Some hormones secretion and personality in anorexia nervosa syndrome

The relationship between plasma leptin, some hormones (GH, IRI, IGF-1, DHEA-S, LH, FSH, T, E2, TSH, fT3, fT4), glucose level, personality dispositions and adipose tissue content in 22 women with anorexia nervosa were evaluated. Some personality features as: defensiveness, domination and aggression necessities, high self-control, bad self-estimation, retiring, expectation of custody--correlated with some hormones (LH, E2, IGF-1, fT3, F, T) and leptin level. The ascertained relationships suggest that still unexplained causes generate simultaneous disturbances in the endocrine and psychic processes in central nervous system of anorexia nervosa patients. Probably hormonal and neurotransmitter derangement are the adaptive changes allowing longer survival, as the low leptin secretion in the severest undernutrition states is.     

Serum Sex Hormones Are Altered in Patients with Chronic Temporal Lobe Epilepsy Receiving Anticonvulsant Medication

Summary: Purpose: To evaluate the changes in serum sex hormones of gonadal or adrenal origin, the gonadotropic hormones, and sex hormone-binding globulin (SHBG) in men and women with chronic temporal lobe epilepsy (TLE), who are undergoing monotherapy with carbamazepine or receiving carbamazepine in combination with other anticonvulsant drugs.
Methods: Gonadal hormones (estradiol, testosterone, free testosterone, and inhibin B), adrenal hormones [cortisol, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and 17a-hydroxyprogesterone], and gonadotropic hormones (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) were measured in 22 women and 26 men with TLE. The study also measured prolactin; human growth hormone and its major mediator, insulin-like growth factor–I; thyroid hormones (free thyroxine and free triiodothyronine); thyroid–stimulating hormone (TSH); and SHBG. The results were compared with those obtained from 60 healthy women and 106 healthy men.
Results: In the female patients, TSH, DHEAS, follicularphase LH, and luteal-phase estradiol were significantly lower than in the control groups, with prolactin and SHBG significantly higher. In the male patients, DHEAS, 17α-hydroxyprogesterone, free testosterone, inhibin B, and the testosterone LH ratio were significantly lower than in the control group, with LH, FSH, and SHBG significantly higher. Increased FSH in 31% of the men indicates an impairment of spermatogenesis; lowered inhibin B in 12% indicates an impaired Sertoli's cell function; and the decreased testosterone LH ratio in 50% indicates an impaired Leydig's cell function.
Conclusions: The case patients had endocrine disorders, mainly concerning the gonadotropic and gonadal functions in both sexes; the adrenal function, with lowered DHEAS levels in both sexes; and lowered 17α-hydroxyprogesterone levels in the men. SHBG levels were increased in patients taking anticonvulsant medications.     

Neuroendocrinological investigations during sleep deprivation in depression. II. Longitudinal measurement of thyrotropin, TH, cortisol, prolactin, GH, and LH during sleep and sleep deprivation

Thyrotropin (TSH), thyroxin (T4), triiodothyronine (T3), free T3 (fT3), cortisol, prolactin, and human growth hormone (HGH) were measured every 2 hr during a night of sleep, the following day, and a night of sleep deprivation (SD) in 14 patients with major depressive disorder. In subgroups fT4 (n = 5), reverse T3 (rT3), and luteinizing hormone (LH) (n = 6) were also investigated. Significant increases in TSH, T4, fT4, T3, fT3, rT3, and cortisol and decreases in prolactin levels occurred during the night of SD, compared to the pattern during the night of sleep. The pre-SD T4 and T3 levels of the responders to SD were already higher than in the nonresponders, and increased less during SD. The cortisol and HGH concentrations of the responders rose higher during SD than those of the nonresponders. Changes in TSH and prolactin were not correlated to clinical response. Analysis of possible neurochemical mechanisms underlying this "pattern" of changes in different endocrine profiles suggests that enhanced noradrenergic activity might play a role in the changes in TSH, cortisol, thyroid hormones, and possibly HGH secretion during SD, and increased dopaminergic tone probably induced the decline in prolactin levels. Additional effects of the serotonergic system cannot be excluded at present. In conclusion, the data suggest that enhanced noradrenergic activity of the locus coeruleus stimulates alpha and/or beta adrenergic receptors in depressed patients during SD. This mechanism could well be involved in the antidepressant effect of this therapy.     

