• All new members please introduce your self here and welcome to the board:
    http://www.professionalmuscle.com/forums/showthread.php?t=259
Buy Needles And Syringes With No Prescription
M4B Store Banner
intex
Riptropin Store banner
Generation X Bodybuilding Forum
Buy Needles And Syringes With No Prescription
Buy Needles And Syringes With No Prescription
Mysupps Store Banner
IP Gear Store Banner
PM-Ace-Labs
Ganabol Store Banner
Spend $100 and get bonus needles free at sterile syringes
Professional Muscle Store open now
sunrise2
PHARMAHGH1
kinglab
ganabol2
Professional Muscle Store open now
over 5000 supplements on sale at professional muscle store
azteca
granabolic1
napsgear-210x65
advertise1
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
ashp210
UGFREAK-banner-PM
esquel
YMSGIF210x65-Banner
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store

My thoughts on Cholesterol - a series

*copied and pasted from some guy named liftsiron at steroidology*

AI's effect on blood lipids

Get ready for a long but worthwhile read.


*The first study below is the typical study, that many BB guru's base their assumption on that AI's are unhealthy for lipid profiles. A study done on
postmenopausal women with breast cancer. Women who have near zero testosterone in their systems. Then take a look at the next three studies on boys in puberty where testosterone is plentiful, there were no adverse effects in regard to lipid profiles. I think that in bodybuilders that poor lipid profiles may be better equated to 17aa orals and a poor diet than to AI's.




Effect of letrozole on the lipid profile in postmenopausal women with breast cancer.

Elisaf MS, Bairaktari ET, Nicolaides C, Kakaidi B, Tzallas CS, Katsaraki A, Pavlidis NA.

Department of Internal Medicine, Medical School, University of Ioannina, GR 451 10 Ioannina, Greece. [email protected]

Hormonal therapy plays a central role in the overall treatment of breast cancer. Aromatase inhibitors can inhibit the aromatase enzyme system resulting in a reduction of oestrogens. letrozole is a non-steroidal aromatase inhibitor that effectively blocks aromatase activity without interfering with adrenal steroid biosynthesis. The drug can significantly reduce the levels of plasma oestrogens, which remain suppressed throughout the treatment. Data are scarce concerning the influence of these drugs on serum lipid levels. In the present study, we evaluated the effects of letrozole on the serum lipid profile in postmenopausal women with breast cancer. A total of 20 patients with breast cancer were treated with letrozole, 2.5 mg once daily. After an overnight fast, serum lipid parameters (total cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglycerides, apolipoproteins A1, B and E and lipoprotein (a)) were measured before treatment and at 8 and 16 weeks afterwards. A significant increase in total cholesterol (P=0.05), LDL cholesterol (P<0.01) and apolipoprotein B levels (P=0.05) in the serum, as well as in the atherogenic risk ratios total cholesterol/HDL cholesterol (P<0.005) and LDL cholesterol/HDL cholesterol (P<0.005) was noticed after letrozole treatment. We conclude that letrozole administration in postmenopausal women with breast cancer has an unfavourable effect on the serum lipid profile.



Posted by JGUNS on CEM
Look at this study done on boys with GH deficiency with anastrozole. There was no use of exogenous test in this study and lipid profiles remained unchanged:

J Pediatr Endocrinol Metab. 2004 Dec;17(12):1597-606. Related Articles, Links

An open label 12-month pilot trial on the effects of the aromatase inhibitor anastrozole in growth hormone (GH)-treated GH deficient adolescent boys.

Mauras N, Welch S, Rini A, Klein KO.

