In prior posts, I have discussed my hypothesis that growth hormone and related growth factors, as a possible therapy for connective tissue/joint degeneration in active populations. The study below finds testosterone therapy (TRT ) appears highly valuable treatment in SCI; to prevent the loss of skeletal muscle post SCI. These results do not surprise me in the least and why this is not a common therapy for people with SCI is a tragedy in my view. If you, or someone you know, has suffered a SCI, I highly recommend you send this info to your/their doctor and pursue this as a possible option. It’s important to note that testosterone deficiency is common after SCI, and according to the U.S. Department of Veterans Affairs SCI unit:
“These findings confirm both a substantial population of men with SCI and with testosterone deficiency, and a significant association between testosterone level and severity of SCI. Measuring serum total testosterone levels should be included in standard screenings for patients with SCI…”
I can say, a very common report of those who go on TRT is a big reduction in general aches and pains in my experience, and again, it makes perfect sense to me. The future treatment of SCI will be the of use various growth factors and other modalities (such as stem cell therapy) to re grow/re connect the spinal cord. That technology is much closer than people realize, but it seems the med/sci community very slow to pursue this area as quickly as they should. Obviously, this approach could be used to repair damaged nerves and other tissues far less challenging than repairing a severely damage or severed spinal cord.
Useful summary info from this study Effects of testosterone replacement therapy on skeletal muscle after spinal cord injury:
“The most important finding of this study was that TRT ameliorated the decrease in fiber CSA resulting from SCI. TRT also attenuated the slow to fast fiber type shift as well as the decrease in oxidative enzyme activity. To our knowledge, this is the first study to investigate the potential of TRT to prevent atrophy in SCI. TRT in aging sarcopenia and in other diseases with muscle wasting (for example, AIDS) results in favorable effects on bone, muscle size and strength in both low-average and hypogonadal men.19 Increases in muscle CSA were equal, if not greater in TRT only groups than in exercise groups without TRT.20 These data and ours for SCI both demonstrate a positive effect of TRT on muscle size without traditional overload…”
Study design: Randomized control.
Objective: To examine the effects of testosterone replacement therapy (TRT) on skeletal muscle 11 weeks after complete SCI.
Setting: Athens, Georgia USA.
Methods: Soleus (SOL), gastrocnemius (GA), tibialis anterior (TA), vastus lateralis (VL) and triceps brachii (TRI) muscles were taken from twelve young male Charles River rats 11 weeks after complete SCI (T-9 transection, n=8) or sham surgery (n=4). Rats received either TRT (two 5 cm capsules, n=4) or empty capsules (n=8) implanted at surgery. Muscle samples were sectioned and fibers analyzed qualitatively for myosin ATPase and quantitatively for succinate dehydrogenase (SDH), alpha-glycerol-phosphate dehydrogenase (GPDH) and actomyosin ATPase (qATPase) activities using standard techniques.
Results: SCI decreased average fiber size (49plusminus4%) in affected muscles and the percentage of slow fibers in SOL (93plusminus3% to 17plusminus2%). In addition, there was a decrease in SDH and an increase in GPDH and qATPase activities across the four hind-limb muscles of the SCI animals. Fiber size in the TRI was increased (31plusminus2%) by SCI while enzyme activities were not altered. Average fiber size across the four hind limb muscles was decreased by only 30% in TRT SCI animals and their SOL contained 39plusminus2% slow fibers. TRT also attenuated changes in enzyme activities. There was no effect of TRT on the TRI relative to SCI.
Conclusions: TRT was effective in attenuating alterations in myofibrillar proteins during 11 weeks of SCI in affected skelatal muscles.
Additional related studies of interest:
Exogenous testosterone prevents motoneuron atrophy induced by contralateral motoneuron depletion.
Fargo KN1, Sengelaub DR. J Neurobiol. 2004 Sep 5;60(3):348-59.
Gonadal steroids exhibit neuroprotective and neurotherapeutic effects. The lumbar spinal cord of male rats contains a highly androgen-sensitive population of motoneurons, the spinal nucleus of the bulbocavernosus (SNB), whose morphology and function are dependent on testosterone in adulthood. Unilateral SNB motoneuron depletion induces dendritic atrophy in contralateral SNB motoneurons, but this atrophy is reversed in previously castrated males treated with testosterone. In the present experiment we test the hypothesis that the morphology of SNB motoneurons is protected from atrophy after contralateral motoneuron depletion by exogenous testosterone alone (i.e., with no delay between castration and testosterone replacement). We unilaterally depleted SNB motoneurons by intramuscular injection of cholera toxin conjugated saporin. Simultaneously, some saporin-injected rats were castrated and immediately given replacement testosterone. Four weeks later, contralateral SNB motoneurons were labeled with cholera toxin conjugated HRP, soma sizes were measured, and dendritic arbors were reconstructed. Contralateral SNB motoneuron depletion induced somal atrophy and dendritic retraction, but testosterone treatment prevented both of these effects. Thus, the presence of high-normal levels of testosterone prevents motoneuron atrophy induced by contralateral motoneuron depletion. These data support a therapeutic role for testosterone in preventing atrophy induced by motoneuron injury.
To define the prevalence of testosterone deficiency in persons with chronic spinal cord injury (SCI) and to identify factors associated with this deficiency.
A U.S. Department of Veterans Affairs SCI unit.
Participants (n = 60) included male veterans completing annual evaluations from July 2006 to April 2007.
In addition to routine annual evaluation laboratory examination, which included measurements of serum albumin levels, participants underwent measurements of serum total testosterone, luteinizing hormone, follicle stimulating hormone, and prolactin levels. Outcome measures included the prevalence of testosterone deficiency (defined as total serum testosterone <325 ng/dL) and the relationship of testosterone level with participant’s age, serum albumin level, narcotic medication use, time since injury, American Spinal Injury Association Impairment Scale (AIS) grade, and neurologic level of injury.
A low serum testosterone level (<325 ng/dL) was detected in 43.3% of participants. The testosterone level was significantly associated with severity of injury as defined by AIS grade (t = -2.59, P = .012). The prevalence of testosterone deficiency was significantly greater in participants with motor complete (AIS A and B) injuries compared with those with motor incomplete (AIS C, D, and E) injuries. Testosterone levels were significantly lower in participants who were taking narcotic medications for pain management (t = -0.25, P < .05). There was no relationship between the use of narcotic medications and severity of injury. Given the small number of participants, the SCI levels, age, duration of injuries, serum albumin levels, and serum levels of luteinizing hormone, follicle stimulating hormone, and prolactin did not reach statistical significance in predicting testosterone level.
These findings confirm both a substantial population of men with SCI and with testosterone deficiency, and a significant association between testosterone level and severity of SCI. Measuring serum total testosterone levels should be included in standard screenings for patients with SCI, particularly those with motor complete injuries.