arimidex, also known as anastrozole, is shown to be an effective aromatase inhibitor in men. These case studies used arimidex to successfully stimulate testosterone production by limiting testosterone to estrogen production. This was found to be useful in the treatment of gynecomastia.
this study revealed increased breast cancer risk in women on "estrogen" and "testosterone" therapy. Now, several problems here: first, are these synthetic hormone or bioidentical. Second, the dosages appear, in what is written, to be supra physiologic. Third, giving supra physiologic estradiol and testosterone will obviously create imbalances and growth potential. Fourth, how were the women evaluated prior to starting hormone therapy and then were they remonitered (unlikely), fifth, were hormone metabolites evaluated (too, also unlikely). This study has serious flaws and very little can be extrapolated other than: don't take supra physiologic hormone levels without appropriate evaluation. Enough said
women using statin therapy to lower cholesterol have increased type II Diabetes. Variables were accounted for and this existed across all classes of statins.
ERα-positive cells respond to E2 with increased proliferation
ERβ was artificially introduced into these cells, E2-induced proliferation was inhibited
The proliferative response to E2 seems to be determined by the ratio of ERα/ERβ. The functions of ERβ in the breast are probably related to its antiproliferative as well as its prodifferentiative functions
The risk of developing PC seems to be related to the diet
In the human prostate, ERβ is expressed in the basal epithelial cells and AR in the luminal epithelium.
For many years, DHT was considered to be the main hormone guiding prostate development and function. However, the idea was challenged when in 2001 Mahendroo et al. showed that mice in which both forms of 5α-reductase had been inactivated, have a normal functional prostate [50]. The question was then raised as to what is the real function of DHT in the prostate. In 1989 we hypothesized that DHT is a precursor of an oestrogen, 5α-androstane-3β,17β-diol (3β-Adiol) and that physiological levels of an oestrogen could be produced in the total absence of aromatase [51]. We later demonstrated that 3β-Adiol is abundant in the prostate and is a good natural ligand for ERβ
The overall effect of oestrogens in the immune system is determined by a balance between ERα and ERβ signalling
The hypothesis of our group is that ERβ plays an important role in regulating the differentiation of pluripotent haematopoietic progenitor cells whereas ERα induces proliferation
In tissues and cell lines of mammary epithelium for example, it has been noticed that E2 in the presence of ERα elicits proliferation, but in the presence of ERβ it inhibits proliferation
ERα and ERβ have distinctive tissue distributions and to the great surprise of endocrinologists [7] many tissues previously thought to be ‘oestrogen-insensitive tissues’ were found to be ERβ positive and oestrogen sensitive. The most notable of the ERα-negative ERβ-abundant tissues were the epithelium of the rodent ventral prostate [8], the granulosa cells of the ovaries [9] and the parenchyma of the lungs
Awesome article discusses the different balance of ER alpha and ER beta and the effects on tissue as it relates to proliferation versus differentiation. This has clear implications in disease. Physicians prescribing hormones without a knowledge and understanding of this are only causing potential harm to their clients.
