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Traumatic Brain Injury & Hypogonadism In The General Population

| By: Joseph Hearnshaw

If you read my last article, you’ll have been introduced to Traumatic Brain Injury (TBI) and it’s potential consequences. As the name suggests, TBI is an injury of the brain.  It’s a particular issue among Army veterans, where out of a cohort of 4620 UK military personnel returning from Afghanistan and Iraq, there were a total of 4.4% with TBI (1). But it’s not just our brave veterans who have been exposed to the risk of TBI.

TBI could be induced by car or motorcycle crashes, falls, sports injuries, and assaults. Anything that strikes a blow to your head could be a cause. It presents itself in various forms, which can range from mild alterations of consciousness to unrelenting comatose states, to even death (2).

This article will review the risk of TBI or mild TBI (mTBI) in the general population, particularly focusing around causes from sports (football and rugby), combat, and what subsequent risks there are associated with hypogonadism.

How Common is TBI Among the Average Population?

We’ve probably all hit our heads at some point, either when playing games as a child or when doing DIY and bumping your head on the shelf above as an adult, just like I did (clumsy me). If enough force is exerted, you could cause TBI. More commonly, they are caused by sports injuries, vehicle crashes, or bad falls within the general population.

It’s worth noting that there are different classifications of TBI:

  1. Mild TBI – mortality is only 0.1%
  2. Moderate TBI – mortality is 10%
  3. Severe TBI – mortality is 40%

The incidence among the general population varies from country to country. In the US, an annual incidence rate of ~31.5/100,000 population was demonstrated (3). The most common cause in sports-related mTBI and moderate TBI cases was getting kicked during American Football (38.1%), followed by fall injuries in sports (20.3%) and it affected mostly adolescents aged 12-18 (120.6/100,000 population). Severe TBI was more associated with off-road vehicular sport and repeated head trauma with equestrian sport and associated falls (3). To little surprise, the majority of cases belonged to men, which is likely due to riskier, often reckless, behaviour (I can imagine Lydia is nodding her head as she reads this!). Women of course aren’t immune from it and have been increasingly affected over the past decade (3). In the UK there are over 1.4 million TBI cases, with many and the most severe arising from vehicle accidents in the elderly, caused predominantly by younger drivers, with many under the influence of alcohol (4, 5).

TBI & Hypogonadism in the General Population

In the previous article, I mentioned that TBI increases the risk of hypothalamic-pituitary deficiencies which can lead to low Testosterone. This often exists as chronic hypogonadism, though with a higher incidence among veterans due to the added increased risk of PTSD.

Pituitary dysfunction has been reported to occur in the range of 15-46.6% of sports related cases, with growth hormone deficiency being one of the most commonly reported pituitary hormone deficiency cases in athletes (6). In general, there’s a reported 15-68% of pituitary hormone deficiency cases among TBI survivors in the long-term, of which can include low Testosterone (7, 8).

Treatment in Hypogonadism Associated TBI Cases

Prevention is always key to avoiding a diseased state, though we appreciate that you can only put so much red tape on your life. You should be aware though that sports such as boxing, rugby and football all carry higher risks of TBI and it’s therefore sensible to wear protective gear accordingly. I always wear a helmet when I cycle because on the low (but ever-present) risk that I do fall, I will have better protected myself from a potential head injury than if I didn’t wear a helmet. I wore headgear in rugby for a reason too. Use common sense here; assess the risk and what precautions are necessary to prevent injury.

Of course, some things will be out of your control, and you can’t always wear a helmet; it isn’t practical. With many cases of TBI, treatment for a hormone deficiency may be essential. Persistent hypogonadism following TBI can be properly detected after approximately 12 weeks from the injury. Your medical practitioner will need to assess you for a range of hormone deficiencies related to pituitary deficiency. You could be presented with the following hormonal dysregulation following TBI:

  1. Adrenal Insufficiency – Due to alterations in ACTH produced, wrestling in weight loss, low blood pressure, vomiting, and dehydration (can be life-threatening if not treated).
  2. Diabetes Insipidus – Due to a lack of ADH made in the pituitary, leads to frequent urination and extreme third
  3. Hyponatremia – Leading to an upset balance of salt and water in the body, resulting in headache, fatigue, vomiting, confusion, and convulsions
  4. Hypothyroidism – Leading to fatigue, constipation, weight gain, and cold intolerance
  5. Hypogonadism – Leading to low testosterone & oestradiol symptoms in men
  6. Growth Hormone Deficiency – Leading to increased fat mass, loss of muscle & bone, and decreased energy
  7. Hyperprolactinemia – Leading to potential hypogonadism, in addition to nipple discharge.

You will then be treated accordingly to the issue.  I’ve dived deeper into this in the ‘What Can We Do?’ section of the previous article, which is well worth the read.


TBI isn’t just limited to veterans; it can affect you and I. It can lead to hypogonadism and other hormone deficiencies. But they can be treated under medical expert supervision with the combination of medical treatment, exercise, and diet; something that our clinic is well experienced in. Remember to be mindful of your head whenever you play sports and to take care to protect it; you only get one head.

The Men’s Health Clinic is revolutionising how we treat hypogonadism related TBI in the UK. Keep tuned to find out more about what we have to offer.


  1. R. J. Rona et al., J. Head Trauma Rehabil. 27, 33–44 (2012)
  2. M. Galgano et al., Cell Transplant. 26, 1118–1130 (2017)
  3. A. W. Selassie et al., Ann. Epidemiol. 23, 750–756 (2013)
  4. T. Lawrence et al., BMJ Open. 6, e012197 (2016)
  5. E. W. Steyerberg et al., PLoS Med. 5, e165 (2008)
  6. A. Hacioglu, F. Kelestimur, F. Tanriverdi, Pituitary. 22, 322–331 (2019)
  7. A. Hohl, T. L. Mazzuco, M. H. C. Coral, M. Schwarzbold, R. Walz, Arq. Bras. Endocrinol. Metabol. 53, 908–914 (2009)
  8. D. J. Barton et al., J. Head Trauma Rehabil. 31, 277–287 (2016)