Quote from: Pipes on December 14, 2016, 07:13:03 PM
My endo is of the opinion that that anything higher than 200 is not advisable.
I wonder what your endo's opinion of ciswomen is, since their levels are as high as 650 pg/ml during a menstrual cycle, or levels as high as 75,000 pg/ml during pregnancy? Have they consulted studies on women, men and even transsexual women where high levels were attained with minimal or no side-effects?
QuoteNot sure what to make of these results...
Use your common sense and intelligence. You will soon know what to make of these findings. Do some research, read actual studies, talk to other doctors.
QuoteAm I harming/decreasing/stunting my feminization by following his 'playing it safe' regimen???
Not necessarily. Some do very well on lower levels, some need more. Individuals vary. Your doctor and you, ideally together, should figure out what is best for you, for your feminization and health. If you're doubting your doctor's credibility and position, you can always go see other experts in the matter, get a second and third opinion.
Two other things worth mentioning:
- the female range is WIDE and even overlaps that of men so chances are wherever you may be, low, medium, high or very high, you are in female range.
- levels vary from one moment to another so that levels may be quite different depending on when your blood is drawn. So while a target is desired, levels may exceed or be below it, at various points in time, and sometimes be within that target range. So, I ask you, are blood tests for this purpose really useful?
Quote from: Clara Kay on December 14, 2016, 08:56:54 PM
I'm convinced that there is no agreement on what level is best for trans women either before or after GRS.
Because individuals VARY in their requirements. Is the same concentration of alcohol in the blood going to have the same effect in every person? Or even in the same person at different times?
Quote from: EmilyMK03 on December 15, 2016, 04:55:15 AM
Every body is different. For some, it may not be safe to have levels above 400. One of the primary concerns for people who are on E is the increased risk of developing deep vein thrombosis (DVT), a potentially deadly complication. This is much more likely to happen if you are overweight, less active, older, and/or are a smoker. If you have any of those risk factors, your doctor may be keeping your levels lower out of concern for your safety.
I have to add that type of estrogen is very important as bio-identical estradiol is more quickly metabolized by the body and has a significantly lower impact on coagulation. The route of administration also matters as the hormone is delivered directly into the blood and much less makes it to the liver and in the portal vein.
High levels, taken non-orally (intramuscular injections, patches, pellets), even in older populations of men (up to 700 pg/ml) and women (up to 3,200 pg/ml) have shown to have minimal to no side-effects and even desirable as they could PROTECT against the risk of thrombosis and improve cardiovascular morbidity and mortality. I have several times posted these studies.
QuoteThere is also an increased risk of developing higher cholesterol with higher levels of estrogen.
It's a little more complicated than that. Depends on the type of estrogen and route of administration. In general, it appears bio-identical estradiol is favorable, even more so, non-orally, regardless of levels.
Am J Obstet Gynecol. 1983 Sep 1;147(1):77-81"Oral administration of estradiol resulted in a significant increase in triglycerides (20% to 44%, p less than 0.05) and very low-density lipoprotein (VLDL) triglycerides (30% to 40%, p less than 0.05) and a decrease in low-density lipoprotein cholesterol (14% to 17%, p less than 0.05). In contrast,
despite a substantial increase in serum estrogen levels, percutaneous estradiol induced a significant decrease in triglyceride (from 0.78 +/- 0.04 to 0.67 +/- 0.05 mmol/L, p less than 0.001) and VLDL triglyceride (from 0.44 +/- 0.16 to 0.35 +/- 0.12 mmol/L p less than 0.05) levels and no significant change in cholesterol levels. The increases of high-density lipoprotein cholesterol levels observed in the three groups were not significant. These data indicate that the route of administration modulates the metabolic and hormonal responses to estrogen therapy."
Lipids Health Dis. 2012 Oct 9;11:133."The effects of intranasal and percutaneous estradiol were similar, regardless of the addition of progesterone. Similarly, for the overall group of 86 women, micronized progesterone did not alter the response to E2. Blood pressure, glucose, insulin, HDL-c, triglycerides, and usCRP remained constant with or without micronized progesterone.
Total cholesterol decreased after E2, and progesterone maintained this reduction. LDL-c levels were similar at baseline and with E2, and lower during E2+P in relation to baseline."
Hum Reprod. 2002 Mar;17(3):825-9."We examined metabolic parameters in cohorts of women with and without subcutaneous estrogen therapy
with concomitant supra-normal concentrations of estradiol (SE)."