Disturbances in the hypothalamo-pituitary-adrenal and other neuroendocrine axes in bulimia

Disturbances in the hypothalamo-pituitary-adrenal (HPA) and other endocrine axes were assessed in 24 women with bulimia and healthy controls. Overnight blood samples for measuring nocturnal plasma cortisol, prolactin (PRL), growth hormone (GH), luteinizing hormone (LH), and follicle stimulating hormone (FSH) were obtained at 30-min intervals. A 1.5 mg dexamethasone suppression test (DST) and a TRH-test were performed. Patients were monitored closely while their nutritional intake was recorded over 21 days. Compared with healthy controls, nocturnal cortisol plasma levels were not elevated in the bulimics. There was a trend toward insufficient cortisol suppression in the DST in patients with bulimia, which was most pronounced in patients with signs of restricted caloric intake. Plasma dexamethasone levels were significantly reduced in bulimics compared with healthy controls. There was a trend for blunted thyrotropin stimulating hormone (TSH) responses to thyrotropin releasing hormone (TRH) in bulimia. The prolactin response to TRH was significantly reduced in bulimics with a history of anorexia nervosa. Plasma LH and plasma FSH were significantly reduced in bulimics with signs of reduced caloric intake [low T3, high levels of beta-hydroxy-butyric acid (BHBA), reduced daily caloric intake, high number of fasting days] as compared with healthy controls. Bulimics with high BHBA levels had significantly reduced nocturnal prolactin plasma levels. Results show that multiple neuroendocrine disturbances exist in bulimia in a milder form than in anorexia nervosa. Evidence for the impact of caloric intake on endocrine functions is presented. Endocrine dysfunctions in our bulimic sample did not show a positive association with the presence of depressive symptoms.     

Endocrine studies in heroin addicts.

In 10 heroin addicts actively taking the drug, 5 males, 5 females, a number of endocrine abnormalities were identified. These included especially: (1) Increased thyroid function manifested by high total T₄ (and occasionally T₃) and T₃ resin uptake, and by blunted TSH response to TRH. (2) Changes in sex hormones, LH and FSH, and LH/FSH responsiveness to GnRH compatible with either primary gonadal failure or disturbance of the hypothalamopituitary regulations of the reproductive functions. (3) Abnormal increase in growth hormone in response to TRH/GnRH. (4) Occasionally increased baseline prolactin; blunted response or slightly increased responsiveness of PRL to TRH/GnRH. (5) No apparent change in the adrenocortical function. The results are best explained by multiglandular abnormalities due possibly to multiple effects of heroin on the endocrine system and its regulations.     

Circadian patterns of rat anterior pituitary and target gland hormones in serum: determination of the appropriate sample size by statistical power analysis

(1) Experiments were performed to ascertain circadian fluctuations in the serum concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (PRL), testosterone (T), growth hormone (GH), thyroid stimulating hormone (TSH), and corticosterone in rats. (2) Serum LH, TSH, T and corticosterone varied throughout the 24-hr period, but the magnitude of change for LH, TSH and T was small compared with the range of individual animals' hormone concentrations at a given time point. (3) Statistical power analyses were performed on the LH, TSH, and corticosterone data in order to determine retrospectively the sample size necessary to reduce the possibility of a Type II (beta) statistical error to an acceptable level. (4) The results of these analyses indicate that many similar studies already published used too few animals and thus were biased toward not rejecting the null hypothesis.     

