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Erectile dysfunction is a common finding in the aging male. A prevalence of over 70% was found in men older than 70 in a recent cross-sectional study (Ponholzer et al 2005). Treatment with phosphodiesterase-5 (PDE-5) inhibitors is proven to be effective for the majority of men but some do not respond (Shabsigh and Anastasiadis 2003). The condition is multi-factorial, with contributions from emotional, vascular, neurological and pharmacological factors. The concept of erectile dysfunction as a vascular disease is particularly interesting in view of the evidence presented above, linking testosterone to atherosclerosis and describing its action as a vasodilator.
Another benefit of the increased muscle mass was that I got stronger. My bench press, squat, and deadlift all enjoyed significant gains during my experiment. It’s great to be able to bench press 225 pounds again for 5 sets of 5 like I used to in high school, and I’m on track to beat my maxes on the bench and squat that my 18-year-old self set over 12 years ago.
I’ve also got a thyroid nodule (benign), and should have it burned out very soon. So I’ve been battling a little more than low T for several years to say the least… a lot of the symptoms of low T can overlap with hyper and/or hypothyroidism… I highly recommend having your TSH, T4 and T3 levels checked along with your Testosterone for anyone experiencing symptoms.
Oral/buccal (by mouth). The buccal dose comes in a patch that you place above your incisor (canine or "eyetooth"). The medication looks like a tablet but you should not chew or swallow it. The drug is released over 12 hours. This method has fewer harmful side effects on the liver than if the drug is swallowed, but it may cause headaches or cause irritation where you place it.
The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
Men who produce more testosterone are more likely to engage in extramarital sex. Testosterone levels do not rely on physical presence of a partner; testosterone levels of men engaging in same-city and long-distance relationships are similar. Physical presence may be required for women who are in relationships for the testosterone–partner interaction, where same-city partnered women have lower testosterone levels than long-distance partnered women.
Cross-sectional studies conducted at the time of diagnosis of BPH have failed to show consistent differences in testosterone levels between patients and controls. A prospective study also failed to demonstrate a correlation between testosterone and the development of BPH (Gann et al 1995). Clinical trials have shown that testosterone treatment of hypogonadal men does cause growth of the prostate, but only to the size seen in normal men, and also causes a small increase in prostate specific antigen (PSA) within the normal range (Rhoden and Morgentaler 2005). Despite growth of the prostate a number of studies have failed to detect any adverse effects on symptoms of urinary obstruction or physiological measurements such as flow rates and residual volumes (Snyder et al 1999; Kenny et al 2000, 2001). Despite the lack of evidence linking symptoms of BPH to testosterone treatment, it remains important to monitor for any new or deteriorating problems when commencing patients on testosterone treatment, as the small growth of prostate tissue may adversely affect a certain subset of individuals.
Ben has mentioned APOE many times, as in this podcast, with the reference in this transcript as something like 34/44. I’ve always assumed that meant a number of different genes that related to APOE having the homozygous or heterzygous mutations. I’ve only been able to find one rs in my 23andme raw data that seems meaningful to this, rs429358. How do you all figure out your APOE status? Are you getting this from one of the other companies that analyzes part of your raw data for you?
With the exception of increasing my fat and cholesterol intake, my diet wasn’t that unconventional. I didn’t follow a strictly low-carb or Paleo diet because recent research has suggested that a diet high in protein and low in carbs actually causes T levels to decrease. With that said, I was judicious with the carbs. I tried to get most of my carbs from veggies and fruit, but I didn’t freak out if my wife made us spaghetti for dinner.
I am 45 years old and have been diagnosed with low testosterone levels. In 2014 my levels were 16.5 and in 2016 that dramatically reduced to a score of 10.4. My doctor prescribed me Testo gel which I rub on every morning and have done so for the last 6 weeks. I keep myself fit, gym twice a week and martial arts twice a week and found my energy levels were depleting and didn’t seem to recover quickly the next day. I started to feel exhausted and experienced low libido,lack of motivation and mental focus. I actually thought oh well this is what happens when you get older.
Testosterone is the primary sex hormone in men, and it is responsible for the development of many of the physical characteristics that are considered typically male. Women also produce the hormone in much smaller amounts. Testosterone, part of a hormone class known as androgens, is produced by the testicles after stimulation by the pituitary gland, which is located near the base of the brain, and it sends signals to a male's testicles (or to a woman's ovaries) that spark feelings of sexual desire. (1)