Unlock the Truth About Hypogonadism and Weight Loss: What You Need to Know!

Introduction

Low testosterone (male hypogonadism) is a medical condition that can affect people with testicles at any age from birth through adulthood. It is a condition in which the testicles don’t produce enough testosterone (the male sex hormone). More specifically, the Leydig cells in your testicles make testosterone.

Testosterone stimulates the development of male characteristics and is essential for sperm production (spermatogenesis). Levels are typically highest in the morning and decline through the day.

Understanding Low Testosterone (Male Hypogonadism)

Low testosterone, also known as male hypogonadism, is a condition where the testicles do not produce sufficient amounts of testosterone, the primary male sex hormone. Other names for low testosterone and male hypogonadism include:Testosterone deficiency syndrome.Testosterone deficiency.Primary hypogonadism.Secondary hypogonadism.Hypergonadotropic hypogonadism.Hypogonadotropic hypogonadism.

The American Urology Association (AUA) defines low blood testosterone as levels below 300 nanograms per deciliter (ng/dL) for adults. However, some researchers and healthcare providers disagree with this and feel that levels below 250 ng/dL are low. Providers also take symptoms into consideration when diagnosing low testosterone.

Several factors can lead to low testosterone, including issues with the testicles, hypothalamus, or pituitary gland. The hypothalamus releases gonadotropin-releasing hormone (GnRH), which triggers the pituitary gland to release luteinizing hormone (LH). LH then travels to the gonads (testicles or ovaries) and stimulates the production and release of testosterone. The pituitary also releases follicle-stimulating hormone (FSH) to cause sperm production.

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Data suggest that about 2% of men may have low testosterone. And other studies have estimated that more than 8% of men aged 50 to 79 years have low testosterone.

Symptoms of Low Testosterone

Symptoms of low testosterone can vary considerably, particularly by age.

In men, symptoms that highly suggest low testosterone include:

Reduced sex drive
Erectile dysfunction
Loss of armpit and pubic hair
Shrinking testicles
Hot flashes
Low or zero sperm count (azoospermia), which causes male infertility

Other symptoms of low testosterone in men include:

Depressed mood
Difficulties with concentration and memory
Increased body fat
Enlarged male breast tissue (gynecomastia)
Decrease in muscle strength and mass
Decrease in endurance

In children, low testosterone before or during puberty for boys can manifest as:

Slowed growth in height, but their arms and legs may continue to grow out of proportion with the rest of their body.
Reduced development of pubic hair
Reduced growth of their penis and testicles
Less voice deepening
Lower-than-normal strength and endurance

Causes of Low Testosterone

There are several possible causes of low testosterone. The two types of male hypogonadism are:

Primary hypogonadism (testicular disorder)
Secondary hypogonadism (pituitary/hypothalamus dysfunction)

Causes of primary and secondary hypogonadism are also divided into either congenital (at birth) or acquired (developed later in childhood or adulthood).

Primary Hypogonadism

Primary hypogonadism occurs when there is an issue with the testicles that prevents them from producing normal levels of testosterone. Another name for primary hypogonadism is hypergonadotropic hypogonadism.

In this type, the pituitary gland produces more luteinizing hormone (LH) and follicle-stimulating hormone (FSH) (known as gonadotropins) in response to low testosterone levels. The high levels of these hormones would normally tell your testicles to produce more testosterone and sperm. However, if you have damaged (most commonly related to prior chemotherapy) or missing testicles, they can’t respond to the increased levels of gonadotropins. As a result, your testicles make too little or no testosterone and sperm.

Sometimes in primary hypogonadism testosterone levels are within the normal range and gonadotropins are high. Your specialist will help you understand if you need treatment, even with normal testosterone levels.