Hormonal and biochemical disturbances in Down's syndrome

ABSTRACT. Clinical and laboratory endocrine variables in 29 adult institutionalized patients with Down's syndrome were compared with those of matched controls consisting of other mentally retarded patients from the same institution. Of the clinical variables, testes volume and body height were significantly lower in patients with Down's syndrome than in control patients. The thyroid function tests documented a higher average TSH level in Down's syndrome than in other mentally retarded patients. However, there was no clear-cut correlation between TSH and thyroid hormone levels. The data indicate that there is a tendency towards primary thyroid dysfunction in Down's syndrome. In addition, there is some evidence indicating a relative failure of TSH secretion. In male patients, estradiol was elevated compared to controls. FSH and LH also seemed slightly higher in the study group, but the differences only reached statistical significance when patients on chronic medication were omitted. Prolactin was significantly greater in the Down's syndrome patients than in the controls, both over the entire sample and in the subgroup of men with Down's syndrome, with P -values of around 0.001. The elevation of prolactin was not due to medication and did not correlate to thyroid function or difficulties during blood sampling. In females, the difference was not statistically significant. Laboratory tests that may be associated with endocrine disease or might indicate disease which could influence the endocrine status, were also included in this study. Compared with the controls, ESR, creatinine and uric acid levels were higher in Down's syndrome patients, while albumin was lower, all with P-values lower than 0.001. Vitamin B₁₂ was moderately lower in Down's syndrome patients than in controls (P<0.05).     

In vivo and in vitro effects of cholecystokinin on gonadotropin, prolactin, growth hormone and thyrotropin release in the rat

Varying doses of cholecystokinin (CCK) dissolved in 2 μl of 0.9% NaCl or 2 μl of saline alone were injected into the third ventricle of conscious ovariactomized (OVX) rats bearing 3rd ventricular cannulae. Plasma luteinizing hormone (LH), prolactin (PRL), growth hormone (GH), thyrotropin (TSH) and follicle stimulating hormone (FSH) levels were measured by RIA in jugular blood samples drawn through an indwelling silastic cannula. Control injections of saline i.v. or into the 3rd ventricle did not modify plasma hormone levels. Intraventricular injections of 4, 40 and 500 ng CCK produced a significant suppression of plasma LH within 5 min of injection. Injection of 4 or 500 ng doses of CCK has no effect on plasma PRL levels, but injection of the 40 ng dose produced a significant elevation of plasma PRL within 15 min. Plasma GH levels increased significantly within 15 min of the 3rd ventricular injection of each dose of CCK. The 40 ng dose of CCK caused a progressive reduction of plasma TSH which was significant by 15 min and lasted through the 60 min of experimentation. The highest dose of 500 ng reduced plasma TSH levels within 5 min. Plasma FSH was not altered by any dose of CCK. Intravenous injection of CCK caused a dose-related increase in plasma prolactin levels within 5 min, but only the highest dose of 1000 ng produced a significant decrease in plasma LH. No significant changes in GH, TSH or FSH levels were observed after i.v. injection of CCK. In vitro incubation of hemipituitaries from male rats with doses of CCK ranging from 10 ng to 5 μg had no effect on pituitary hormone release into the medium. The results indicate that CCK can alter pituitary hormone release via a hypothalamic action and suggest that it may act as t transmitter or modulator of neuronal activity controlling the release of hypothalamic releasing and/or inhibiting hormones.     

Neuroendocrinological investigations during sleep deprivation in depression. I. Early morning levels of thyrotropin, TH, cortisol, prolactin, LH, FSH, estradiol, and testosterone

Measurements of 12 hormones were conducted in patients with major depressive disorder at 8 AM on the morning before and at 8 AM on the morning after total sleep deprivation (SD). Thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), and free T3 (fT3) were measured in 50 patients, free T4 in 39 patients, reverse T3, cortisol, prolactin, luteinizing hormone, and follicle-stimulating hormone in 21, estradiol in 20 (women), and testosterone in 14 (men). After SD, there was a significant rise in TSH, T4, T3, and fT3 concentrations and a significant fall in testosterone levels. The increases in TSH levels were significantly correlated to clinical response. Responders to SD had higher T4, fT4, rT3, and testosterone concentrations before SD. Neither age, gender, polarity, nor antidepressant medication had a clearly significant effect on the response to SD.     

