Try diet and exercise changes as your health permits. Losing weight, eating the right foods, and getting more exercise are great ways to naturally increase testosterone while also improving your overall health. While mild to moderate changes are likely safe in most teenage boys, you should consult your doctor before making any significant changes to make sure those changes will be right for your specific health needs.
Elevated testosterone levels have been demonstrated to increase the growth of body muscles and contribute to better activation of the nervous system, resulting in more power and strength, a better mood, enhanced libido, and many other benefits. Previous researches done on the anabolic role of testosterone and its impact on muscular strength in training-induced adaptations has provided rather conflicting findings, and a positive correlation between testosterone-mediated responses and both functional performance and body composition was found.[4,5] There are a number of naturally occurring substances that can boost testosterone levels in the body. Foods containing such substances are known as testosterone-foods; and they tend to be rich in vitamins, antioxidants, and minerals like zinc, which plays a key role in testosterone production.[2,6-8]
Consume vegetable carbohydrates and healthy fats. Your body requires the carbohydrates from fresh vegetables rather than grains and sugars. In addition to mono- or polyunsaturated fats found in avocados and raw nuts, saturated fats are also essential to building your testosterone production. According to research, there was a decrease in testosterone stores in people who consumed a diet low in animal-based fat.11 Aside from avocados and raw nuts, ideal sources of healthy fat that can boost your testosterone levels include:
Cardiovascular disease, and its underlying pathological process atherosclerosis, is an important cause of morbidity and mortality in the developed and developing world. Coronary heart disease in particular is the commonest cause of death worldwide (AHA 2002; MacKay and Mensah 2004). As well as increasing with age, this disease is more common in the male versus female population internationally, which has led to interest in the potential role of sex hormones in modulating risk of development of atherosclerosis. Concerns about the potential adverse effects of testosterone treatment on cardiovascular disease have previously contributed to caution in prescribing testosterone to those who have, or who are at risk of, cardiovascular disease. Contrary to fears of the potential adverse effects of testosterone on cardiovascular disease, there are over forty epidemiological studies which have examined the relationship of testosterone levels to the presence or development of coronary heart disease, and none have shown a positive correlation. Many of these studies have found the presence of coronary heart disease to be associated with low testosterone levels (Reviews: Jones, Jones et al 2003; Jones et al 2005).
Findings that improvements in serum glucose, serum insulin, insulin resistance or glycemic control, in men treated with testosterone are accompanied by reduced measures of central obesity, are in line with other studies showing a specific effect of testosterone in reducing central or visceral obesity (Rebuffe-Scrive et al 1991; Marin, Holmang et al 1992). Furthermore, studies that have shown neutral effects of testosterone on glucose metabolism have not measured (Corrales et al 2004), or shown neutral effects (Lee et al 2005) (Tripathy et al 1998; Bhasin et al 2005) on central obesity. Given the known association of visceral obesity with insulin resistance, it is possible that testosterone treatment of hypogonadal men acts to improve insulin resistance and diabetes through an effect in reducing central obesity. This effect can be explained by the action of testosterone in inhibiting lipoprotein lipase and thereby reducing triglyceride uptake into adipocytes (Sorva et al 1988), an action which seems to occur preferentially in visceral fat (Marin et al 1995; Marin et al 1996). Visceral fat is thought to be more responsive to hormonal changes due to a greater concentration of androgen receptors and increased vascularity compared with subcutaneous fat (Bjorntorp 1996). Further explanation of the links between hypogonadism and obesity is offered by the hypogonadal-obesity-adipocytokine cycle hypothesis (see Figure 1). In this model, increases in body fat lead to increases in aromatase levels, in addition to insulin resistance, adverse lipid profiles and increased leptin levels. Increased action of aromatase in metabolizing testosterone to estrogen, reduces testosterone levels which induces further accumulation of visceral fat. Higher leptin levels and possibly other factors, act at the pituitary to suppress gonadotrophin release and exacerbate hypogonadism (Cohen 1999; Kapoor et al 2005). Leptin has also been shown to reduce testosterone secretion from rodent testes in vitro (Tena-Sempere et al 1999). A full review of the relationship between testosterone, insulin resistance and diabetes can be found elsewhere (Kapoor et al 2005; Jones 2007).
Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).
Decreased testosterone production in men with rheumatoid arthritis is a common finding (Stafford et al 2000), and it is now generally recognized that androgens have the capacity to suppress both the hormonal and cellular immune response and so act as one of the body’s natural anti-inflammatory agents (Cutolo et al 2002). This known anti-inflammatory action of testosterone has led to studying the effect of testosterone therapy in men with rheumatoid disease. Although not all studies have reported positive effects of testosterone treatment (Hall et al 1996), some studies do demonstrate an improvement in both clinical and chemical markers of the immune response (Cutolo et al 1991; Cutolo 2000). This observation would go along with more recent evidence that testosterone or its metabolites protects immunity by preserving the number of regulatory T cells and the activation of CD8+ T cells (Page et al 2006).