"
Women with SE have similar triglyceride and HDL cholesterol levels but lower LDL cholesterol concentrations compared with post-menopausal women not taking ERT."
Acta Endocrinol (Copenh). 1986 Mar;111(3):419-23."
Despite the high oestradiol levels produced by both types of implant, the only significant finding was a reduced LDL cholesterol"
"Oral oestrogens have been shown to elevate HDL cholesterol and reduce LDL cholesterol (Tikkanen et al. 1978). Reports on the effects of parenteral oestrogen on lipoproteins have been conflicting. Fähraeus et al. (1982), who studied oestradiol-17ß, administered as a cream, and Buckmand et al. ( 1980). who studied depo-oestradiol cypionate noted little change in lipoproteins. However, Brook et al. ( 1982) found that sc oestrogen caused a marked increase in HDL cholesterol and reduced VLDL cholesterol and LDL cholesterol, whereas Lobo et al. (1980) found that oestrogen implants increased HDL cholesterol, the other lipid fractions remaining unchanged. In a previous study (Farish et al. 1984), we followed lipoprotein levels for 6 months in bilaterally oophorectomised women who were treated with sc implants containing either oestradiol alone or oestradiol and testosterone. We found that both therapv regimens lowered LDL cholesterol and the oestrogen only implants also caused an increase in HDL cholesterol."
CLIMACTERIC 2005;8(Suppl 1):3–63"Implants of estradiol showed only minor effects on lipid metabolism with a slight decrease in LDL cholesterol and a slight increase in HDL cholesterol"
"In women with supraphysiological estradiol levels during treatment with implants, no adverse effects on lipid metabolism, but a reduction in LDL cholesterol and fasting insulin were observed."
J Lipid Res. 2006 Feb;47(2):349-55."This prospective pilot study of 18 men with androgen-independent prostate cancer receiving ADT measured effects of TDE on lipid and inflammatory CVD risk factors before and after 8 weeks of TDE.
During treatment, estradiol levels rose 17-fold;
total cholesterol, LDL cholesterol, and apolipoprotein B levels decreased. HDL2 cholesterol increased, with no changes in triglyceride or VLDL cholesterol levels. Dense LDL cholesterol decreased and LDL buoyancy increased in association with a decrease in HL activity. Highly sensitive C-reactive protein levels and other inflammatory markers did not worsen. Compared with ADT, short-term TDE therapy of prostate cancer improves lipid levels without deterioration of CVD-associated inflammatory markers and may, on longer-term follow-up, improve CVD and mortality rates."
TDE = transdermal estradiol
ADT = androgen deprivation therapy
Aust N Z J Obstet Gynaecol. 1978 Aug;18(3):198-201."The effect of oestradiol valerate on levels of blood cholesterol, triglycerides, free oestradiol and coagulation factors, as well as on urinary oestrogens and free cortisol was measured in 10 oöphorectomised women.
Despite the very high urinary oestrogen levles obtained, there was no significant change found in the other parameters during and after treatment."
Maturitas. 1980 Jul;2(2):95-100."During the course the
serum estradiol level increased 5-6 fold from the postmenopausal levels."
"
No significant changes occurred in the serum triglycerides and total cholesterol, whereas in the control group the triglycerides decreased. The proportional concentration of beta-lipoproteins decreased. There was also a slight decrease in the pre-beta-lipoproteins. The proportional concentration of beta-lipoproteins increased, as also serum high density lipoprotein (HDL) cholesterol."
Fertil Steril. 2001 May;75(5):898-915."Two-hundred forty-eight studies provided information on the effects of 42 different HRT regimens.
All estrogen alone regimens raised HDL cholesterol and lowered LDL and total cholesterol. Oral estrogens raised triglycerides. Transdermal estradiol 17-beta lowered triglycerides."
Obstet Gynecol. 2015 Mar;125(3):605-10."All transgender women had estradiol levels at least in the physiologic female – range at 6 months,
with 3/16 (19%) having supraphysiologic levels > 1000pg/dl (including the one transgender woman using intramuscular estradiol valerate)."
Typo: should read 1,000 pg/ml
"transgender people receiving cross-sex hormone therapy
do not develop abnormal blood pressure or lipids in the short term."
Whether total cholesterol is a really important gauge of cardiovascular risk is seriously put into question by several findings from studies. Studies showing an association do not prove anything as there is no cause and effect established.
BMJ 2016;353:i1246"Unpublished documents with completed analyses for the randomized cohort of 9423 women and men aged 20-97; longitudinal data on serum cholesterol for the 2355 participants exposed to the study diets for a year or more; 149 completed autopsy files."