急性颅脑损伤后垂体前叶激素的动态变化及意义

目的探讨急性颅脑损伤患者垂体前叶激素水平的变化与颅脑损伤程度及预后的关系。方法随机抽取90例颅脑损伤患者作为观察组,采用酶联免疫定量分析法动态检测伤后第1、3、5、7、14、30d血清催乳素(PRL)、卵泡刺激素(FSH)、黄体生成激素(LH)和促甲状腺激素(TSH)水平;30例正常人作对照组,损伤程度采用GCS评分评估,预后采用GOS评分评估。结果观察组血清PRL、FSH、LH较对照组显著升高(P<0.05),TSH较对照组略降低(P>0.05);观察组血清PRL、FSH、LH水平伤后升高(72h内尤为明显),后逐渐降低,血清TSH的水平伤后略降低,后逐渐回升;GCS评分较低者垂体前叶激素变化幅度较大;预后恶劣的颅脑损伤患者垂体前叶激素变化幅度较大。结论急性颅脑损伤后血清垂体前叶激素PRL、FSH及LH水平明显升高,变化程度与颅脑损伤严重程度及预后有关。     

Hormonal changes in headache patients.

Seventy-three patients with headache underwent serum and cerebrospinal fluid (CSF) radioimmunoassays of follicle-stimulating hormone (FSH), luteinizing hormone (LH), cortisol and prolactin. Serum FSH showed significant increases in all headache patients while serum LH increased only in females. Such a rise of serum FSH and LH is attributed to disturbances of the sleep-wake cycle. On the other hand, serum cortisol was significantly decreased in the male headache patients, probably due to altered circadian rhythm. Serum prolactin remained within normal limits. CSF prolactin, FSH and LH showed detectable levels in all headache sufferers compared to undetectable levels in control subjects, while CSF cortisol was significantly reduced.     

Circulating IGF-1, IGFB-3, GH and TSH levels in multiple sclerosis and their relationship with treatment

Objectives: Improving the proficiency of oligodendrocytes in their ability to repair myelin damage is one of the major goals of multiple sclerosis treatment. Insulin-like growth factor-1 (IGF-1) is one of several polypeptides that are considered to have potential benefits in that sense. In the present study, we aimed to determine serum levels of IGF-1 and insulin-like growth factor binding protein-3 (IGFBP-3), thyroid stimulating hormone (TSH) and growth hormone (GH) among treated and non-treated patients with Relapsing-Remitting Multiple Sclerosis (RRMS) and a healthy control group.

Methods: The study enrolled 100 RRMS patients and 100 age- and sex-matched control subjects diagnosed with definite multiple sclerosis (MS). Serum GH, IGF-1, IGFBP-3, and TSH levels were studied.

Results: The number of relapses and Expanded Disability Status Scale were negatively correlated and IGFBP-3 and GH were positively correlated with IGF-1. A statistically significant difference was not observed when patients were divided into two subgroups as patients treated with a MS-specific therapy (n = 54) and non-treated patients (n = 46). TSH and IGFBP-3 values were significantly lower in patient group vs. control group.

Conclusion: While no difference was determined with in IGF-1 levels, low levels of IGF-1 was in correlation with the least levels of IGFBP-3. To understand the relation between IGF-1 and IGFBP-3, the role of low levels of IGFBP-3 and TSH may be studied with clinic isolated syndrome patients and the evolution of these patients to definite MS.     

Hypothalamic-pituitary function in myotonic dystrophy

Summary Function of the hypothalamic-pituitary axis was investigated in seven patients with myotonic dystrophy (MD).HGH and ACTH secretion were normal.TSH response to TRH was impaired in about half the cases, without concomitant thyroid dysfunction. LH and FSH levels were often elevated, with inconsistant response to LH-RH stimulation. Gonadotrophin disturbances in MD have previously been attributed to a primary gonadal lesion, characteristically seen in this disease. High prolactin levels in six of our seven patients however suggest that gonadal failure may also be due to hyperprolactinemia through the direct anti-gonadal effect of prolactin and its interference with hypothalamic-pituitary regulation of gonadotrophin secretion.