Nemours Children's Clinics in Jacksonville, FL, USA. [email protected]

OBJECTIVE: To investigate whether 12 mo treatment with the aromatase inhibitor anastrozole can achieve sustained suppression of estrogen production and delay epiphyseal fusion in growth hormone deficient (GHD) adolescent males. STUDY DESIGN: 20 adolescents with GHD were recruited (mean age +/- SE: 14.7 +/- 0.5 yr). Ten continued on GH (control group), and 10 on GH and anastrozole (Rx group) for 12 mo. RESULTS: After 12 mo E2 concentrations declined 60% in the Rx group (from 1.8 +/- 0.5 to 0.7 +/- 0.3 pg/ml, p <0.05) whereas they increased in controls (from 1.2 +/- 0.7 to 1.8 +/- 0.7, p <0.05). Testosterone increased 117% in the Rx group (from 304 +/- 31 to 626 +/- 64 ng/dl), 47% in controls (from 274 +/- 89 to 398 +/- 51) (p = 0.03, ANOVA between groups). IGF-I increased 42% in controls (454 +/- 22 to 711 +/- 109 ng/ml, p <0.05), but remained invariant in the Rx group (446 +/- 29 to 540 +/- 80, p = NS). Bone markers, plasma lipids, insulin, glucose, and liver function tests were all unchanged between groups with no differences either in body composition or bone mineral density accrual. There were no differences in growth velocity, height SDS, bone age advancement, predicted adult height or testicular volumes between groups after 12 mo. CONCLUSIONS: Anastrozole treatment potently decreases estrogen concentrations in adolescent males with GHD while allowing normal virilization, without deleterious effects on body composition, plasma lipids, bone metabolism or the tempo of puberty. Twelve months of treatment, however, did not increase predicted adult height. Further studies are needed to ascertain whether more prolonged estrogen blockade is helpful in the treatment of growth retardation in puberty.




Posted by JGUNS on CEM
and with letrozole:

J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):345-56. Related Articles, Links
Click here to read
Novel treatment of short stature with aromatase inhibitors.

Dunkel L, Wickman S.

Hospital for Children and Adolescents, University of Helsinki, PO Box 281, Helsinki 00029 HUS, Finland. [email protected]

Estrogens have an essential role in the regulation of bone maturation and importantly in the closure of growth plates in both sexes. This prospective, randomized, placebo-controlled study was undertaken to evaluate whether suppression of estrogen synthesis in pubertal boys delays bone maturation and ultimately results in increased adult height. A total of 23 boys with constitutional delay of puberty (CDP) received a conventional, low-dose testosterone treatment for inducing progression of puberty. Eleven of these 23 boys were randomized to receive a specific and potent P450-aromatase inhibitor, letrozole, for suppression of estrogen action, and 12 boys were randomized to receive placebo. Estradiol concentrations in the letrozole-treated boys remained at the pretreatment level during the administration of letrozole, whereas the concentrations increased during the treatment with testosterone alone and during spontaneous progression of puberty. Testosterone concentrations increased in all groups, but during the letrozole treatment, the increase was more than fivefold higher than in the group treated with testosterone alone. The inhibition of estrogen synthesis delayed bone maturation. The slower bone maturation in the boys treated with testosterone and letrozole, despite higher androgen concentrations, than in the boys treated with testosterone indicate that estrogens are more important than androgens in regulation of bone maturation in pubertal boys. During the 18 months follow-up, an increase of 5.1 cm in predicted adult height was observed in the boys who received testosterone and letrozole, but no change was seen in the boys who received testosterone alone or in the untreated boys. This finding indicates that an increase in adult height can be attained in growing adolescent boys by inhibiting of estrogen action.





Posted by JGUNS on CEM
Eur J Endocrinol. 2002 Mar;146(3):339-46. Related Articles, Links
Click here to read
The role of sex steroids in the regulation of insulin sensitivity and serum lipid concentrations during male puberty: a prospective study with a P450-aromatase inhibitor.

Wickman S, Saukkonen T, Dunkel L.

