP coarsely ground flax seed (365 Organic)
  • 1 TBSP organic sunflower seed butter (Once Again)
  • One small banana – about 6-6.5 inches or so
  • Mega Chunks by Enjoy Life (or any other soy free, dairy free, gluten free, chocolate chips!)
  • 1/2 cup water
  • 1/8  to 1/4 cup butter
  • Sea Salt

IMG_5714

  1. Pre-heat oven to 350 F.
  2. Add all ingredients to a large mixing bowl, and mix well!
  3. Use an ice cream scooper to scoop out about 10 cookies onto a parchment paper lined baking sheet.
  4. Bake at 350 F for about 25 minutes, or until solid and slightly browned.
  5. Melt a little bit of butter in the microwave, and use a culinary brush to brush the top of the cookies with some butter.
  6. Sprinkle sea salt on top.
  7. ENJOY!

*Store in an airtight container in the fridge!

Macros: Screen Shot 2015-03-06 at 6.09.25 PM

Maximize Muscle

Hello lovely people!

It’s been a little while.

But I’m back with more knowledge to share !🙂

First, I’d like to say that I’m currently sipping organic Mexican Chiapas coffee with grass-fed heavy cream and a few drops of vanilla creme stevia. I’ve never put heavy cream in my coffee before. It is the best  thing in the entire world. Try it!

This is the cream I used. I found it at Whole Foods.

heavy_cream

So tips for gaining muscle and maximizing fat loss!

  • Lift weights, but vary your training. Your training should include a mixture of endurance, agility, and speed training. Resistance training is catabolic. It breaks down muscle fibers, but it triggers an anabolic process when muscle fibers have to rebuild themselves in order to handle more stress in the future.advancedtriangle
  • Train for your goals. Velocity and high speed training will more likely develop lean muscle. Muscular strength is acquired through maximizing resistance and minimizing endurance. Training only for strength can minimize muscle endurance. The body has a muscle mass set point. The body will try to remain at that set point. At a certain point, as long as your not using steroids, your muscle gain will cease.keep-calm-and-set-your-goals-4
  • Vary your food intake. Periods of under eating can actually be beneficial. When you under eat, you trigger a mechanism that detoxes your body. It clears out unused proteins and recycles nutrients. However, under eating should never exceed 24 hours. Muscle breakdown will occur if under eating is sustained for too long. If you under eat for a few days, you should compensate by overeating during one meal the next day. This will help you avoid metabolic decline and muscle breakdown. Overtime, under eating and then overeating will allow you to increase your metabolic capacity.kefir-duo-230w
  • Vary your macronutrients. Slow twitch muscle fibers are endurance muscles. They have more mitochondria. Mitochondria use fat for energy. If you are going to perform mostly endurance training, it may be best to eat a higher fat, lower carb diet. It will take your body a few weeks to months to adjust to this diet, but once you adjust you will have tons of energy. If you’re training for  strength, velocity, and speed, your diet should be higher in carbohydrates because these muscles use glucose more readily. There is apparently a “super muscle fiber” that can use both sources of fuel efficiently. By varying your training you can help to create “super muscle fibers”. Macronutrient_Ratios
  • Post recovery meals are essential. It is so important to eat a recovery meal after a workout to stimulate insulin release and IGF1. Protein with fast and slow release is the best source of protein. The fast will immediately be used in the damaged muscles, while the slow releasing protein will sustain anabolic activity throughout the day. Low glycemic carb sources are the best to help rebuild muscles. There is no need to overly spike insulin to recieve the benefits of carbohydrates in muscle repair and growth. Whey protein is naturally high in IGF1 and can promote muscle growth. The best fat sources to eat post workout are MCT oil fat sources because these are short chain fatty acids that are able to be used immediately and help to repair the muscle. Avoid cheap, overly processed, chemical foods that can cause hormonal deregulation and stress the liver.
    • Most commercial protein powders do not include all the essential amino acids.
    • Minerals are important to replenish after a workout too.
    • Carbs should come from non-fructose sources, fibrous sources, and low glycemic sources.
    • Incorporating high fat and high carb days will increase mitochondrial density and glycogen reserves, as well as increase performance in the gym.
  • Keep your detox organs healthy! Liver detoxification is critical to fat loss. Your liver needs to be functioning at its optimally capacity to maximize fat loss. The liver plays a roll in processing nutrients for fuel and producing steroid hormones.liver-detox1
  • Eliminate the reasons for fat tissue to exist. Fat tissues produces hormones, hold toxins, and protects the body from chronic over feeding or underfeeding.
    • Avoid chronic calorie restriction.
    • Avoid long-term low carb diets.
    • Avoid hormone disrupting substances (plastics, fertilizers, chemicals, herbicides, etc.)

Above all: TRIAL AND ERROR. Find what works for YOU and your specific body type! We are all different!

Blog photo

 

You can read more about this in the book: “Maximum Muscle, Minimum Fat”

 

Have a blessed day!

