Why Replace Testosterone?

Testosterone is what you call an androgen or male hormone. It is the hormone that gives men AND women the competitive advantage to “survive” (This would be the main reason why athletes abuse it.) When you lose it, people lose the ability to “compete”.

Testosterone deficiency in men is called andropause. In women, testosterone deficiency through traditional medicine is routinely overlooked as a medical issue. In fact, this is a problem for women since they typically have 10 times less testosterone than men, so if they lose an equal amount as compared to a male, it generally affects them more radically.

Testosterone loss typically happens gradually and is often misconstrued as part of “normal aging” for both men and women. This would be a logical assumption if we didn’t artificially increase our lifespan through our technological advances reducing the effects of environmental stressors. We technically should be gone by the time we hit deficiency because we would succumb to some disease or predator by then. However, as you all know, this is not the case.

What happens when testosterone drops? Besides the loss of libido and sexual dysfunction, men AND women see an increase in body fat and decreased lean muscle mass, decreased energy, an increase in cardiovascular disease, increase in risk of osteoporosis, and increased brain aging. There is also an overall decrease in a sense of wellbeing. Testosterone deficiency may occur on average as young as 35 years of age for both men and women.

When replacing testosterone, we shoot for optimal levels — levels you would typically see in your twenties.

Rumor has it that testosterone replacement therapy increases the risk of prostate cancer or an enlarged prostate (BPH). NOT TRUE: there is no clinical evidence to support these claims.

On the plus side for women, there are studies that show that testosterone reduces the risk of breast cancer.

Are you ready to get your testosterone to OPTIMAL? Call for a free medical consultation to see if you may benefit from testosterone therapy.

OBJECTIVE: To evaluate the efficacy and safety of a testosterone patch for the treatment of women with hypoactive sexual desire disorder after natural menopause.

DESIGN: A multicenter, randomized, double-blind, placebo-controlled, parallel-group trial was conducted in naturally menopausal women with hypoactive sexual desire disorder receiving a stable dose of oral estrogen with or without progestin (N = 549). Women were randomized to receive testosterone 300 microg/day or placebo patches twice weekly for 24 weeks. The primary efficacy measure was change from baseline in frequency of total satisfying sexual activity over a 4-week period (weeks 21-24).

RESULTS: A total of 483 women (88%) were included in the primary analysis population (those with baseline sex hormone binding globulin levels < or = 160 nmol/L). The change from baseline in number of total satisfying sexual episodes was significantly greater for testosterone compared with placebo (participants with baseline sex hormone binding globulin levels < or = 160 nmol/L, mean change of 2.1 +/- 0.28 versus 0.5 +/- 0.23 episodes/4 weeks; P < 0.0001; intent-to-treat population, mean change from baseline of 1.9 +/- 0.26 versus 0.5 +/- 0.21 episodes/4 weeks, P < 0.0001). Testosterone also produced statistically significant improvements compared with placebo in all secondary efficacy measures, including sexual desire and personal distress. The testosterone patch was well tolerated.

CONCLUSIONS: Testosterone patch treatment increased the frequency of satisfying sexual activity and sexual desire, decreased personal distress, and was well tolerated in naturally menopausal women with hypoactive sexual desire disorder.

Why should you care? If you are an adult, this will be one of the most likely reasons you die. Sound drastic? We agree, but you can change your fate by taking the right actions now. Studies show that maintaining a healthy HDL level reduces your risk of heart disease by FOUR times.

How to Improve good cholesterol:

1. Take fish oil supplements, or eat fatty fish (salmon, cod, tuna, sardines, mackerel, and trout), walnuts, oatmeal, and oat bran. These have all been shown to improve good cholesterol (HDL) and reduce bad cholesterol (LDL).

2. Take Niacin, a B vitamin. This is the only effective ‘medicine’ at both lowering bad cholesterol and elevating good cholesterol. It is all natural and you don’t need to see a Doctor to get started! We would still love to see you, but we would rather see you healthy!

3. Start BHRT (bio-identical hormone replacement therapy) and start exercising.

How to Lower bad cholesterol:

1. Watch your diet – avoid fatty meats (bacon, sausage, hamburger, chicken with the skin), fried food, butter, ice cream. These foods and others that are high in saturated fats can be a large culprit in raising your cholesterol. Try to avoid or eat them sparingly!

2. Begin weight loss – What is your BMI? Lowering you BMI and losing body fat can improve your bad cholesterol.

3. Take statins – prescription medicine (see the information below though as there are some “cons” to taking these).

4. Take Niacin – it’s all-natural!

5. Take Omega-3 oils – it’s all-natural!

Statins like Lipitor, Zocor or Crestor do not raise good cholesterol. In fact, they can actually lower it.

