Androsterone Lowers Cholesterol and Mimics Thyroid Hormone

Research shows that the sex hormone Androsterone has the capabilities to lower bad cholesterol (LDL), and increase oxygen consumption similar to active thyroid hormone (T3).  These findings indicate that Androsterone may have the ability to keep your heart healthy while stimulating a better metabolic rate – via – increased oxygen consumption.

Researcher’s investigated Androsterones effects on 3 patients with hypercholsteremia (high cholesterol), normal cholesterol, and a patient with myxedema (hypothyroidism/low thyroid).  The steroid (androsterone), in a single daily dosage of 50 mgs was given intra-muscularly in sesame oil & benzyl alcohol.  This procedure was adhered to for 34 days.

Some interesting findings were reported –

There was a significant decline in the serum cholesterol level in all 3 subjects. The cholesterol lowering effect was most profound in the patient with hypothyroidism (low thyroid), which caused an 18 to 40 percent decrease in elevated serum cholesterol levels. The decrease was obvious in both free and esterified cholesterol fractions.

However, following the Androsterone treatment, after cessation of the steroid hormone, serum cholesterol concentrations returned to pre-treatment levels EXCEPT in the patient with hypothyroidism (low thyroid). Researcher’s experimented with several other steroid hormones only to find that they all INCREASED bad cholesterol opposing Androsterones effects.

How about Androsterones activity replicating thyroid-like functions?

It has been documented that the level of thyroid function significantly influences the production of endogenous androgen levels. People with hypothyroidism (low thyroid) are characterized by an absolute and relative DECREASE in Androsterone levels. Patients that had low and normal thyroid functions underwent cytomel (prescription T3 hormone) treatment, they produced both an absolute and relative INCREASE in Androsterone levels. Patients with HYPERthyroidism (over-active thyroid) displayed higher endogenous Androsterone levels.

It is clear that Androsterone demonstrates a thyromimetic characteristic due to increasing a person’s rate of oxygen consumption, which in turn can also lower cholesterol levels. Androsterone is pretty exciting because it seems to be a possible treatment for people displaying hypercholesteremia (elevated cholesterol) symptoms. This is fascinating because the androgens in which Androsterone is derived from are often associated with hyperlipidemic states (elevated cholesterol).

In men, androgenic hormones decline in the aging process, therefore, it may be in a male’s best interest to supplement with Androsterone to defend against atherosclerosis (clogged arteries), and a compromised rate of oxygen consumption due to decreased thyroid output.

References:

1.) Skovasted, J. Molholm Hansen , M. Kristernsen and L Korsgaard Christensen, The androsterone-etiocholanolone extretion ratio in Hyper- and Hypothyroidism. Vol. 180, fasc. 3 1966

2.) Samuel G Kahn, Thyroid-androgen interrelation in the dietary hypercholesterolemic rat, April, 1965

3.) LEON HELLMAN, M.D, H. LEON BRADLOW , ph D, B ZUMOFF, M.D., DAVID k FUKISHIMA, pH d. AND T.F. GALLEGHER, pH d. THYROID-ANDROGEN INTERRELATIONS AND HYPERCHOLESTERMIC EFFECT OF ANDROSTERONE, FEBRUARY 11, 1959

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Carbs Plus Stress Increases Estrogen

If you are a person who wants to attain a leaner, more define physique, than you need to take action to lower cortisol levels and lower your carbohydrate consumption.

                     … And here is why 

There was a fascinating study performed by researchers from the University of Birmingham that examined Glucocorticoid (cortisol) & insulin regulation and how it affects aromatase activity in human adipose tissue, revealing different outcomes in men and women.

In this study, researchers wanted to examine insulin & cortisol’s role in potentiating aromatase activity in men and women by taking samples of subcutaneous and omental (visceral) adipose tissue for rigorous testing.

The research candidates were premenopausal women (7) and postmenopausal women (10) and 9 men.  The researchers found that the male candidate’s basal aromatase activity was significantly higher in the subcutaneous tissues opposed to omental (visceral) tissue with cortisol + insulin present. Insulin appeared to exacerbate cortisol’s effect in promoting aromatase activity.

The female test subjects had similar results as the males, but even more aromatase activity with insulin + cortisol present. This small piece of the study reveals that subcutaneous adipose tissue has a much greater affinity for aromatase activity than omental (visceral) fat in both genders.

When they examined the differences between pre & postmenopausal women and their reaction to insulin + cortisol the results revealed that postmenopausal women had high aromatase in the omental (visceral) tissues than premenopausal women. However both pre & postmenopausal women revealed the same response to aromatase activity in the subcutaneous tissues.

