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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Until a decade ago the ailments of elderly men, such as atherosclerosis, hypertension, diabetes mellitus, lower urinary tract symptoms and erectile dysfunction (ED), were regarded as distinct diagnostic/therapeutic entities but there is a growing awareness that these entities are not disparate and, to improve the health of the ageing male, require an integral approach. There is an inter-dependence between the metabolic syndrome, ED and patterns of testosterone in ageing men. The main features of the metabolic syndrome are abdominal obesity, insulin resistance, hypertension and dyslipidaemia, significant factors in the aetiology of erectile function. The metabolic syndrome is associated with lower-than-normal testosterone levels. A new concept of the role of testosterone in male physiology suggests that testosterone plays also a significant role in the development and maintenance of bone and muscle mass and is a determinant of glucose homeostasis and lipid metabolism. Testosterone is not only a factor in libido but exerts also essential effects on the anatomical and physiological substrate of penile erection. With these recent insights, the health problems of elderly men must be placed in a context that allows an integral approach. Treatment of testosterone deficiency is to become part and parcel of this approach.
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PMID:Metabolic syndrome, testosterone deficiency and erectile dysfunction never come alone. 1960 30

Blood pressure (BP) is more salt sensitive in men than in premenopausal women. In Dahl salt-sensitive rats (DS), high-salt (HS) diet increases BP more in males than females. In contrast to the systemic renin-angiotensin system, which is suppressed in response to HS in male DS, intrarenal angiotensinogen expression is increased, and intrarenal levels of ANG II are not suppressed. In this study, the hypothesis was tested that there is a sexual dimorphism in HS-induced upregulation of intrarenal angiotensinogen mediated by testosterone that also causes increases in BP and renal injury. On a low-salt (LS) diet, male DS had higher levels of intrarenal angiotensinogen mRNA than females. HS diet for 4 wk increased renal cortical angiotensinogen mRNA and protein only in male DS, which was prevented by castration. Ovariectomy of female DS had no effect on intrarenal angiotensinogen expression on either diet. Radiotelemetric BP was similar between males and castrated rats on LS diet. HS diet for 4 wk caused a progressive increase in BP, protein and albumin excretion, and glomerular sclerosis in male DS rats, which were attenuated by castration. Testosterone replacement in castrated DS rats increased BP, renal injury, and upregulation of renal angiotensinogen associated with HS diet. Testosterone contributes to the development of hypertension and renal injury in male DS rats on HS diet possibly through upregulation of the intrarenal renin-angiotensin system.
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PMID:Testosterone-dependent hypertension and upregulation of intrarenal angiotensinogen in Dahl salt-sensitive rats. 1921 90

A considerable body of evidence exists suggesting that androgen deficiency contributes to the onset, progression, or both of cardiovascular disease (CVD). The aim of this review is to evaluate the relationships between testosterone (T) deficiency and risk factors of CVD and to discuss the implications of androgen deficiency in men with cardiovascular risk factors. The relationship between androgen deficiency and endothelial function, lipid profiles, inflammatory responses, altered vascular smooth muscle reactivity, and hypertension are discussed with regard to CVD. A comprehensive literature search was carried out with the use of Pub Med from 1980 through 2009, and relevant articles pertinent to androgen deficiency and vascular disease were evaluated and discussed. Low T, whether attributed to hypogonadism or androgen deprivation therapy, in men with prostate carcinoma, produces adverse effects on cardiovascular health. Androgen deficiency is associated with increased levels of total cholesterol, low-density lipoprotein, increased production of proinflammatory factors, and increased thickness of the arterial wall and contributes to endothelial dysfunction. Testosterone supplementation restores arterial vasoreactivity; reduces proinflammatory cytokines, total cholesterol, and triglyceride levels; and improves endothelial function but also might reduce high-density lipoprotein levels. Testosterone is an anabolic hormone with a wide range of beneficial effects on men's health. The therapeutic role of T in men's health, however, remains a hotly debated issue for a number of reasons, including the purported risk of prostate cancer. In view of the emerging evidence suggesting that androgen deficiency is a risk factor for CVD, androgen replacement therapy could potentially reduce CVD risk in hypogonadal men. It should be emphasized, however, that androgen replacement therapy should be done with very thorough and careful monitoring for prostate diseases.
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PMID:The dark side of testosterone deficiency: III. Cardiovascular disease. 1934 98