Hospital for Children and Adolescents, University of Helsinki, PL281, FIN-00029 HUS, Helsinki, Finland. [email protected]

OBJECTIVE: Our purpose was to study the sex steroid-mediated changes in serum insulin and lipid concentrations in boys during puberty. DESIGN AND METHODS: We treated boys with constitutional delay of puberty either with testosterone plus placebo or with testosterone plus an aromatase inhibitor, letrozole, which inhibits the conversion of androgens to oestrogens. We demonstrated previously that during treatment with testosterone plus letrozole the increase in testosterone concentration was more than 5-fold higher than during treatment with testosterone plus placebo. The concentrations of 17beta-oestradiol, IGF-I and IGF-binding protein-3 increased during testosterone-plus-placebo treatment, but during testosterone-plus-letrozole treatment the concentrations remained unchanged. These divergent changes in the two groups enabled us to study the effects of sex steroids and GH on insulin sensitivity and lipid concentrations. RESULTS: The insulin concentration in the testosterone-plus-placebo-treated group did not change. In contrast, in the testosterone-plus-letrozole-treated group, the concentration decreased during letrozole treatment, indicating improved insulin sensitivity. Changes in insulin and IGF-I concentrations within 12 and 18 months were correlated. In the testosterone-plus-placebo-treated group, the high-density lipoprotein cholesterol concentration did not change but in the testosterone-plus-letrozole-treated group the concentration decreased. The concentrations of low-density lipoprotein cholesterol (LDL-cholesterol) and triglycerides did not change in either of the groups. CONCLUSIONS: The findings indicate that androgens do not directly alter insulin sensitivity in boys during puberty. In contrast, the observations suggest tight regulation of glucose--insulin homeostasis by GH in boys at this stage. Furthermore, our findings indicate that sex steroids do not significantly participate in the regulation of serum concentrations of LDL-cholesterol or triglycerides in boys during early and mid-puberty.

*There you have it: no exogenous test, but LDL remained unchanged with letrozole in boys. Anastrozole appeared to have no effect on lipids in the previous study I posted.








*However on every parade some rain may fall. Although the study below was done with mice, it could relate to us.



Posted by Nandi12 on CEM
The studies that show little if any change in plasma lipid profiles with aromatase inhibition may be very deceptive. There is an emerging view that the local aromatization of T to E2 within the coronary vessel walls is what is cardioprotective, not circulating E2.

Note that in the study below the testes intact/anastrazole administered mice had no significant difference in plasma lipids as compared to controls, but had accelerated plaque development.


Pharmacology
Testosterone inhibits early atherogenesis by conversion to estradiol: Critical role of aromatase

Communicated by C. Kumar N. Patel, University of California, Los Angeles, CA, January 2, 2001 (received for review December 18, 2000)


Abstract

The effects of testosterone on early atherogenesis and the role of aromatase, an enzyme that converts testosterone to estrogens, were assessed in low density lipoprotein receptor-deficient male mice fed a Western diet. Castration of male mice increased the extent of fatty streak lesion formation in the aortic origin compared with testes-intact animals. Administration of anastrazole, a selective aromatase inhibitor, to testes-intact males increased lesion formation to the same extent as that observed with orchidectomized animals. Testosterone supplementation of orchidectomized animals reduced lesion formation when compared with orchidectomized animals receiving the placebo. This attenuating effect of testosterone was not observed when the animals were treated simultaneously with the aromatase inhibitor. The beneficial effects of testosterone on early atherogenesis were not explained by changes in lipid levels. Estradiol administration to orchidectomized males attenuated lesion formation to the same extent as testosterone administration. Aromatase was expressed in the aorta of these animals as assessed by reverse transcription-PCR and immunohistochemistry. These results indicate that testosterone attenuates early atherogenesis most likely by being converted to estrogens by the enzyme aromatase expressed in the vessel wall.
 
Ray Peat: Cholesterol, longevity, intelligence, and health

Really liked this article and I like alot of his stuff

Cholesterol, longevity, intelligence, and health.

Some interesting blurbs from the article if you don't care to read thru..