---

Zusammenfassung Bei sieben Patienten mit Myotonia Dystrophica (MD) wurde die hypothalamische-hypophysäre Funktion untersucht. Die Sekretion von HGH und ACTH waren normal. Die TSH-Produktion nach Stimulation mit TRH war in ungefähr der Hälfte der Fälle gestört, ohne begleitende Schilddrüsendysfunktion. LH- und FSH-Werte waren öfters erhöht mit wechselnder Reaktion auf LHRH-Stimulation.Die bisher beschriebenen Gonadotrophinstörungen bei der MD wurden bisher immer dem primären Gonadenleiden zugeschrieben. Erhöhte Prolactin-Werte in sechs unserer sieben Patienten sprechen zugunsten der Möglichkeit, daß die Gonadeninsuffizienz auch eine Folge der Hyperprolactinämie sein könnte sowohl durch eine direkte antigonadale Wirkung, wie durch Interferenz mit der hypothalamisch-pituitären Regulation der Gonadotrophin-Sektretion.

---

Abbreviations ACTH adrenocorticotrophic hormone - FSH follicle stimulating hormone - HGH human growth hormone - LH luteinizing hormone - LH-RH luteinizing hormone-releasing hormone - PRL prolactin - TRH thyrotrophic releasing hormone - TSH thyroid stimulating hormone     

Studies using releasing factors in Klinefelter's Syndrome: The responses of LH and FSH to luteinizing hormone-releasing hormone and of prolactin and TSH to thyrotropin-releasing hormone before and after testosterone

(1) During an investigation of their pituitary function, the TSH prolactin (PRL) and gonadotropin, (LH, FSH) response to TRH was measured in four patients with documented euthyroid Klinefelter's syndrome. (2) In all four patients, the serum testosterone was low, the gonadotropins were elevated and thyroid antibodies undetectable. (3) The identical study was repeated after each patient had received intramuscular testosterone cypionate 200 mg bi-weekly for three doses. This raised the serum testosterone at least four-fold. (4) Basal TSH was normal in all four patients but its response to TRH was blunted (mean peak TSH 9.6 μU/ml), compared with normal controls (mean peak TSH 18 μU/ml). Following testosterone this response to TRH was further suppressed to a mean peak of 3.4 μU/ml TSH. (5) Basal PRL levels were also normal and the mean peak response to TRH, 28 ng/ml. When repeated after testosterone, TRH produced a mean peak PRL of 58 ng/ml. (6) LH and FSH, both elevated basally, did not change with TRH administration, but both were stimulated by LHRH 100 μg i.v., LH briskly, FSH more variably. (7) FSH was suppressed sharply but LH only partially with testosterone therapy. (8) Our studies indicate that the TSH response to TRH in Klinefelter's syndrome is blunted and further suppressed with short term testosterone replacement. The PRL response to TRH under these same circumstances, however, is enhanced. Previous reports of abnormal LH feedback control are confirmed. (9) Klinefelter's syndrome is associated with subtle abnormalities in hypothalamic pituitary regulation not expected in typical primary hypogonadism.     

Chronic cognitive sequelae after traumatic brain injury are not related to growth hormone deficiency in adults

Objective: The objective of the study was to asses the possible influence of hypothalamo–pituitary deficiencies, and growth hormone (GH) deficiency in particular, on cognition in adult patients with traumatic brain injury (TBI). TBI is a recently identified risk factor for cognitive deficits and hypopituitarism. Even the patients with favorable outcome after TBI may present with persistent bodily, psychosocial, and cognitive impairments, resembling patients with untreated partial or complete pituitary insufficiency. Design: We performed retrospective and cross‐sectional study of endocrine and cognitive function in TBI in 61 patients (aged 37.7 ± 1.7 years) of both sexes (44 m,17 f), at least 1 year after TBI (3.9 ± 0.6 years). Serum insulin‐like growth factor 1 (IGF‐I), thyroxin, thyroid‐stimulating hormone (TSH), follicle‐stimulating hormone (FSH), luteinizing hormone (LH), testosterone (in men), prolactin, and cortisol were measured, and GH secretion was assessed by growth hormone releasing hormone (GHRH) + growth hormone releasing peptide‐6 (GHRP‐6) test. Cognitive function was assessed by using a standard neuropsychological battery. Results: GH deficiency (GHD) and GH insufficiency (GHI) were found in 20 patients (32.8%). After adjustment for confounders [age, body mass index (BMI), education level, time elapsed from TBI], there were no significant differences in results of neuropsychological tests between patients with TBI with GHD, GHI, and normal GH secretion. There were no correlations of neuropsychological variables with stimulated peak GH secretion or IGF‐I level. Conclusions: GHD persists long after the TBI, independently of trauma severity and age at traumatic event. GH secretion is more sensitive to TBI than other pituitary hormones. No evidence is found for an association of cognitive function impairment and somatotropic axis impairment in adult patients tested more than 1 year after the TBI.     