Cons for Statin Drugs:

1. Reduce CoQ10 which is important for maintaining cardiovascular health, reducing damage to blood vessels, and increasing energy
2. May cause liver and muscle dysfunction
3. Are expensive
4. Have poor tolerance and compliance
5. Are over-prescribed 90% of the time
6. Have shown to increase breast cancer risk in some studies
7. Can cause cataracts

Heart disease runs in families so your genetics plays a part in your cholesterol levels, BUT there are things you can do TODAY to improve your fate. “Genetics loads the gun, but we pull the trigger”

Would you know how likely you are to develop heart disease? A REVITA physician can help. Would you also like to know how likely you are to develop about 50 other types of disease? REVITA’s Genetic testing can answer those questions for you.

If you would like more information on this subject email us or call 704-319-5530.

Division of Medicine (UMDS), St. Thomas’ Hospital, London.

The availability of recombinant human growth hormone (GH) has resulted in investigation of the role of GH in adulthood and the effects of GH replacement in the GH-deficient adult. These studies have led to the recognition of a specific syndrome of GH-deficiency, characterized by symptoms, signs and investigative findings. Adults with long-standing growth hormone deficiency are often overweight, have altered body composition, with reduced lean body mass (LBM), increased fat mass (FM), reduced total body water and reduced bone mass. In addition, there is reduced physical and cardiac performance, altered substrate metabolism and an abnormal lipid profile predisposing to the development of cardiovascular disease. Adults with GH deficiency report reduced psychological well-being and quality of life. These changes may contribute to the morbidity and premature mortality observed in hypopituitary adults on conventional replacement therapy. GH treatment restores LBM, reduces FM, increases total body water and increases bone mass. Following GH therapy, increases are recorded in exercise capacity and protein synthesis, and “favorable” alterations occur in plasma lipids. In addition, psychological well-being and quality of life improve with replacement therapy. GH is well tolerated; adverse effects are largely related to fluid retention and respond to dose adjustment. It is likely that GH replacement will become standard therapy for the hypopituitary adult in the near future. The benefits of GH replacement in the GH-deficient adult have been unequivocally demonstrated in studies lasting up to 3 years. The results of longer term studies are awaited to determine whether these benefits are sustained over a lifetime.

Department of Urology, Johns Hopkins University School of Medicine, James Buchanan Brady Urological Institute, Johns Hopkins Hospital, Baltimore, MD 21287-2101, USA.

Abstract

Androgens are thought to play a role in the pathogenesis of prostate cancer. We evaluated androgen levels in 3 age-matched groups of men who were part of the Baltimore Longitudinal Study of Aging: 1) 16 men with no prostatic disease by urologic history and exam (control group); 2) 20 men with a histologic diagnosis of benign prostatic hyperplasia (BPH) who had undergone simple prostatectomy; and 3) 20 men with a histologic diagnosis of prostate cancer (16 with local/regional cancer, and 4 with metastatic cancer). Luteinizing hormone (LH), total testosterone (T), and free T were measured on stored AM sera by radioimmunoassay (RIA). Free T was also calculated from the measured concentrations of total T and sex hormone binding globulin (SHBG). The median number of repeated sex steroid measurements ranged from 6-9 over a period from 7-25 years prior to the diagnosis of prostate disease. There were no significant differences in age-adjusted LH, total T, SHBG, or calculated free T levels among the groups at 0-5, 5-10, and 10-15 years before diagnosis. These data suggest that there are no measurable differences in serum testosterone levels among men who are destined to develop prostate cancer and those without the disease.

Estrogen is important to BOTH women and men. Wait … but isn’t that just a female hormone? No it is not! In fact, the protective estrogen called estradiol is responsible for reducing the risk of heart disease, osteoporosis and Alzheimer’s disease in both women AND men!

In women specifically, when estrogen begins to drop to a point of deficiency it manifests as menopause. The symptoms of menopause include vaginal atrophy or dryness, skin changes that include thinning and dryness, incontinence, temperature dysregulation that include hot flashes and night sweats, breast changes, fatigue, and decreased libido. In short, a woman’s overall wellbeing is decreased.

In both men and women, estrogen not only has been shown to protect against the above ailments, it has also been shown to be protective against strokes, macular degeneration, colon cancer, tooth loss and memory loss. Therefore, it is not good to block estrogen in men UNLESS they develop breast tissue and/or swelling.

How does one keep their estrogen up at the optimal level? Unfortunately, once your body begins to lose estrogen, it is difficult if not near impossible to keep it up naturally.

For women: The most effective way is replacement with the bio-identical estrogen in the form of estradiol.

For men, testosterone converts to estradiol. Therefore, the best way for men is via replacing testosterone.

Is your estrogen level optimal? Yes? No? Don’t know? Regardless – REVITA can help.