the energy supplied to rephosphorylate
adenosine diphosphate (ADP) to adenosine triphosphate (ATP) during and following intense
exercise is largely dependent on the amount of phosphocreatine (PCr) stored in the
muscle
Creatine is chemically known as a non-protein nitrogen
It is synthesized in the liver and pancreas from the amino acids arginine, glycine,
and methionine
Approximately 95% of the body's creatine is stored in skeletal muscle
About two thirds of the creatine found in skeletal muscle is stored as phosphocreatine
(PCr) while the remaining amount of creatine is stored as free creatine
The body breaks down about 1 – 2% of the creatine pool per day (about 1–2 grams/day)
into creatinine in the skeletal muscle
The magnitude of the increase in skeletal muscle creatine content is important because
studies have reported performance changes to be correlated to this increase
"loading" protocol. This protocol is characterized by ingesting approximately
0.3 grams/kg/day of CM for 5 – 7 days (e.g., ≃5 grams taken four times per day) and
3–5 grams/day thereafter [18,22]. Research has shown a 10–40% increase in muscle creatine and PCr stores using this
protocol
Additional research has reported that the loading protocol may only need to be 2–3
days in length to be beneficial, particularly if the ingestion coincides with protein
and/or carbohydrate
A few studies have reported protocols with no loading
period to be sufficient for increasing muscle creatine (3 g/d for 28 days)
Cycling protocols involve the consumption of "loading" doses for 3–5 days every 3
to 4 weeks
Most of these forms of creatine have been reported to be no
better than traditional CM in terms of increasing strength or performance
Recent studies do suggest, however, that adding β-alanine to CM
may produce greater effects than CM alone
These investigations indicate that the
combination may have greater effects on strength, lean mass, and body fat percentage;
in addition to delaying neuromuscular fatigue
creatine
phosphate has been reported to be as effective as CM at improving LBM and strength
Green et al. [24] reported that adding 93 g of carbohydrate to 5 g of CM increased total muscle creatine
by 60%
Steenge et al. [23] reported that adding 47 g of carbohydrate and 50 g of protein to CM was as effective
at promoting muscle retention of creatine as adding 96 g of carbohydrate.
It appears that combining CM with carbohydrate or carbohydrate and protein produces
optimal results
Studies suggest that increasing skeletal muscle creatine uptake may
enhance the benefits of training
Nearly 70% of these studies have
reported a significant improvement in exercise capacity,
Long-term CM supplementation appears to enhance the overall quality of training,
leading to 5 to 15% greater gains in strength and performance
Nearly all studies indicate that "proper" CM supplementation increases body mass
by about 1 to 2 kg in the first week of loading
short-term adaptations reported from
CM supplementation include increased cycling power, total work performed on the bench
press and jump squat, as well as improved sport performance in sprinting, swimming,
and soccer
Long-term adaptations when combining CM supplementation with training include increased
muscle creatine and PCr content, lean body mass, strength, sprint performance, power,
rate of force development, and muscle diameter
subjects taking CM typically gain about twice as much body
mass and/or fat free mass (i.e., an extra 2 to 4 pounds of muscle mass during 4 to
12 weeks of training) than subjects taking a placebo
The gains in muscle mass appear to be a result of an improved ability to perform
high-intensity exercise via increased PCr availability and enhanced ATP synthesis,
thereby enabling an athlete to train harder
there is no evidence to support the notion
that normal creatine intakes (< 25 g/d) in healthy adults cause renal dysfunction
no long-term side effects have been observed in athletes (up to 5 years),
One cohort of patients taking 1.5 – 3 grams/day of CM has been monitored since 1981
with no significant side effects
DHT at 70 mg daily shown to have no adverse effects in the prostate of "healthy" men older than 50. However, it did increase DHT metabolites (3 alpha androstane-diol and 3 beta androstane-diol), decreased LH, Testosterone, Estradiol, FSH, increased hemoglobin, creatinine, lean mass and decreased fat.
sex hormones such as E1, E2, FEI, T and FAI were also strongly positively associated with age-adjusted CRP levels whereas SHBG showed a strong negative association
An intriguing aspect is the observation that higher plasma concentrations of both oestrogenic and androgenic components were related to increased CRP
Study finds that lower SHBG, higher Estradiol, Estrone, Testosterone levels, and free androgen index is associated with increased CRP in "healthy" postmenopausal women.
Review finds that low SHBG and higher Testosterone levels are associated with increased CVD risk in post menopausal women. Exact relationship is undetermined.
Meta-analysis finds no improvement with cardiovascular risk from low saturated fats. This is not the first study to show this. The weakness of this is that this study is a meta-analysis. This needs to be taken in context and applied individually. The take home is that universal restriction of saturated fats is not the holy grail of nutrition.