A little goes a long way for men, but clinically many men do well with 5 to 10 mg of a topical progesterone cream at bedtime, again, only under your doctor’s supervision. Arginine is important for nitric oxide (NO) production and should be taken twice daily. I've also been recommending Testoplex™ for years. It's Xymogen’s formulation—featuring mungbean sprout powder—to address healthy testosterone levels and provide support for libido and overall vitality.
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Get good quality sleep on a regular basis. A chronic lack of quality sleep can significantly reduce the amount of testosterone a teenager or man produces, which then reduces muscle growth and promotes fat gain. Research has shown that quantity of sleep is associated with morning testosterone levels in males. More specifically, male testosterone levels in the morning increase with a longer duration of sleep. At least seven hours of restful sleep is recommended, although for many teenagers, nine hours is ideal to feel refreshed.
It seems like today it’s a badge of honor to train every day until exhaustion. The ethos is to push yourself harder and harder every day. If that’s your philosophy towards exercise, you might be sabotaging your testosterone levels (as well as your 20 Mile March). Studies have shown that overtraining can reduce testosterone levels significantly. Yes, it’s important to exercise hard, but it’s even more important to give your body rest so it can recuperate from the damage you inflicted upon it.
Like other steroid hormones, testosterone is derived from cholesterol (see figure). The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids. In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.
Beast Sports recommends taking four capsules twice per day. The pills are about the same size as a multivitamin or a Tylenol liquid gel pill — not tiny tablets, unfortunately, but they aren’t horse pills. They smell like the boxes of raisins your Mom packed into your school lunch, but stale, like they were forgotten in the pantry for a few years, and a little spicy, like she sprinkled curry powder on them. If you follow this eight pills per day regime, your $46 bottle will last you twenty-two days, and cost you about $2 per day.
A study published in the Journal of Steroid Biochemistry studied the effects of diet on serum sex hormones in healthy men. Results showed that when men decreased their healthy fat intake, serum concentrations of androstenedione, testosterone and free testosterone also decreased. (8) This indicates you can add low testosterone to the list of low-fat diet risks.
Testosterone is a sex hormone that plays important roles in the body. In men, it’s thought to regulate sex drive (libido), bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm. A small amount of circulating testosterone is converted to estradiol, a form of estrogen. As men age, they often make less testosterone, and so they produce less estradiol as well. Thus, changes often attributed to testosterone deficiency might be partly or entirely due to the accompanying decline in estradiol.
A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).
“I'm a truck driver and for 13 hours a night I sit in my truck and I drive. Out of boredom, I'd stop and eat. That was all until Andro400 – ever since then my life has changed. I started out weighing 341 pounds, and since taking Andro400 I've dropped 85 pounds! There's no cravings – I actually don't even think about food anymore. One thing that Andro400 said on the radio ad is it attacks belly fat – well let me tell you it did – the 2nd month is where I saw a drastic change in the size of my stomach. I've lost 6 inches! I'm sleeping better. My knee pain went away. I've had some lower back issues and that went away, and I can only attribute that to Andro400. It's a Life Changer for me!”
Reduce stress levels. Stress is ubiquitous in the modern world, particularly for teenagers who face a variety of pressures and expectations. High levels of stress triggers the release of the stress hormone cortisol, which tends to counteract the negative physiological effects of stress. That's certainly beneficial, but cortisol also blocks the effects and impact of testosterone within the body, which can cause significant problems for teenage boys. As such, try to provide a low-stress, stable environment for your teenager and give him opportunities to vent his frustrations and other emotions. Exercising, playing sports and developing enjoyable hobbies are all great at reducing stress.
Some of them can benefit dieters or competitive athletes. These individuals often experience significant decreases in their testosterone levels as a result of the restrictive or stressful exercise or diet regimen. It is worth mentioning that many of them can actually benefit healthy and hyper-active individuals (for example, professional weight lifters), but we can’t know that for sure because there aren’t enough studies to back up this claim.
The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).
A: Testosterone is the male androgen, or sex hormone. It controls too many things to list here. While it does help regulate mood, sex drive, and metabolism, it does this by working in tandem with other hormones in your body. It's produced by the male testes and the adrenal glands. For more information, go to //www.everydayhealth.com/drugs/testosterone. Matt Curley, PharmD
This content is strictly the opinion of Dr. Josh Axe and is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of medical advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. Neither Dr. Axe nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this educational content. All viewers of this content, especially those taking prescription or over-the-counter medications, should consult their physicians before beginning any nutrition, supplement or lifestyle program.
Heavy metal, fluoride, chlorine, pesticides, dioxins and other dangerous chemicals that are in our food, products and even the air we breath are wreaking absolute havoc on our endocrine systems (responsible for testosterone production). It’s hard to avoid these (especially if you’re a smoker) but they are major contributors to man’s decline in testosterone.
Some of these signs and symptoms can be caused by various underlying factors, including medication side effects, obstructive sleep apnea, thyroid problems, diabetes and depression. It's also possible that these conditions may be the cause of low testosterone levels, and treatment of these problems may cause testosterone levels to rise. A blood test is the only way to diagnose a low testosterone level.