Sex steroids such as Dhea, Androstenedione, Estrone, Testosterone etc… may regulate adipose mass by increasing preadipocyte proliferation, differentiation, and adipocyte size through effects on lipolysis (fat-loss) and lipogenesis (fat accrural).

Insulin plays a crucial role in adipocyte proliferation and differentiation, however in this study, insulin ALONE has no effect on aromatase expression, whereas insulin + cortisol demonstrated an additive effect on aromatase activity.

You know what that means for most people who utilize high carbohydrate diet’s to either keep dietary fat low or to gain weight?

It means that relatively high doses of insulin (think dextrose & white rice) in combination with cortisol (think low blood sugar from spiked insulin) increases aromatase activity, which promotes estrogen levels in excess.

This is extremely undesirable for favorable body composition as this phenomenon will promote proliferation and differentiation of preadipocytes, enhancing central adiposity (fat mass accrural).

  Now what you should do

I hope after reading this article you recognize that ingesting copious amounts of carbohydrates in your plight for ultimate muscle mass or general health (because you still abide by the USDA outdated food pyramid which is simply asinine) you understand that manipulating your insulin and cortisol levels through meticulous nutrition planning will be in your best interests.

I am NOT telling you to switch to an Atkins or Ketogenic Diet by any means, simply just to pay attention to your carbohydrate choices (high glycemic VS low glycemic) and also your glycemic loads (grams of carbs per meal). If you absolutely insist you MUST incorporate carbohydrates around the clock with each meal, make sure to keep the gram allotment low, at around 20-30 grams per meal, as this keeps the glycemic load under control. Also, employ high glycemic carbs ONLY around your weight training or high activity event. The remainder of your carbs (if you insist you need them) should be low glycemic.

I would suggest you to just use carbohydrates INFREQUENTLY, meaning pre & post training, while the rest of your meals consist of top quality protein sources and raw, undenatured fats.

Incorporating a supplement that increases growth hormone production while lowering the stress hormone cortisol would be beneficial for those striving to get as lean as possible while dieting for fat-loss or gaining mass while keeping body fat lower.

Look no further than Primordial’s EndoAmp Max, which will do just that – Increase GH & lower cortisol, while enhancing mental acuity and focus.

  Helpful tips to lower cortisol & insulin –

  • Deep tissue massages will relax your muscles and mind, which will lower cortisol

  • Keeping the glycemic load small at each carbohydrate meal will keep insulin stable

  • Sleeping in a silent pitch black room will initiate high quality sleep for lowering cortisol and boosting GH release

  • Combining essential fats to each low glycemic load meal will further lower insulin release

  • Supplementing with adaptogenic herbs such as magnolia bark & rhodiola lower cortisol

  • Incorporating fiber into each meal will keep insulin levels low

  • Supplementing with Primordial Performance EndoAmp will boost GH & lower cortisol

 

References:  J Clin Endocrinol Metab. 2002 Mar;87(3):1327-36.  Glucocorticoid regulation of p450 aromatase activity in human adipose tissue: gender and site differences.  McTernan PG, Anderson LA, Anwar AJ, Eggo MC, Crocker J, Barnett AH, Stewart PM, Kumar S.

Post-Exercise Protein Consumption is Mandatory

In order to gain muscle, you MUST undergo intense resistance training.  In order to gain muscle, you MUST consume protein to re-build muscle tissue.

These two variables work synergistically with each other and to maximize your chances of gaining lean muscle tissue you simply must consume protein alongside a resistance training routine.

The timing of protein ingestion is a highly debatable subject and has been unresolved as to whether precise timing is truly essential for measureable repair/growth opposed to simply consuming enough protein at other times of the day.

A very interesting study was conducted that investigated whether immediate protein consumption or a 2-hour delayed protein consumption had measureable impact on muscle hypertrophy and strength.

13 men with a body mass index (BMI) of 25 ± 1 kg m− 2 (means ± SEM) completed a 12-week resistance training program, training 3 times a week receiving oral protein in liquid form (10 g protein, 7 g carbohydrate, 3 g fat) immediately post workout, OR 2 hours post workout.

Scientists examined muscle hypertrophy by magnetic resonance imaging (MRI) and from muscle biopsies and muscle strength was examined using dynamic and isokinetic strength measurements. They also measured body composition from dual-energy X-ray absorptiometry (DEXA) and food records were recorded over 4 days. 

