Obesity and Hypogonadism

Lamm, Steven; Chidakel, Aaron; Bansal, Rohan

doi:10.1016/j.ucl.2016.01.005

Cited by 44 publications

(38 citation statements)

References 46 publications

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“…Different studies have investigated the relationship between obesity, MetS, and hypogonadism or drop in serum TT (Laaksonen et al ., , ; Allan & McLachlan, ; MacDonald et al ., ; Brand et al ., ; Wang et al ., ; Yassin et al ., ). Obesity is an important risk factor for health and could be the single most common cause of a drop in T levels, with about 52.4% of all obese men presenting T levels <300 ng/dL (Mulligan et al ., ; Lamm et al ., ). Various studies show an inverse linear relationship between TT and BMI and an inverse relationship between free and total T levels in serum and visceral fat mass, demonstrating a positive correlation between hypogonadism and obesity in obese males (Kapoor et al ., ; Dandona et al ., ; Dandona & Rosenberg, ; Szulc et al ., ; Defeudis, ).…”

Section: Checklist Featuresmentioning

confidence: 97%

The CATCH checklist to investigate adult‐onset hypogonadism

et al. 2018

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Adult-onset hypogonadism is a syndrome often underdiagnosed, undertreated, or incompletely explored. There are various reasons for this: firstly, undefined age range of men in whom testosterone levels should be investigated and then no definitive serum cutoff point for the diagnosis of hypogonadism; and finally, variable and non-specific signs and symptoms; men and physicians do not pay adequate attention to sexual health. All these factors make the diagnostic criteria for hypogonadism controversial. The evaluation of the clinical features and causes of this syndrome, its link with age, the role of testosterone and other hormone levels, and the presence of any comorbidities are all useful factors in the investigation of this population. The purpose of this manuscript, after an accurate analysis of current literature, is to facilitate the diagnosis of hypogonadism in men through the use of the CATCH acronym and a checklist to offer a practical diagnostic tool for daily clinical practice. A narrative review of the relevant literature regarding the diagnosis of late-onset hypogonadism or adult-onset hypogonadism was performed. PubMed database was used to retrieve articles published on this topic. A useful new acronym CATCH (Clinical features [symptoms] and Causes, Age, Testosterone level, Comorbidities, and Hormones) and a practical checklist to facilitate the evaluation of hypogonadism in aging men were used. The evaluation of the clinical features and causes of hypogonadism, the link with age, the role of Testosterone and other hormones, and the evaluation of comorbidities are important in investigating adult-onset hypogonadism. The CATCH checklist could be helpful for clinicians for an early diagnosis of both hypogonadism and associated comorbidities. We suggest the use of this acronym to advocate the investigation of declining testosterone in aging men.

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Section: Checklist Featuresmentioning

confidence: 97%

The CATCH checklist to investigate adult‐onset hypogonadism

et al. 2018

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“…Testosterone is then release into the systemic circulation to reach the extragonadal target organs. In the bloodstream, testosterone is mostly transported bound to sex hormone‐binding globulin (SHBG) or to serum albumin, where only 1% to 2% of the hormone is transported in the unbound or “free” form and thus biologically active . Testosterone action is mediated through androgen receptor binding or conversion to other two active metabolites, namely, estradiol or dihydrotestosterone (DHT) resulting from testosterone conversion by the aromatase or 5‐α reductase enzymes, respectively.…”

Section: Introductionmentioning

confidence: 99%

“…In the bloodstream, testosterone is mostly transported bound to sex hormone-binding globulin (SHBG) or to serum albumin, where only 1% to 2% of the hormone is transported in the unbound or "free" form and thus biologically active. 19 Testosterone action is mediated through androgen receptor binding or conversion to other two active metabolites, namely, estradiol or dihydrotestosterone (DHT) resulting from testosterone conversion by the aromatase or 5-α reductase enzymes, respectively. Estradiol prompts a negative feedback on the hypothalamus, more specifically through its inhibitory action on kisspeptin-producing KNDy neurons, via oestrogen receptors, which inhibits GnRH production and, subsequently, suppresses the synthesis and secretion of gonadotropins.…”

