BREAKING! COVID-19 Latest: Study Reveals That COVID-19 May Deplete Testosterone Levels In Men!
Source: COVID-19 Latest Sep 29, 2020 3 years, 6 months, 3 weeks, 6 days, 8 hours, 46 minutes ago
COVID-19 Latest: Adding to the confusions and contradictions, a new study by researchers from the University of Mersin and the Mersin City Education And Research Hospital in Turkey found as men's testosterone level at baseline decreases, the probability for them to be in the intensive care unit (ICU) significantly increases.
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The study findings suggest that the COVID-19 disease might actually be deteriorating men's testosterone levels.
The study findings were published in the peer-reviewed journal: The Aging Male.
https://www.tandfonline.com/doi/full/10.1080/13685538.2020.1807930
Testosterone is the principal male sex hormone, and decreases on average by 0.8–2% per year after the age of 40 years. The prevalence of male hypogonadism has been ranged from 2.1 to 9.5% in men aged 40–70 years . Its rate significantly increases, ranging 10–80% in several morbid diseases. Male late-onset hypogonadism has been reported as a risk factor for diabetes, chronic obstructive pulmonary disease, metabolic syndrome, dyslipidemia, thrombotic and cardiovascular disease, leading to increased mortality in the general population. The prevalence of hypogonadism in age hospitalized male patients has been reported as 53.3% . Low levels of testosterone have been found as an association with higher rates of infection-related hospitalization and all-cause mortality in male hemodialysis and intensive care unit patients. In a double blind, placebo controlled, randomized study, testosterone replacement therapy provided improvement in peak oxygen consumption in elderly patients with chronic heart failure.
https://pubmed.ncbi.nlm.nih.gov/19712802/
Dr Selahittin Çayan, lead author and Professor of Urology, states that while it has already been reported that low testosterone levels could be a cause for poor prognosis following a positive SARS-CoV-2 test, this is the first study to show that COVID-19 itself depletes testosterone.
The researchers hope that the new development could help to explain why so many studies have found that male prognosis is worse than those females with COVID-19, and therefore to discover possible improvement in clinical outcomes using testosterone-based treatments.
Dr Cayan explained to Thailand Medical News, "Testosterone is associated with the immune system of respiratory organs, and low levels of testosterone might increase the risk of respiratory infections. Low testosterone is also associated with infection-related hospitalization and all-cause mortality in male in ICU patients, so testosterone treatment may also have benefits beyond improving outcomes for COVID-19.”
He added, "In our research, the mean total testosterone decreased, as the severity of the COVID-19 increased. The mean total testosterone level was significantly lower in the ICU group than in the asymptomatic group. In addition, the mean total testosterone level was significantly lower in the ICU group than in the Intermediate Care Unit group. The mean serum follicle stimulating hormone level was significantly higher in the ICU group than in the asymptomat
ic group.’
He further added, "
We found hypogonadism ie a condition in which the body does not produce enough testosterone in 113 (51.1%) of the male patients. The patients who died, had significantly lower mean total testosterone than the patients who were alive. However, even 65.2% of the 46 male patients who were asymptomatic had a loss of loss of libido."
The study team looked at a total of 438 patients. This included 232 males, each with laboratory confirmed SARS-CoV-2. All data were prospectively collected. A detailed clinical history, complete physical examination, laboratory and radiological imaging studies were performed in every patient. All data of the patients were checked and reviewed by the two physicians.
The detailed cohort study was divided into three groups: asymptomatic patients (n: 46), symptomatic patients who were hospitalized in the internal medicine unit (IMU) (n: 129), and patients who were hospitalized in the intensive care unit (ICU) (n: 46).
It was found that in the patients who had pre-COVID-19 serum gonadal hormones test (n: 24), serum total testosterone level significantly decreased from pre-COVID-19 level of 458 ± 198 ng/dl to 315 ± 120 ng/dl at the time of COVID-19 in the patients (p =0.003).
Interestingly death was observed in 11 of the male adult patients (4.97%) and 7 of the female patients (3.55%), revealing no significance between the two genders (p > 0.05).
Dr Çayan commenting on the results of the study, added, "It could be recommended that at the time of COVID-19 diagnosis, testosterone levels are also tested. In men with low levels of sex hormones who test positive for COVID-19, testosterone treatment could improve their prognosis. More research is needed on this."
The study team noted that the limitations of this study include it not including a control group of patients with conditions other than COVID-19, this was due to the restrictions placed on the hospital that they were monitoring the patients in.
The study team state that future studies should look at the concentration levels of ACE2 (Angiotensin-converting enzyme 2) an enzyme attached to the cell membranes of cells that are receptors to the novel coronavirus in relationship with the total testosterone levels.
Angiotensin-converting enzyme 2 (ACE2) is primarily expressed in the adult type Leydig and Sertoli cells, and has an important role in lung protection. Therefore, viral binding to the ACE2 receptor may decrease its expression causing deterioration in a lung protective pathway, and might affect testosterone production, leading to increases in pro-inflammatory cytokines in SARS-CoV-2 infected patients. Very few studies have investigated the relationship between testosterone and mortality with the contradictory results in patients with COVID-19 with a small sample size and short follow-up period.
https://onlinelibrary.wiley.com/doi/full/10.1111/andr.12821
https://pubmed.ncbi.nlm.nih.gov/32387456/
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