Hyperestrogenemia and hypotestosteronemia have been observed in association with myocardial infarction (MI) and its risk factors. To determine whether these abnormalities may be prospective for MI, estradiol and testosterone, as well as risk factors for MI, were measured in 55 men undergoing angiography who had not previously had an MI. Testosterone (r = -.36, P = .008) and free testosterone (r = -.49, P < .001) correlated negatively with the degree of coronary artery disease after controlling for age and body mass index. When the patient group was successively reduced to a final study group of 34 men by excluding the patients with other major disorders, the testosterone and free testosterone correlations persisted (r = -.43, P < .02 and r = – .62, P < .001, respectively). Neither estradiol nor the risk factors, except for high-density lipoprotein cholesterol, correlated with the degree of coronary artery disease in the final group. Testosterone correlated negatively with the risk factors fibrinogen, plasminogen activator inhibitor-1, and insulin and positively with high-density lipoprotein cholesterol. The correlations found in this study between testosterone and the degree of coronary artery disease and between testosterone and other risk factors for MI raise the possibility that in men hypotestosteronemia may be a risk factor for coronary atherosclerosis.

Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio 782847762, USA.

That free radical destruction of macromolecules is a basis of aging and age related diseases has considerable experimental support. Melatonin, a hormone produced in organisms as diverse as algae and humans, is produced primarily during the daily period of darkness, with only small amount being synthesized during the day. In mammals including man, melatonin is produced by and secreted from the pineal gland during the night; however, the night-time production of melatonin falls markedly with aging such that in senescent animals a night –time melatonin rise is barely measurable.

This may be significant in terms of aging in the light of recent observation which shows that melatonin is a highly efficient free radical scavenger and antioxidant both in vitro and in vivo. In vitro, melatonin has been shown to directly scavenge both the hydroxyl and peroxyl, radical, and it does so more efficiently than other known antioxidants; Furthermore, melatonin greatly potentates the efficiency of previously-discovered endogenous and exogenous. In vivo, both physiological and pharmacological levels of melatonin reportedly counteract the devastatingly destructive actions of free radical generating chemical. For example, melatonin effectively combats DNA damage in rats given massive doses of the chemical carcinogen safrole, and the indole overcomes much of the genomic damage inflicted by ionizing radiation. Also, lipid per oxidation induced by paraquat, bacterial lipopolysaccharide or H202 is highly significantly reduced by concurrent melatonin administration. Finally, cataracts produced in newborn rats by the depletion of the endogenous antioxidant glutathione are prevented by melatonin. These findings provide evidence that melatonin is operative in the-cell nucleus, in the aqueous cymosely and in lipoid-rich cellular membranes as an antioxidant. Considering this, the loss of this potent antioxidant during aging may be consequential in terms of cellular and organismal aging as well as the onset of age-related diseases. These experimental results from a variety of sources suggest that a more determined approach to the study of melatonin as an anti-aging factor is warranted.

Publication types:

Review

Review tutorial

If you are like me, you may be a little confused about all the carb-talk. Good Carbs, Bad Carbs, No-Carb, All Carb?!?! What’s it all mean?

I want to help you understand a few key truths about carbohydrates that can help you on your Journey to Wellness.

#1 – Which carbs should I avoid?
There are 5 key carbs that you should avoid in your diet.
1. Bread
2. Pasta
3. Rice
4. Potatoes
5. Alcohol

Why are these forbidden? They quickly turn to sugar which causes your body to begin to store fat (YUCK!) and they cause spikes in your insulin levels which can lead to type 2 diabetes. FYI – Diabetes is the 7th biggest killer in the United States now!

#2 – Which carbohydrates should I eat?
Do not eat any food above 50 on the glycemic index.
Search your favorite foods glycemic index by going to: http://www.glycemicindex.com/

#3 – How do I eat carbohydrates properly?
Always eat carbs with a serving of protein ( and try to eat protein with every meal). Please know that this doesn’t mean you have to eat carbs with each meal. When you pair a carbohydrate with a protein you will further lower the gylcemic rating. TIP: You may also pair the carb with a fiber supplement which will have the same benefit.

#4 – When should I avoid carbohydrates?
Do not eat carbs after dinner (no cereal, no ice cream nor chips). Instead, find a high protein snack if you are hungry. Nuts are a great snack choice.

Start to make steps towards eating healthier, low-glycemic, carbohydrates and you will live longer, look better, have more energy… make it happen! It’s never too late.

“The best time to plant a tree is 20 years ago. The second best is now.”

Start your transformation today.

In health and wellness,
Don

Since 1946, the UK Medical Research Council has collected medical, psychological, and demographic data on more than 5000 people on everything for verbal and nonverbal reasoning to algebra and visual memory. Tapping in this data base, psychologist Marcus Richards of University College London and his colleagues found that the smarter women is during childhood, the more likely she will begin menopause later in life. After adjusting for factors such as education, number of children, and socioeconomic states, they found that higher cognitive scores correlated with later menopause.

The finding, reported in the 22 July issue of Neurology, suggests that the link between hormones and brain development might be stronger than researchers suspected, pushing the connection and back to an earlier age. Other research has shown that hormones including estrogen can influence both brain development and reproductive aging.

Education, knowledge and advances in reproductive techniques are rapidly growing.

From Biomedicine: January 2000, Vol.3 No1