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Congenital conditions that affect your testicles and can lead to primary hypogonadism include:

Absence of testicles at birth (anorchia)
Undescended testicles (cryptorchidism)
Leydig cell hypoplasia (underdevelopment of Leydig cells in your testicles)
Klinefelter’s syndrome (a genetic condition in which males are born with an extra X chromosome: XXY instead of XY)
Noonan syndrome (a rare genetic condition that can cause delayed puberty, undescended testicles or infertility)
Myotonic dystrophy (part of a group of inherited disorders called muscular dystrophies)

Acquired conditions that affect your testicles and can lead to primary hypogonadism include:

Testicle injury or removal
Orchitis, which is inflammation of one or both testicles. This is most often the result of a bacterial infection, such as a sexually transmitted infection, but it can be due to viral infections, such as mumps.
Chemotherapy or radiation therapy to your testicles
Certain types of tumors
Anabolic steroid use

Secondary Hypogonadism

Conditions that affect how your hypothalamus and/or pituitary gland cause secondary hypogonadism. This is known as hypogonadotropic hypogonadism because there are low levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Those low levels cause decreased testosterone and sperm production.

Congenital conditions that can lead to secondary hypogonadism include:

Isolated hypogonadotropic hypogonadism (a condition that causes low levels of gonadotropin-releasing hormone from birth)
Kallmann syndrome (a rare genetic condition that causes loss of the development of nerve cells in your hypothalamus that produce gonadotrophin-releasing hormone. It can also cause a lack of smell.)
Prader-Willi syndrome (a rare genetic multisystem disorder than can cause hypothalamus dysfunction)

Acquired conditions that can lead to secondary hypogonadism include:

Hypopituitarism (This condition may result from an adenoma, infiltrative disease, infection, injury, radiation therapy or surgery that affects your pituitary gland.)
Hyperprolactinemia
Iron overload (hemochromatosis)
Brain or head injury
Cushing’s syndrome
Cirrhosis of the liver
Kidney failure
HIV/AIDS
Alcohol use disorder
Poorly managed diabetes
Obesity
Obstructive sleep apnea
Certain medications, including estrogens, psychoactive drugs, metoclopramide, opioids, leuprolide, goserelin, triptorelin and newer androgen biosynthesis inhibitors for prostate cancer.

Late-onset hypogonadism (LOH) is a type of secondary male hypogonadism that results from normal aging. As males age they have a deterioration of hypothalamic-pituitary function and Leydig cell function that decrease testosterone and/or sperm production.

LOH and low testosterone are more common in men who have Type 2 diabetes, overweight and/or obesity.

In one study, 30% of men who were overweight had low testosterone, compared to only 6% of those with weight in the normal range. In another study, 25% of men with Type 2 diabetes had low testosterone, compared to 13% of those without diabetes.

The Link Between Obesity and Hypogonadism

Obesity is one of the major public health issues globally, since it is associated with a higher morbidity and mortality, leading to a relevant economic impact on the affected people, their families, and the health care system. Subjects with obesity have a higher risk of a number of comorbidities, including insulin resistance, type 2 diabetes mellitus (T2DM), dyslipidemia, hypertension, cardiovascular disease, some types of cancer, hyperuricemia, deep vein thrombosis and pulmonary embolism, sleep-related breathing disorders, osteoarthritis, and hypovitaminosis D. In males, obesity represents the clinical condition most strongly associated with hypogonadism, leading to erectile dysfunction and infertility due to oligospermia/azoospermia. In addition, in a vicious cycle, male hypogonadism impairs body composition (reduced muscle mass, higher fat mass), fat metabolism, bone mineralization, and cognitive function. Particularly, central fat accumulation has been linked with all the disorders above, and waist circumference has been found as the most reliable predictor of both lower serum testosterone (T) and risk of developing metabolic and cardiovascular diseases.