Episodic hormone secretion during sleep in Kleine-Levin syndrome: evidence for hypothalamic dysfunction

"Acute" hypothalamic-pituitary function tests including insulin tolerance test, LRH, ACTH and TRH stimulation tests and nocturnal secretory pattern of human growth hormone, 11-OHCS, prolactin, FSH, LH and TSH were studied in a 23-year-old male with Kleine-Levin syndrome during the course of a typical hypersomnic attack. The "acute" tests revealed paradoxical growth-hormone response to TRH stimulation, borderline high basal plasma prolactin levels with normal response to TRH. The hormonal secretory pattern during sleep revealed abnormalities in LH, 11-OHCS and prolactin secretion. These together with the results of the "acute" tests are indicative of an abnormality in the hypothalamic regulation of various pituitary hormones. This observation may indeed be the first laboratory demonstration confirming a long-standing hypothesis that Kleine-Levin syndrome is related to hypothalamic dysfunction.     

Changes in anterior pituitary function during ACTH therapy of patients with infantile spasms

Serum cortisol, prolactin (PRL), TSH, GH, LH and FSH levels were measured before and immediately after daily ACTH-Z therapy (0.01 mg/kg/day, 1-2 weeks) for 5 patients with infantile spasms and one patient with myoclonus epilepsy. Total number of ACTH-Z therapy were 8 times, and all patients became seizure free after ACTH-Z therapy. In 6 occasions, TRH, LH-RH and insulin tolerance tests were performed before and after daily ACTH-Z therapy. Serum cortisol levels were significantly increased after daily ACTH-Z therapy but all other hormone levels were significantly decreased. In TRH and LH-RH tolerance tests, peak levels and increments of PRL, LH and FSH were significantly decreased after daily ACTH-Z therapy and those of TSH were mildly decreased. In one case insulin tolerance test revealed an adequate decrease of blood glucose before and after ACTH-Z therapy, and there was a poor GH response after ACTH-Z therapy. Daily ACTH-Z therapy was thought to suppress secretion of anterior pituitary hormones.     

Evaluation of Endocrine Profile,Hypothalamic–Pituitary–Testis Axis and Semen Quality in Multiple Sclerosis

Several endocrine and sexual disturbances have been demonstrated in multiple sclerosis (MS) patients of both sexes. The endocrine profile, hypothalamic–pituitary–testis (HPT) axis and semen quality were evaluated in male patients with MS. A total of 68 male MS patients aged 18 years or older were recruited. Forty‐eight age‐matched healthy male volunteers served as controls. All subjects underwent complete physical examination and routine semen analysis. Two blood samples were drawn from each participant at 15‐min intervals for the determination of the resting levels of: luteinising‐hormone (LH), follicle‐stimulating hormone (FSH), prolactin, testosterone, oestradiol and sex hormone binding globulin. The HPT axis was assessed using gonadotrophin‐releasing hormone (GnRH) and human chorionic gonadotrophin tests. The mean basal serum levels for LH, FSH and testosterone in MS patients were significantly lower than the mean for normal controls (P = 0.01). The injection of GnRH analogue did not yield a significant increase in FSH and LH levels in the MS patients compared to normal controls (P = 0.001). Total sperm count, sperm motility and percent normal sperm morphology were lower in MS patients compared to controls. MS subjects with progressive disease had higher and more severe HPT axis abnormalities than that for patients with relapsing remitting MS. Most subjects with MS have hypogonadotrophic hypogonadism state and fertility impairment. It appears that the damage to HPT axis is both in pituitary and testicular levels. Further studies are needed to better elucidate the underlying pathophysiology of HPT axis dysregulation.     

