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.
Meat. Meat, particularly beef, provides our bodies with the protein it needs to create muscle (more muscle = more T) and the fats and cholesterol to make testosterone. My meat topping of choice was sliced up chuck steak. I grilled two of them on Monday and it lasted me until the next Monday. Every now and then I’d slow-cook some ribs or brisket to use as my meat topping. My philosophy was the fattier, the better.
A4M, which stands for “The American Academy of Anti-Aging Medicine” is dedicated to the advancement of tools, technology, and transformations in healthcare that can detect, treat, and prevent diseases associated with aging. They promote the research of practices and protocols that have the potential to optimize the human aging process. The organization is also dedicated to educating healthcare professionals and practitioners, scientists, and members of the public on biomedical sciences, breakthrough technologies, and medical protocols through our advanced education entity: Metabolic Medical Institute (MMI). Their event in Vegas each year is, in my opinion, well worth checking out.
Epidemiological evidence supports a link between testosterone and glucose metabolism. Studies in non-diabetic men have found an inverse correlation of total or free testosterone with glucose and insulin levels (Simon et al 1992; Haffner et al 1994) and studies show lower testosterone levels in patients with the metabolic syndrome (Laaksonen et al 2003; Muller et al 2005; Kupelian et al 2006) or diabetes (Barrett-Connor 1992; Andersson et al 1994; Rhoden et al 2005). A study of patients with type 2 diabetes using measurement of serum free testosterone by the gold standard method of equilibrium dialysis, found a 33% prevalence of biochemical hypogonadism (Dhindsa et al 2004). The Barnsley study demonstrated a high prevalence of clinical and biochemical hypogonadism with 19% having total testosterone levels below 8 nmol/l and a further 25% between 8–12 nmol/l (Kapoor, Aldred et al 2007). There are also a number longitudinal studies linking low serum testosterone levels to the future development of the metabolic syndrome (Laaksonen et al 2004) or type 2 diabetes (Haffner et al 1996; Tibblin et al 1996; Stellato et al 2000; Oh et al 2002; Laaksonen et al 2004), indicating a possible role of hypogonadism in the pathogenesis of type 2 diabetes in men. Alternatively, it has been postulated that obesity may be the common link between low testosterone levels and insulin resistance, diabetes and cardiovascular disease (Phillips et al 2003; Kapoor et al 2005). With regard to this hypothesis, study findings vary as to whether the association of testosterone with diabetes occurs independently of obesity (Haffner et al 1996; Laaksonen et al 2003; Rhoden et al 2005).
Before we go any further, know that fenugreek is an herb of Asian origin, commonly used in Indian cuisine. The Indians have been consuming it as an aphrodisiac and an herbal cure-all for centuries which might explain why that waiter in your local Indian restaurant is always smiling. As it turns out, there is actually some validity to the purported claims.
There is a negative correlation of testosterone levels with plasminogen activator inhibitor-1 (PAI-1) (Glueck et al 1993; Phillips 1993), which is a major prothrombotic factor and known to be associated with progression of atherosclerosis, as well as other prothrombotic factors fibrinogen, α2-antiplasmin and factor VII (Bonithon-Kopp et al 1988; Glueck et al 1993; Phillips 1993; De Pergola et al 1997). There is a positive correlation with tissue plasminogen activator (tPA) which is one of the major fibrinolytic agents (Glueck et al 1993). Interventional trials have shown a neutral effect of physiological testosterone replacement on the major clotting factors (Smith et al 2005) but supraphysiological androgen administration can produce a temporary mild pro-coagulant effect (Anderson et al 1995).