-Fitgirlfab

 

 

 

 

Whole-30 Review

So!

A few months back I did the whole-30!

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(This was an awesome excerpt right from the awesome book!)

It’s basically eating super clean paleo for 30 days to look and feel your best. No, it’s not easy, but if you want it bad enough it is definitely doable!

I ate no grains, dairy, sweets, added sugars, and very little fruit. I ate mostly protein like fish, lamb, beef, chicken, turkey, and pork. I also ate large servings of vegetables of all kinds, and starchy tubers too for more carbohydrates. I consumed a ton of coconut while doing the whole 30–Coconut flakes, coconut butter, coconut oil, coconut milk! Coconut is very gut healing and an anti fungal. I also tried my hand at making some bone broth. Bone broth is just that, broth that is made from leaving bones in a crock pot for over 24 hours. It is supposedly rich in amino acids and also gut healing. It’s a magical drink. (side note: The La Lakers drink some with every meal to promote faster healing and joint recovery!)

I did not do it to lose weight. I did it to “reset” my biological hormones like leptin, insulin, and coritsol. I also did it to help fix my satiety signals. Sometimes we keep eating because the food we’re eating is hyper-palatable. Our bodies naturally crave sugar, salt, and fat as a survival mechanism. So, when you begin eating something like potato chips, it can be nearly impossible to stop at just one.

Also, blood sugar spikes make you crave more food even when you’re not really hungry. Dairy, more specifically whey, will spike insulin and cause you to want more.

I loved it! At first I was a little lethargic, but as a week and a half went by, I became more energized and felt great.

I was not even trying to lose weight, but I managed to do so. The whole-30 advocates that you get out of your old “comfort foods” mentality. That means stop thinking you need a dessert with every meal or something sweet after dinner. Breaking these cultural cues is hard. Basically, you ask yourself, “am I really hungry, or am I just bored, angry, sad, tired, or just craving something?” My go to question that I got off of the whole 30 website to check if I was really hungry when I wanted more food at night was, “Could I eat fish with broccoli right now?” If the answer was yes, then I would eat more food, if no, then I would entertain myself with some other tasks.

I think the whole-30 is awesome because it works. It resets all your hormones, makes you more aware of what your eating and how good, real food should taste. It does not advocate artificial sweeteners or anything processed. It is an eye-opening experience that will change how you feel and look. I recommend it for anyone! No matter how fit you are, how out of shape you are, or whatever your situation the whole-30 helps you to “reset” and find balance!

I HIGHLY recommend the book, it is pack full of good information. You can get it on amazon, click here!

 

Here are some of my favorite meals I ate:

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First picture is Chilean Sea Bass on top of a bed of spinach, second is sweet potatoes, third is sautéed spiraled zucchini, and the fourth was one of my go to drinks. I enjoyed hot cups of green tea with lemon!

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I’m italian, so no pasta is no bueno! However, this was awesome! Italian sausage from whole foods, peppers and onions, and I put it all on top of a huge spinach salad with lots of sugar free tomato sauce!

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Eggs wrapped in pork–enough said.

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And this was my favorite of all time! I got the recipe off of civilized caveman’s website. It was SO darn good!

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My go-to breakfast was two eggs over easy, turkey breast, kale, onions, butternut squash, and half an avocado–all sprinkled with salt of course!🙂

And here’s my transformation picture:

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Currently, I am still eating the same way the whole-30 promotes, but I slowly added certain foods back into my diet. To do this, I used Chris Kresser’s book, “Your Personal Paleo Code”. This book advocates slowly re-introducing foods back into your diet to see if you react to them.

For example, I added dairy and did not react to it, so I can eat dairy. However, when I tired to add corn, I felt bloated and lethargic, so I will no longer be eating corn.

I’m still in the process of finding what works for me and my body. It is a learning experience. Everyone is different, so you have to find what works for you.

I HIGHLY recommend Chris’s book too. You can find it on amazon at this link!

 

Hope this helped some people! If you have any questions, feel free to ask!🙂

God Bless,

Fitgirlfab

 

Been so long!

Hey guys! It’s been forever! But I’m back!

 

Quick update for now, I’ll do a more in-depth post later.

Life has been crazy! I’ve been studying to finish my degree. I’ll be graduating in May with a degree in Economics!

It’s so exciting!😀

Anyway, here’s a quick look at my life in pictures:

 

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I did the “whole-30” – I’ll do a post on this later.

 

 

Got these versa grips!, they work pretty well for lifting and helping grip!

 

 

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I’ve been eating healthy, REAL, foods! – more to come on this too!

 

I’ve also been learning a ton. NOT just in school, but doing my own research too. I’ve read a few books: The whole-30 book, the calorie myth by Jonathan Bailor, Robb Wolf’s book, and many more!

I’m also writing my senior economics paper on health/nutrition/agriculture/corruption. So, I will be sharing all of that too! 

 

STAY TUNED FOR SOME AWESOME INFO!!🙂 — off to get my workout on and then take a Calc quiz!