Among adult males, the most common form of hypogonadism is functional secondary hypogonadism, also known as dysmetabolic hypogonadotropic hypogonadism or male obesity secondary hypogonadism (MOSH). The pathogenesis of this disorder is multifactorial and generally related to chronic diseases, including obesity, T2DM, and the metabolic syndrome. Regardless of the latter diseases, an inverse relationship between T and excess body weight has been reported in men of all ages, with lower T levels found in subjects with higher body mass index (BMI). Indeed, low total testosterone (TT) primarily reflects reduced concentrations of sex hormone-binding globulin (SHBG) in mild obesity, with no clear evidence of clinical androgen deficiency or defective spermatogenesis. Conversely, more severe forms of obesity lead to overt hypogonadotropic hypogonadism, due to the suppression of the HPT axis, and lower levels of both TT and free testosterone (FT) and even of inhibin B. Interestingly, this mechanism of HPT axis damage seems to be already present at puberty in boys with obesity. Gonadotropins (follicle-stimulating hormone [FSH] and luteinizing hormone FSH [LH]) may be inappropriately normal or low in mild obesity, and a specific decrease in pulse amplitudes of LH has been reported in middle-aged men with severe obesity. Several factors are involved in the pathogenesis of this form of hypogonadism, in particular, a role of estradiol, insulin, leptin, and other pro-inflammatory cytokines has been proposed.

In men with obesity, a part of androgens is converted to estrogens through peripheral aromatization in adipose tissue. The most represented estrogen is estradiol, and this has been suggested to induce functional secondary hypogonadism due to the suppression of the HPT axis. Indeed, early studies showed higher estradiol concentrations in young to middle-aged subjects with obesity compared to lean controls, and following studies reported the treatment of hypogonadal subjects with obesity with selective estrogen receptor modulators (SERM) or anti-aromatase inhibitors (AI) to be successful in stimulating the HPT axis and in achieving physiological T levels. In recent years, this hypothesis has been questioned. Different studies found low levels of both estradiol and TT in men with obesity as well as in hypogonadal men with T2DM. Indeed, given that up to 40% of circulating estradiol is synthesized from the peripheral conversion of T to estradiol, it is much more likely that men with obesity and low serum T may have low estradiol levels too. Accordingly, no changes in estradiol levels after weight loss were reported, thus supporting the picture of hypogonadal men with obesity as not being characterized by a chronic estrogen excess. Given the findings above, one would raise the question whether a vicious cycle is there for obesity and estrogens, as the one described for T. Indeed, in preclinical studies, adipose tissue inflammation and insulin resistance were found to reduce aromatase expression, which returned to normal levels with improvements in the factors above. In addition, adequate estradiol concentrations were linked with favorable metabolic effects, including reduced white adipose tissue accumulation, preserved insulin sensitivity in skeletal muscles and liver, reduced apoptosis of pancreatic β-cells driven by oxidative stress, amyloid polypeptide toxicity, or lipotoxicity, and enhance glucose-stimulated insulin biosynthesis. In all, circulating estradiol is primarily dependent on T, and there is growing evidence that its levels tend to decrease rather than to increase along with the progressive increase of fat mass.

Weight Loss and Testosterone: A Bidirectional Relationship

It is generally accepted that hypogonadism secondary to obesity is functional since it is reversible following weight loss.

The association among obesity, and in particular visceral obesity, and other comorbidities, such as dyslipidemia, glucose impairment, and hypertension, is clustered in the concept of MetS. MetS is essentially a diagnostic category, helping physicians to identify subjects at major risk for metabolic and cardiovascular complications.

Life-style modifications have documented that weight-loss and physical exercise are able to improve obesity-associated functional hypogonadism and its related sexual symptoms. Physicians should strongly adapt all the reasonable strategies to remove/mitigate the known conditions underlying functional hypogonadism, including MetS and obesity. Physical limitations, including reduced muscle mass and increased fat mass, along with low self-confidence, also due to the sexual problems, might limit a subject's propensity to increase physical activity and dieting.

WL, particularly through fat reduction, has a positive influence on testosterone levels. Both moderate and significant reductions in BMI are associated with notable increases in serum testosterone levels.