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confidence: 99%

Obesity and male hypogonadism: Tales of a vicious cycle

et al. 2019

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Summary Obesity prevalence, particularly in children and young adults, is perilously increasing worldwide foreseeing serious negative health impacts in the future to come. Obesity is linked to impaired male gonadal function and is currently a major cause of hypogonadism. Besides signs and symptoms directly derived from decreased circulating testosterone levels, males with obesity also present poor fertility outcomes, further evidencing the parallelism between obesity and male reproductive function. In addition, males with androgen deficiency also exhibit increased fat accumulation and reduced muscle and mineral bone mass. Thus, compelling evidence highlights a vicious cycle where male hypogonadism can lead to increased adiposity, while obesity can be a cause for male hypogonadism. On the opposite direction, sustained weight loss can attain amelioration of male gonadal function. In this scenario, a thorough evaluation of gonadal function in men with obesity is crucial to dissect the causes from the consequences in order to target clinical interventions towards maximized improvement of reproductive health. This review will address the causes and consequences of the bidirectional relationship between obesity and hypogonadism, highlighting the implicit male reproductive repercussions.

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“…The bidirectional causal relationship between sex hormone levels and chronic inflammation processes represents reciprocal regulatory pathways capable of generating reproductive dysfunction. In fact, a low level, but chronic pro‐inflammatory state is now well recognized to be a driver of several inflammatory conditions such as rheumatoid arthritis, inflammatory bowel disease, and other age‐related lifespan conditions, like obesity and cardiovascular diseases (Politch et al ., ; Tigas & Tsatsoulis, ; Keith et al ., ; Morrison & Brannigan, ; Lamm et al ., ; Kahn & Brannigan, ). The damage of male reproductive tract tissues in response to such conditions can be a result of changes induced by local and/or systemic inflammatory mediators in the hypothalamic–pituitary–testicular axis, and/or direct impact of systemic pathophysiological processes that can also impair male reproductive function (Table ).…”

Section: Inflammation and Impact To Male Reproductive Healthmentioning

confidence: 99%

In search of new paradigms for epididymal health and disease: innate immunity, inflammatory mediators, and steroid hormones

et al. 2019

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The primary job of the epididymis is to mature and protect the luminally transiting spermatozoa. Mounting evidence is showing that innate immune components [including Toll‐like receptors (TLRs) and antimicrobial proteins, among which are β‐defensins] and inflammatory mediators, under the primary influence of androgens, participate in the cellular and molecular processes that define this tissue. Here, we present an overview of the contributions of these signaling pathway components during epididymal homeostasis and discuss the hypotheses as to their involvement in epididymitis, the most common urological inflammatory condition in men, frequently impairing their fertility. Drawing primarily from rodent models, we also focus on how the distribution and functional expression of innate immune components are differentially regulated in the prenatal developing epididymis, providing new insights into the disruption of these signaling pathways throughout the lifespan. Male infertility is caused by a variety of conditions, such as congenital malformations, genetic and endocrine disorders, exposure to environmental toxicants, and inflammatory/infectious conditions. More than one‐third of infertile men with an idiopathic condition cannot currently be adequately diagnosed. Thinking about the innate immunity and inflammation context of the epididymis may provide new insights and directions as to how these systems contribute to male fertility, as well as also uncover urological and andrological outcomes that may aid clinicians in diagnosing and preventing epididymal pathologies.

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Obesity and Hypogonadism

Cited by 44 publications

References 46 publications

The CATCH checklist to investigate adult‐onset hypogonadism

The CATCH checklist to investigate adult‐onset hypogonadism

Obesity and male hypogonadism: Tales of a vicious cycle

In search of new paradigms for epididymal health and disease: innate immunity, inflammatory mediators, and steroid hormones

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