Testosterone determination in an old men population has demonstrated its about the as general health marker, not only sexual, prompting a greater in to arrest for this analytic determination and the potential relations of testosterone with other markers of cardiovascular health, obesity, hypertension, erectile dysfunction, sarcopenia, metabolic syndrome, ageing, and other conditions. We specifically review the relationship between cardiovascular health, erectile dysfunction, and androgen deficiency, processes easily recognizable, prevented and treated. Current information gives such a prominence to testosterone as a health reference that its determination seems to be inexcusable in the ageing male consult.
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PMID:[Testosterone, endothelial function, cardiovascular health and androgen deficiency in the old man]. 1954 88

Changing lifestyles and an excess of food supply in developed countries have resulted in an increasing prevalence of overweight and obesity. As a consequence, a disorder of complex pathophysiology involving visceral adipose tissue as an endocrine organ, dyslipidemia, insulin resistance and hypertension has emerged-the so-called metabolic syndrome. This disorder can lead to the manifestation of type 2 diabetes mellitus and cardiovascular disease. In men, testosterone deficiency may contribute to the development of the metabolic syndrome. In turn, states of hyperinsulinemia and obesity lead to a reduction of testicular testosterone production. Testosterone has reciprocal effects on the generation of muscle and visceral adipose tissue by influencing the commitment of pluripotent stem cells and by inhibiting the development of preadipocytes. Insulin sensitivity of muscle cells is increased by augmenting mitochondrial capacity and fostering expression of oxidative phosphorylation genes. Testosterone has a protective effect on pancreatic beta cells, which is possibly exerted by androgen-receptor-mediated mechanisms and influence of inflammatory cytokines. As some, but not all, epidemiological and interventional studies indicate, testosterone substitution might be helpful in preventing or attenuating the metabolic syndrome in aging men with late-onset hypogonadism and in hypogonadal patients with type 2 diabetes mellitus, but larger controlled trials are needed to confirm such hypotheses.
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PMID:Testosterone deficiency, insulin resistance and the metabolic syndrome. 1985 74

Metabolic syndrome is characterized by central obesity, dyslipidemia, hypertension, and insulin resistance. Each lifestyle disease and also metabolic syndrome are closely associated with decreased serum testosterone. In general, it is believed that testosterone is inversely related to adiponectine level, which is thought to be a key molecule in the etiology of metabolic syndrome. However, no inverse correlation exists between them in patients with LOH. Testosterone replacement treatment is expected to be one of treatments for metabolic syndrome.
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PMID:[Bone and Men's Health. Testosterone and lifestyle disease]. 2011 14

A 57 yr old man presented to endocrinology clinic with a six year history of poorly controlled hypertension which was treated with Metoprolol 200 mg/day and Enalapril 20 mg/day. He was asymptomatic but incidentally hypokalaemia was detected while having cholecystectomy, two years prior to his clinic appointment. He had never been on diuretics or laxatives. He was started on potassium supplements (120 mmol/d) and advised to increase dietary potassium by the surgical team. A detailed personal history revealed ingestion of 300-500 g licorice per day. Physical examination was unremarkable apart from increased blood pressure of 180/105 mmHg. Following the initial visit, his serum electrolyes (K+3.7 mmol/l) were normal with potassium supplementation and as were morning cortisol, ACTH, 11-deoxycortisol and plasma metanephrines. 17 OH-P, DHEAS and androstenedione were normal but testosterone was low. Morning ambulant aldosterone was slightly increased at 801 pmol/L and renin activity was undetectable. Urinary 24 h aldosterone excretion was significantly increased at 162 ng/24 h with normal cortisol and catecholamine excretion. Four weeks following advice to stop licorice, serum potassium decreased to 3.4 mmol/L despite continuous supplementation. Morning plasma aldosterone increased to 1 449 pmol/ml, renin activity remained undetectable but 24 h urine aldosterone excretion increased to 434 ng/24 h with a reduction in urinary cortisol excretion. Interestingly 17 OH-P and androstenedione levels, although within the reference range, were slightly higher compared to the levels whilst on licorice. Testosterone level had significantly increased to be within normal range. Abdominal imaging with US and MRI showed a 2.7 cmx2.2 cmx1.7 cm left adrenal mass. He underwent laparoscopic left adrenalectomy and histology confirmed aldosterone producing adrenal adenoma. Post-operatively his aldosterone and serum potassium levels normalized and he became normotensive without any antihypertensive medication.
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PMID:Licorice - or more? 2021 99