Dietary Interventions

The clinical practice guidelines for medical care of patients with obesity from the American Association of Clinical Endocrinologists and the American College of Endocrinology indicate that reducing total caloric intake should be the main component of any weight-loss intervention, irrespective to the macronutrient composition. We previously meta-analyzed the effect of any low-calorie diet in 13 studies published until mid-2012 and addressing the effect of caloric restriction on HPT. We found that an average diet-induced weight loss of 9.8% was associated with a significant increase in total T (TT) of 2.8 nmol/L (1.68-4.07 nmol/L) and 2.05 (0.93-3.16 nmol/L), when paired and non-paired t-test models were applied. At that time, not enough studies were available to evaluate in a sub-analysis the effect of diet-induced weight reduction on gonadotropin levels. However, when data from diet were combined with those from bariatric surgery (see below), we reported a significant weight loss-induced increase in luteinizing hormone (LH) (1.31 mU/L [0.80-1.82 mU/L]) and follicle stimulating hormone (1.79 mU/L [1.28-2.30 mU/L]). Since that time, several new studies have been published.

Combining the results of those trials, low calorie diet results in a significant increase in TT levels at endpoint. Meta-regression analysis showed that a higher Δ-weight is associated with a higher T increase, meaning that each 5 kg of weight reduction results in one nmol/L increases.

Dietary interventions, particularly low-carbohydrate and Mediterranean diets, have been linked to increased testosterone production in men with obesity.

Physical Exercise

Overall, 8 studies evaluated the effect of physical exercise on T levels. Combining the results of those trials, physical exercise resulted in a significant increase in TT levels at endpoint. A multivariate regression analysis was performed using (Δ-TT) as the dependent variable and age, trial duration as well as percent reduction of weight (Δ-weight) after physical exercise as putative predictors. The standardized coefficients suggest that a greater weight loss and a longer trial duration are significantly associated with an increase in TT levels, independently of age.

Exercise, particularly resistance training, has also been shown to improve hormonal profiles by lowering fat mass and boosting testosterone levels.

Regular physical activity reduced the odds ratio for ED by 50%.

Bariatric Surgery

So far, five systematic meta-analyses have been published concerning changes in sex hormone levels upon bariatric surgery. Despite differences in the number of studies analyzed and in the inclusion criteria for the study selection, all the meta-analyses found a significant, sustained increase in TT and free T after bariatric surgery, as compared with the pre-surgical values. The mean increase in T was comparable in all the available meta-analyses ranging from 8 to 10 nmol/L for TT and from 75 to 90 pmol/L for free T. A significant increase in SHBG and gonadotropins was also consistently found in all these meta-analyses. Total estradiol was significantly decreased after bariatric surgery, with a mean reduction of about 20 pmol/L, as documented by most meta-analyses.

Bariatric surgery has been identified as one of the most effective methods for increasing testosterone in morbidly obese individuals, with improvements sustained over time.

Liraglutide

Only one study investigated the effect of an anti-obesity drug, i.e., liraglutide, on HPT in obese hypogonadal men with sexual symptoms and poor responses to lifestyle measures. Liraglutide, but not TTh, induced a 6% reduction in weight. Both treatments ameliorated sexual symptoms and increased significantly TT, although the increase was more evident with T gel (5.9 vs. 2.6 nmol/L with liraglutide).

Additional Factors Affecting Testosterone Levels

Besides lifestyle interventions, it's crucial to consider other factors that might influence testosterone levels. These include:

Age: Testosterone levels naturally decline with age, leading to late-onset hypogonadism (LOH).
Underlying Medical Conditions: Conditions like type 2 diabetes, kidney dysfunction, cirrhosis of the liver, HIV/AIDS, and obstructive sleep apnea are associated with low testosterone.
Medications: Certain medications, including estrogens, psychoactive drugs, opioids, and androgen biosynthesis inhibitors, can affect testosterone production.
Genetics: Genetic conditions like Klinefelter's syndrome and Kallmann syndrome can lead to hypogonadism.

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