They also measured insulin response to protein supplementation.  Here are the exciting and convincing results after this experiment was concluded –

  • Cross-sectional area of m. quadriceps femoris (54.6 ± 0.5–58.3 ± 0.5 cm2) and mean fiber area (4047 ± 320–5019 ± 615 μ m2) increased in the P0 group (liquid protein post-exercise group)

  • No significant increase was observed in the 2-hour delayed group

  • Dynamic & isokinetic strength increased by 46% & 15%, respectively (liquid protein post-exercise group)

  • The 2-hour delayed group ONLY improved dynamic strength by 36%

  • No differences in glucose or insulin response were observed between protein intake at 0 and 2 h post-exercise.

 This phenomenal study proves the significance of ingesting a fast acting protein supplement such as; whey protein isolate immediately post-exercise for initiating muscle hypertrophy.

 

References:

1.) B Esmarck,J L Andersen*S Olsen, E A Richter†, M Mizuno, Timing of postexercise protein intake is important for muscle hypertrophy with resistance training in elderly humans. 

August 15, 2001 The Journal of Physiology, 535, 301-311. 

High LDL Cholesterol Builds Big Muscles

The word “cholesterol” is often interpreted as a major health concern regarding cardiovascular health.  When most people think of cholesterol they think of “Good Cholesterol” & “Bad Cholesterol.”  

The “Good Cholesterol” is associated with High Density Lipo-Proteins (HDL) & “Bad Cholesterol” is associated with Low Density Lipo-Proteins (LDL).  Recent research performed by Dr. Riechman from Texas A&M University may have shed some new light in regards to “Bad Cholesterol” not being such a bad guy after all.  Riechman determined that you need a reasonable amount of LDL circulating in your blood to induce adequate muscle hypertrophy.

In fact, he performed a study involving 52 adults from ages 60-69 years old who were in generally good health , but not physically active. None of the subjects were training on a regular basis. The summation of the study concluded that after moderate intense exercise, participants who had accrued the most muscle mass also displayed the highest levels of LDL (bad cholesterol). This was definitely a surprise, and not something that was expected.

This unique finding demonstrates that you need a certain amount of LDL to elicit adequate muscular hypertrophy. It proves that all forms of cholesterol are paramount to a person’s health. You simply cannot remove all of your “bad cholesterol” as that would actually be detrimental to your health.                                                                  

+ =

Low Density Lipo-Proteins gets a bad reputation for its ability to build up in the walls of arteries, which causes a reduction in blood circulation which often leads to heart disease and heart attacks.

High Density Lipo-Proteins often helps facilitate the removal of cholesterol from the arteries. However, LDL is significant in the fact that it serves as a “warning sign” that something is wrong and alerts the body to defend the malady at hand.

People need to understand that you do not want to completely rid yourself of bad cholesterol and understand that everyone needs a certain amount of both forms of cholesterol.

Riechman says “Our tissues need cholesterol, and LDL delivers it,”  “HDL, the good cholesterol, cleans up after the repair is done. And the more LDL you have in your blood, the better you are able to build muscle during resistance training.”

The study Dr. Riechman conducted serves as a useful finding in dealing with conditions such as Sarcopenia (age dependent muscle loss), which could help aging individuals fend off muscular atrophy which shortens one’s life span.

The following findings reveal how imperative essential fatty acids and saturated fat based diets are in overall health, and in a person’s plight for ultimate muscle mass accrual. 

Ghrelin Hormone: An Ectomorph’s Solution to Muscular Weight Gain

The endogenous growth hormone secretagogue Ghrelin may play a paramount role in your quest for muscle growth. This gastric hormone stimulates hunger in mice and in humans by binding to the ghrelin receptors located in the hypothalamus and the hippocampus.


Reasons why people feel the urge to eat

Ghrelin is highest when blood sugar is low and being in a fasted state. Ghrelin is a potent endogenous growth hormone releaser, and is the strongest of the secretagogues. Even though it increases growth hormone release, some of its effects are quite different from growth hormone itself. Ghrelin encourages lipogenesis, whereas growth hormone supports lypolysis. Ghrelin also supports glucose oxidation, while growth hormone suppresses insulin production for inhibited glucose disposal. This equates to ghrelin being highly effective for weight gain through adipogenic pathways and growth hormone supporting weight loss through lipolytic pathways.

Ghrelin Effects:                                            Synthetic Growth Hormone Effects:

-Increases endogenous GH                                -Synthetically derived

-Encourages lipogenesis (fat gain)                     -Encourages lipolysis (fat loss)

-Increases glucose oxidation                             -May promote insulin resistance

-Great for weight gain                                       -Great for fat loss

Knowing such facts makes it very clear that ghrelin would be perfect for the ectomorphic, hard gainer body type. If you are someone who frequents the bodybuilding internet forums, then you are probably aware of the recent surge in popularity with research peptide companies. These companies sell a product called GHRP-6, which is a hexapeptide comprised of 28 amino acids that signals the pituitary to secrete growth hormone through increasing ghrelin production. Using GHRP-6 in conjunction with a regimented weight training program and a meticulously planned diet, the ectomorphic trainee could consume copious amounts of high quality nutrients to achieve muscular weight gain that once seemed impossible.