"The death rate from heart disease in the United States began increasing early in the twentieth century, and it reached its peak from about 1950 to 1975, and then began declining. During the decades in which the death rate was rising, consumption of animal fat was decreasing, and the use of vegetable oil was increasing."

"Despite the growing knowledge about the dangers of polyunsaturated fats, many medical articles are still advocating the "official" heart protective diet (e.g., "... diets using nonhydrogenated unsaturated fats as the predominant form of dietary fat," Hu and Willet, 2002)."

"Dietitians often recommend eating poached salmon, rather than "red meat," to lower cholesterol. Experimenters have measured the toxic oxidized cholesterol in different foods prepared in a variety of ways. Steaming salmon produced several times as much oxidized cholesterol as frying it, because of the longer cooking time that allowed the polyunsaturated fatty acids to break down, producing toxins such as acrolein and free radicals that oxidize the cholesterol and other components of the fish. The toxic cholesterol content of the steamed salmon was much higher than that of beef cooked at a high temperature."

"Many antioxidant nutrients act like a thyroid supplement did in the 1934 rabbit experiments, preventing atherosclerosis even when extra toxic cholesterol is given to the animals. People who eat seafood get much more selenium in their diet than people who eat nothing from the sea, and selenium is one of the extremely protective nutrients that prevent atherosclerosis in animal experiments with excess cholesterol."

"It is well established that several antioxidant nutrients are protective factors in heart disease. The medical establishment has expended a great amount of money and time in the last 60 years fighting the use of vitamin E or selenium for treating or preventing heart disease, though many physicians now take vitamin E themselves. But people who study free radical chemistry recognize that polyunsaturated fats are highly susceptible to oxidation, and that saturated fats tend to slow their degradation, acting to some extent as antioxidants. Several experiments and observations have shown that cholesterol itself can protect against damaging oxidation of polyunsaturated fats, protecting DNA and other vital components of the cell. A consistent program to prevent the oxidation of cholesterol would have to include all of the vitamins and minerals that are involved in antioxidant defense, avoidance of nutrients that exacerbate the destructive oxidations, and an effort to normalize the hormones and other factors, such as carbon dioxide, that have protective effects against free radical oxidation. A low level of cholesterol might increase susceptibility to the oxidants."

"In the healthy organism, cholesterol is constantly being synthesized, and constantly converted into steroid hormones, and, in the liver, into the bile salts that are secreted to emulsify fats in the intestine. Thyroid hormone and vitamin A are used in the process of converting cholesterol into pregnenolone, the immediate precursor of progesterone and DHEA. Anything that interfered with these processes would be disastrous for the organism. The supply of cholesterol, thyroid and vitamin A must always be adequate for the production of steroid hormones and bile salts. When stress suppresses thyroid activity, increased cholesterol probably compensates to some extent by permitting more progesterone to be synthesized."

"Simply injecting cholesterol into animals can improve their learning ability. In the Framingham heart study of 1894 people extending over a period of about 20 years, people with cholesterol naturally in the "desirable" range, below 200 mg.%, scored lower on "verbal fluency, attention/concentration, abstract reasoning, and a composite score measuring multiple cognitive domains" than those with higher cholesterol (Elias, et al., 2005)."

"After the age of fifty, low cholesterol is clearly associated with an increased risk of dying from a variety of causes. A study of old women indicated that a cholesterol level of 270 mg. per 100 ml. was associated with the best longevity (Forette, et al., 1989). "Mortality was lowest at serum cholesterol 7.0 mmol/l [=270.6 mg%], 5.2 times higher than the minimum at serum cholesterol 4.0 mmol/l, and only 1.8 times higher when cholesterol concentration was 8.8 mmol/l. This relation held true irrespective of age, even when blood pressure, body weight, history of myocardial infarction, creatinine clearance, and plasma proteins were taken into account."

"The recent discovery that the size of the LDL particle is a predominant factor in the development of atherosclerosis is one of those things that the editors and medical professors should find embarrassing.