High‐Cholesterol Diet Disrupts the Levels of Hormones Derived from Anterior Pituitary Basophilic Cells

Emerging evidence shows that elevated cholesterol levels are detrimental to health. However, it is unclear whether there is an association between cholesterol and the pituitary. We investigated the effects of a high‐cholesterol diet on pituitary hormones using in vivo animal studies and an epidemiological study. In the animal experiments, rats were fed a high‐cholesterol or control diet for 28 weeks. In rats fed the high‐cholesterol diet, serum levels of thyroid‐stimulating hormone (TSH; also known as thyrotrophin), luteinising hormone (LH) and follicle‐stimulating hormone (FSH) produced by the basophilic cells of the anterior pituitary were elevated in a time‐dependent manner. Among these hormones, TSH was the first to undergo a significant change, whereas adrenocorticotrophic hormone (ACTH), another hormone produced by basophilic cells, was not changed significantly. As the duration of cholesterol feeding increased, cholesterol deposition increased gradually in the pituitary. Histologically, basophilic cells, and especially thyrotrophs and gonadotrophs, showed an obvious increase in cell area, as well as a potential increase in their proportion of total pituitary cells. Expression of the β‐subunit of TSH, FSH and LH, which controls hormone specificity and activity, exhibited a corresponding increase. In the epidemiological study, we found a similar elevation of serum TSH, LH and FSH and a decrease in ACTH in patients with hypercholesterolaemia. Significant positive correlations existed between serum total cholesterol and TSH, FSH or LH, even after adjusting for confounding factors. Taken together, the results of the present study suggest that the high‐cholesterol diet affected the levels of hormones derived from anterior pituitary basophilic cells. This phenomenon might contribute to the pituitary functional disturbances described in hypercholesterolaemia.     

Random and Non-Random Coincidence Between Luteinizing Hormone Peaks and Follicle-Stimulating Hormone, Alpha Subunit, Prolactin and Gonadotropin-Releasing Hormone ulsations

We have examined the co-pulsatility of luteinizing hormone (LH) and prolactin, LH and follicle-stimulating hormone (FSH), and LH and α subunit in normal men. We tested whether the degree of physiologically observed co-pulsatility (peak coincidence) significantly exceeded expected random concordance between independently pulsating hormone series. To this end, computer simulations were used to create synthetic endocrine time series pulsating randomly and independently at known frequencies. Resultant predictions of the mean, variance and probability distribution of the number of randomly coincident peaks permitted us to test the null hypothesis that physiologically observed hormone co-pulsatility was due to chance peak associations alone. Physiological observations were made in 33 normal men and in six ovariectomized ewes subjected to combined hypothalamo-pituitary and jugular venous catheterization. The following salient results were obtained: 1) random peak coincidence rates between independently pulsating hormone series were substantial at high pulse frequencies, but such random rates were significantly exceeded in the case of gonadotropin-releasing hormone and LH peaks (P< 0.0001); 2) random coincidence was further increased when coincidence was defined as peak maxima occurring not only simultaneously but also within some defined time window (e.g. ±10 min, as commonly done in the literature); 3) significant co-pulsatility could be demonstrated for simultaneous LH and FSH pulsations in normal men (P< 0.0001); 4) coincidence rates for 10-min lagged (but not for simultaneous) LH and prolactin pulses were significantly more likely than chance associations; 5) observed coincidence between LH and a subunit pulses significantly exceeded expected (random) peak overlap (P<0.001); and 6) in contrast, hormone peaks in different men were only randomly associated. We conclude that based upon the means, variances and probability distributions calculated here, available reports on peak coincidence between pulsatile neuroendocrine time series must be re-examined in the light of high rates of random coincidence observed between independently pulsating hormone series.