– I must  mention one must be very stringent and meticulous with whom they decide to research with, meaning make sure the company is of high quality and the peptides are USA grade ingredients. A company such as Southern Research Co. has a trusted reputation and  is held in high regard in the research peptide community. 

 

References

1.) Cordido, Fernando; Isidro, Maria L.; Nemina, Rosa; Sangiao-Alvarellos, Susana, Ghrelin and Growth Hormone Secretagogues, Physiological and Pharmacological Aspect. Volume 6, Number 1, March 2009 , pp. 34-42(9)

2.) .Cummings DE, Weigle DS, Frayo RS, Breen PA, Ma MK, Dellinger EP, Purnell JQ, Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery.
N Engl J Med. 2002 May 23;346(21):1623-30.

3.) Britt Edén Engström, Pia Burman, Camilla Holdstock and F. Anders Karlsson,
Effects of Growth Hormone (GH) on Ghrelin, Leptin, and Adiponectin in GH-Deficient Patients. The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 11 5193-5198

Anti-inflammatory Benefits of Androstenetriol (5-androstene-3 beta-7 beta-17 beta-triol, beta AET)


Androstene-3 beta-7 beta-17 beta-triol (AET) represents a key naturally occurring 7-hydroxy dehydroepiandrosterone (DHEA) metabolite. Produced from the adrenal gland, DHEA and its sulfate are the major circulating adrenal steroids in humans. Serum levels peak in young adults, but then steadily decline with age, falling over 80% by age 70. DHEA serves as a precursor of male and female sex hormones. (1, 3, 5, 6)


DHEA demonstrates a plethora of anti-aging properties in rodents, including anti-inflammatory, anti-obesity, anti-diabetic, immune enhancing activities, and opposes certain activities of endogenous glucocorticoids (GC). As the literature grew, DHEA became widely used as an anti-aging, anti-stress dietary supplement. Despite these well-documented activities in animal models, DHEA supplementation in humans has yielded inconclusive results and the value of DHEA replacement in humans is controversial. Such widely different outcomes in rodents and humans have been referred to as ‘the DHEA conundrum’. Moreover, the potential therapeutic use of DHEA is limited by its side effects due to its conversion to sex hormones.


One possibility to explain these discrepancies is that a metabolite(s) of DHEA, rather than DHEA itself, may be necessary for its full action in human physiology. DHEA undergoes extensive conversion and derivatization to multiple products by phase 1 reactions involving the cytochrome P450 system, and studies have shown that these phase 1 products can be more potent than parental DHEA. Phase 1 reactions frequently decline in elderly subjects, and since such subjects have been the major participants in human DHEA treatment studies, it is possible that biologically active metabolites of DHEA were not produced in adequate amounts in previous human studies. It is also possible that qualitative changes in DHEA metabolism between rodents and humans will account for these differences.


DHEA oxidation via the action of the enzyme CYP7B leads to the 7-hydroxy derivatives of C-19 steroids, which are collectively present in low nanomolar concentrations in human circulation and are not readily metabolized to potent androgens or estrogens. Many of the functions initially attributed to DHEA from observations in rodents are now thought to be properties of these oxygenated metabolites, particularly AET.

 

Molecular Structure of Androstenetriol


AET possesses some of the anti-inflammatory and GC-opposing activities that have been attributed to DHEA, but with greater apparent potency. Studies with AET demonstrate it markedly up regulates host immune response, prevents immune suppression, modulates inflammation and improves survival after lethal infections by pathogens and lethal radiation. (1, 3, 5, 6)


AET has been shown to be protective against traumatic shock. Traumatic shock activates the hypothalamic-pituitary-adrenal axis (HPA) to mediate a cascade of defensive mechanisms that often include overwhelming inflammatory response and immunosuppression, which may lead to multiple organ failure. In a relevant traumatic hemorrhagic shock rodent model that applies to both combat and civilian sectors, AET provided a significant protective effect and improved survival. In a murine thermal injury model that includes glucocorticoid-induced osteopenia, AET significantly preserved bone mineral content, restored whole body bone mineral content and bone growth, suggesting reversal of GC-mediated adverse effects.