Smaller lipoprotein particles have a greater surface area exposed to the oxidative factors in the serum, and so are more rapidly degraded into toxic substances. People with larger LDL particles are remarkably resistant to heart disease, and the drug companies are looking for a way to turn their lipoproteins into products. But the conditions that govern the size of the LDL particles are physically and chemically reasonable, and are causing confusion among the doctinaire.

There have been several studies in India showing that consumption of butter and ghee is associated with a low incidence of heart disease; for example, according to one study, people in the north eat 19 times more fat (mostly butter and ghee) than in the south, yet the incidence of heart disease is seven times higher in the south. A study in Sweden found that the fatty acids in milk products are associated with larger LDL particles (Sjogren, et al., 2004).

In a 35 day study, when butter (20% of the calories) was compared to various kinds of margarine (with more trans fatty acids) in a similar quantity, the LDL particles were bigger on the butter diet (Mauger, et al., 2003). But in a study of the habitual diet of 414 people, large LDL particles were found to be correlated with increased intake of protein, animal fat, and trans fatty acids (Kim and Campos, 2003)."
 
ALA, Gymnema Sylvestre, Chromium and a little Vanadyl...I can't let the cat out of the bag just yet, but a certain sponsor is about to start carrying something awesome along these lines :)

JM

what are your thoughts on glucophage?
 
So let's talk about this Ancel Keys character. He is one of the most famous players in this whole tale of cholesterol and the lipid hypothesis.

The work of Ancel Keys – This guy was hell bent on proving the lipid hypothesis. Sometime around 1950 he decided to do a massive study involving 6 countries. He definitely did get results that matched his theory. The results showed a perfectly curvilinear correlation between saturated fat intake, cholesterol levels and coronary mortality. There was one slight problem with this though. He had data available for 22 countries and cherry picked the countries that supported his theory, and deleted all the findings from the other countries. Researchers quickly found this out, and included data from the other countries which at the end of the day, blew away his theory. Keys wouldn’t let go though. He then did another massive study called “The 7 Country Study” where he did THE EXACT SAME THING. He picked Finland, Greece, Italy, Japan, Yugoslavia, the Netherlands, and the USA. He was once again called out by many experts. The bottom line was that had he picked Israel, France, Sweden, etc (other countries), he would have actually proved that the MORE saturated fat and cholesterol one ate, the lower the risk of CHD.

Now here is where this gets even more seedy. Keys was on the nutrition adivisary committe for guess who? Yes, the Amercian Heart Association....well as you can guess, they incorporated his theories into their doctrine, and BOOM....so begins the anti saturated fat movement, based off some horrible studies...

Tomorrow I want to post about some more studies...then we'll start to get into what cholesterol is, and more about it's function within the body...


JM

The book Muscle, Smoke, & Mirrors covers this topic extensively. It really was an "eye-opening" experience reading about this! One reason why I'll never allow my Doc to prescribe me any "statins"!!!
 

Staff online

  • pesty4077
    Moderator/ Featured Member / Kilo Klub
  • LATS
    Moderator / FOUNDING Member / NPC Judge
  • rAJJIN
    Moderator / FOUNDING Member

Forum statistics

Total page views
558,063,035
Threads
135,759
Messages
2,768,705
Members
160,343
Latest member
12cc
NapsGear
HGH Power Store email banner
your-raws
Prowrist straps store banner
infinity
FLASHING-BOTTOM-BANNER-210x131
raws
Savage Labs Store email
Syntherol Site Enhancing Oil Synthol
aqpharma
yourmuscleshop210x131
hulabs
ezgif-com-resize-2-1
MA Research Chem store banner
MA Supps Store Banner
volartek
Keytech banner
musclechem
Godbullraw-bottom-banner
Injection Instructions for beginners
Knight Labs store email banner
3
ashp131
YMS-210x131-V02
Back
Top