Testosterone [Figure 1] is the main male sex hormone. It is responsible for male sexuality and is the main hormone-producing the features associated with masculinity such as substantial muscle mass, facial hair, libido, and sperm production. Besides, the hormone has other vital functions as the basic chemical composition of testosterone is steroidal; and steroids are known to have significant physiological, as well as psychological, effects in male individuals, especially adults. Testosterone production is reduced gradually in men starting from the age of 30. Hence, testosterone blood concentrations slowly diminish as age progresses. As a result, men may experience a number of physiological and psychological events, such as a lack of sex-drive, erectile dysfunction, acute depression, fatigue, low energy levels, and insomnia.
Everytime you add Testosterone to your system, be it naturally through producing in the testis, injected, oral, or dermal you will receive a spike in your blood levels. Estrogen is mainly created in men by an action of an enzyme called Aromatase. Aromatase floats around and binds to Testosterone and converts it to Estrogen. When you spike your T your E will follow in this way. The obvious and detrimental effects to many of the already estrogen dominant hypogonadal men will be inappropriate over stimulation of the estrogen receptors in the body. Gynecomastia, fluid retention, weight gain, brain fog, erratic emotions, depression, ect. Higher levels of Estrogen cause SHBG to be created. SHBG binds to Testosterone and transports it to the liver for disposal. On top of this Estrogen can bind to your androgen receptors causing Testosterone to float around with no where to go. If you are taking shots or gel or cream and feel little to no effect even though it’s technically raised your T blood ranges, you now have an multiple answers for why you little to nothing or feel even worse. This has been known for years that you must be prepared to control Estrogen. An Aromatase Inhibitor (AI) or anti estrogen medication (Clomiphene, Tamoxifen) is needed to stop the estrogen from getting out of control. By taking an Aromatase inhibitor and monitoring your E2 levels you can easily control Estrogen, Aromatase, and SHBG from getting out of hand and free up those blocked androgen receptors so you can now reap the benefits of elevating T to a healthy level. If your Doctor is not testing your E2(aka Estrogen, Estradiol) levels before and during talks and administration of TRT or will never prescribe an AI then you shouldn’t be following his advice at all and will be harmed by Testosterone usage. This may sound complicated but in the end it’s simple. Elevate Testosterone. Control Estrogen. Only two medications needed. Don’t settle.
at 54 testestrone was 135 so started TRH. Huge increase in energy and sex drive on 100mg cypriate every 2 weeks. My PSA rose from 1.13 to 1.63 in two years so Dr. ordered a biopsy. I am now almost 56. Came back with 1 out of 12 cores having adenocarcinoma and graded at 3×3.I am scheduled for a pelvic MRI in 4 weeks. DR wants me stay on testosterone for the time being and wants to add a med to block DHT (as I understand it.I got all this today so kind of confused what to do. Lifestyle-I rarely eat red meat maybe twice a month, run 10ks and half-marathons.how crazy is that?
Testosterone is an anabolic steroid hormone that plays a critical role in metabolism, sex drive, muscle building, mood regulation, memory & cognitive function. Normal testosterone levels play a huge role in maintaining optimal weight as well as reducing risk of degenerative diseases such as osteoporosis, heart disease, diabetes, & certain cancers (1, 2, 3).
Increased testosterone can have an impact on body composition. Possible benefits include gains in lean muscle mass, reduced body fat and increased bone density. Testosterone inhibits uptake of triglycerides and increases lipid mobilization from adipose tissue, and the increase or decrease of testosterone will usually have an inverse effect on fat stores, with higher testosterone generally causing a decrease in body fat. "The Journal of Clinical Endocrinology and Metabolism" published a study in 2007 that showed decreases in body fat and increases in lean mass in HIV-positive obese men given testosterone therapy. In 1989, a study of the effects of testosterone on muscle mass at the University of Rochester School of Medicine and Dentistry suggests that increasing testosterone increases protein synthesis in muscles. Body composition changes from increased testosterone were also demonstrated in a 1999 study at the School of Exercise Science and Sports Management, Southern Cross University in Australia performed on male weight-training subjects, which showed increases in arm girth and body weight and decreased body fat following a 12-week cycle of testosterone enanthate.
"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.