Since AET is a naturally occurring compound there is no patent protection leaving the door wide open for AET analogue research. Harbor BioSciences, Inc. – http://www.harborbiosciences.com/ (Public, OTC:HRBR – http://www.google.com/finance?q=OTC:HRBR ) is exploring a synthetic derivative of AET for the treatment of diseases with underlying chronic inflammation. HRBR has developed 17alpha-Ethynyl-5-androsten-3beta, 7beta, 17beta-triol (HE3286), a synthetic derivative AET. (1, 2, 4, 7)


Within the past two years, animal model studies of HE3286 successfully demonstrate the treatment of lung inflammation without immune suppression, the reduction of established disease of rheumatoid arthritis, and both glucose-lowering and cholesterol-lowering effects. Harbor BioSciences most ambitious project to date is their recently released data regarding that plasma levels of AET positively correlate with BMI in healthy men and women.(1) These observations suggest a compensatory role for AET in preventing the development of metabolic syndrome and obesity. The AET structural core may provide the basis for novel pharmaceuticals to treat this disease, HE3286. Stay tuned.



1. Auci DL, Ahlem CN, Kennedy MR, Page TM, Reading CL, Frincke JM. A Potential Role for 5-Androstene-3[beta],7[beta],17[beta]-triol in Obesity and Metabolic Syndrome. Obesity. http://www.nature.com/oby/journal/vaop/ncurrent/abs/oby2010204a.html


2. Conrad D, Wang A, Pieters R, et al. HE3286, an oral synthetic steroid, treats lung inflammation in mice without immune suppression. Journal of Inflammation 2010;7(1):52. http://www.journal-inflammation.com/content/7/1/52


3. Loria RM. Antiglucocorticoid function of androstenetriol. Psychoneuroendocrinology 1997;22 Suppl 1:S103-8.


4. Lu M, Patsouris D, Li P, et al. A new antidiabetic compound attenuates inflammation and insulin resistance in Zucker diabetic fatty rats. American Journal of Physiology – Endocrinology And Metabolism 2010;298(5):E1036-E48. http://ajpendo.physiology.org/content/298/5/E1036.full


5. Malik AK, Khaldoyanidi S, Auci DL, et al. 5-androstene-3?,7?,17?-triol (?-AET) Slows Thermal Injury Induced Osteopenia in Mice: Relation to Aging and Osteoporosis. PLoS ONE;5(10):e13566. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0013566


6. Marcu AC, Paccione KE, Barbee RW, et al. Androstenetriol Immunomodulation Improves Survival in a Severe Trauma Hemorrhage Shock Model. The Journal of Trauma 2007;63(3):662-9.


7. Offner H, Firestein GS, Boyle DL, et al. An Orally Bioavailable Synthetic Analog of an Active Dehydroepiandrosterone Metabolite Reduces Established Disease in Rodent Models of Rheumatoid Arthritis. Journal of Pharmacology and Experimental Therapeutics 2009;329(3):1100-9. http://jpet.aspetjournals.org/content/329/3/1100.full


8. Stiles AR, McDonald JG, Bauman DR, Russell DW. CYP7B1: One Cytochrome P450, Two Human Genetic Diseases, and Multiple Physiological Functions. Journal of Biological Chemistry 2009;284(42):28485-9.

Insulin’s Effect on Blood Pressure

lower blood pressureFebruary 19th, 2010 – In a previous article, I talked about how high carbohydrate diets can increase triglycerides (blood fats), or high cholesterol. It also appears that high carbohydrate consumption can increase hypertension, or high blood pressure.  Check this out.

It’s not actually the carbohydrates doing the damage; rather it’s their corresponding hormone – insulin.  The more carbs we eat, the more insulin our bodies pump into the blood stream to shuttle the glucose into cells for storage.  When we are in a hyperinsulinemic (high insulin) state, like the one you’re in when you eat a high carbohydrate diet, the kidneys will retain more sodium than normal. (1)  This is the body’s protective mechanism to maintain proper electrolyte balance, by retaining water to keep the sodium sufficiently diluted.  More water leads to increased blood volume, and thus more pressure on the walls of the blood vessels.

Insulin also stimulates the smooth muscle cells of the arterial walls, acting like a growth hormone and causing them to enlarge and thicken. (2) As they grow, the interior space of the blood vessels decreases, which further increases blood pressure.  Combine narrowed vessels with increased blood volume and you have a perfect recipe for a heart attack.

References –

1. Insulin and renal sodium retention in obese adolescents.

Rocchini AP, Katch V, Kveselis D, Moorehead C, Martin M, Lampman R, Gregory M.

Hypertension. 1989 Oct;14(4):367-74  PMID: 2676858

2. Protein Power

Dr. Michael Eades

New York, NY: Creative Paradox LLC (2000)

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