Metabolic and morphologic abnormalities in persons with HIV remain common contributors to stigma and morbidity. Increased abdominal circumference and visceral adiposity were first recognized in the late 1990s, soon after the advent of effective combination antiretroviral therapy. Visceral adiposity is commonly associated with metabolic abnormalities including low HDL-cholesterol, raised triglycerides, insulin resistance, and hypertension, a constellation of risk factors for cardiovascular disease and diabetes mellitus known as "the metabolic syndrome". Medline and conference abstracts were searched to identify clinical research on factors associated with visceral adiposity and randomized studies of management approaches. Data were critically reviewed by physicians familiar with the field. A range of host and lifestyle factors as well as antiretroviral drug choice were associated with increased visceral adiposity. Management approaches included treatment switching and metformin, both of which have shown benefit for insulin-resistant individuals with isolated fat accumulation. Testosterone supplements may also have benefits in a subset of individuals. Supra-physiological doses of recombinant human growth hormone and the growth hormone releasing hormone analog tesamorelin both significantly and selectively reduce visceral fat over 12-24 weeks; however, the benefits are only maintained if doping is continued. In summary, the prevention and management of visceral adiposity remains a substantial challenge in clinical practice.
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PMID:Epidemiology, assessment, and management of excess abdominal fat in persons with HIV infection. 2021 6

Male gender is a major risk factor for premature cardiovascular death, a relationship not yet explained. Low testosterone in men is a risk factor for the metabolic syndrome and type 2 diabetes and is associated independently with individual components of the metabolic syndrome--visceral obesity, insulin resistance, hyperglycemia, hypertension and dyslipidemia. Epidemiological studies report increased mortality in men with low testosterone. Testosterone replacement in the short-term reduces waist circumference, cholesterol and circulating pro-inflammatory cytokines and improves insulin sensitivity and glycemic control in diabetics. Testosterone also has beneficial effects on cardiac ischemia, angina and chronic heart failure. This manuscript reviews the current evidence supporting a link between low testosterone and cardiovascular disease, highlighting the need for larger, longer-term studies.
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PMID:Testosterone deficiency: a risk factor for cardiovascular disease? 2038 74

There is a high prevalence of hypogonadism in the older adult male population and the proportion of older men in the population is projected to rise in the future. As hypogonadism increases with age and is significantly associated with various comorbidities such as obesity, type 2 diabetes, hypertension, osteoporosis and metabolic syndrome, the physician is increasingly likely to have to treat hypogonadism in the clinic. The main symptoms of hypogonadism are reduced libido/erectile dysfunction, reduced muscle mass and strength, increased adiposity, osteoporosis/low bone mass, depressed mood and fatigue. Diagnosis of the condition requires the presence of low serum testosterone levels and the presence of hypogonadal symptoms. There are a number of formulations available for testosterone therapy including intramuscular injections, transdermal patches, transdermal gels, buccal patches and subcutaneous pellets. These are efficacious in establishing eugonadal testosterone levels in the blood and relieving symptoms. Restoration of testosterone levels to the normal range improves libido, sexual function, and mood; reduces fat body mass; increases lean body mass; and improves bone mineral density. Testosterone treatment is contraindicated in subjects with prostate cancer or benign prostate hyperplasia and risks of treatment are perceived to be high by many physicians. These risks, however, are often exaggerated and should not outweigh the benefits of testosterone treatment.
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PMID:A practical guide to male hypogonadism in the primary care setting. 2051 42


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