"Serum cholesterol lowering diet that replaced saturated fat with linoleic acid (from corn oil and corn oil polyunsaturated margarine). Control diet was high in saturated fat from animal fats, common margarines, and shortenings."
"The intervention group had significant reduction in serum cholesterol compared with controls (mean change from baseline −13.8% v −1.0%; P<0.001). Kaplan Meier graphs showed no mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup.
There was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol in covariate adjusted Cox regression models (hazard ratio 1.22, 95% confidence interval 1.14 to 1.32; P<0.001). There was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts. Systematic review identified five randomized controlled trials for inclusion (n=10 808). In meta-analyses, these cholesterol lowering interventions showed no evidence of benefit on mortality from coronary heart disease (1.13, 0.83 to 1.54) or all cause mortality (1.07, 0.90 to 1.27)."
BMJ 2016;353:i1512"As expected, the diet enriched with linoleic acid lowered serum cholesterol concentration. But it did not reduce mortality: in fact participants in the intervention group had a higher mortality than controls. The pooled results of the MCE and four similar trials failed to find any reduction in mortality from coronary heart disease.3 4 5 6"
N Engl J Med. 1977 Sep 22;297(12):644-50."
Two well designed contemporaneous27 , 28 trials showed that both niacin and clofibrate reduced cholesteremia by 15 to 20 per cent below starting levels, and yet neither drug had a measurable effect on the behavior of coronary heart disease after five years of observation. This is important evidence (Fig. 3 and 4) because the effect of drugs on cholesteremia is about twice that achieved by the most rigorous, fat-modified diets.29"
Lancet. 1995 Dec 23-30;346(8991-8992):1647-53."After standardization for age,
there was no association between blood cholesterol and stroke except, perhaps, in those under 45 years of age when screened. This lack of association was not influenced by adjustment for sex, diastolic blood pressure, history of coronary disease, or ethnicity (Asian or non-Asian)."
J Epidemiol Community Health. 2002 Feb; 56(Suppl 1): i19–i24."This analysis of the EUROSTROKE project
could not disclose an association of total cholesterol with fatal, non-fatal, haemorrhagic or ischaemic stroke."
Am J Med. 1977 May;62(5):707-14."Lipid and lipoprotein values, including fasting triglycerides and high density lipoproteins (HDL), low density lipoproteins (LDL) and total cholesterol levels, were obtained on
2,815 men and women aged 49 to 82 years chiefly between 1969 and 1971 at Framingham. In the approximately four years following the characterization of lipids, coronary heart disease developed in 79 of the 1,025 men and 63 of the 1,445 women free of coronary heart diseases."
"
At these ages total cholesterol was not associated with the risk of coronary heart disease."
Quote from: SadieBlake on December 15, 2016, 07:27:52 AM
225 made my endo happy. I need to get a blood test soon to see if adding prometrium has changed estrogen levels.
Volume 18a of Elsevier's New Comprehensive
Biochemistry, Titled 'Hormones and Their Actions, Part I', editors BA
Cooke, RJB King and HJ van der Molen. Published 1988. ISBN
0-444-80996-1. Dewey 612.405."Binding of progesterone to its receptors then leads not only to progestational effects, but also antiestrogenic
effects by causing a reduction in estrogen secretion into the systemic circulation; by stimulating the enzyme 17B-hydroxysteroid dehydrogenase which converts estradiol to the less active estrogen estrone"
Post Reproductive Health 2014, Vol. 20(2) 69–72"Micronised progesterone stimulates the 17 beta hydroxy steroid dehydrogenase transformation of
estradiol into less potent estrone E1. E1 competes poorly with estradiol E2 for binding to the estrogen
nuclear receptor and diffuses out of the target cells more easily than E2."
Quote from: DuchessBianca on December 15, 2016, 10:32:07 AM
My doctor tests levels but doesn't really put a lot of weight into them, how I feel/results are what matters most to him.
Personally, I think this makes the most sense. My 2 cents, I'm not a doctor.
QuoteThat being said I don't really know what levels my doctor does prefer and I can only assume that "in the female range" is what he prefers.
Female range is WIDE, from less 20 pg/ml (men have 10-30) to up to 650 pg/ml during cycle, to 75,000 during pregnancy.
QuoteMy first labs were at just about 3 months testosterone was 34 ng/dL and estradiol was 34 93 pg/mL, the latter is what my peak levels would be based on when I was tested after taking my sublingual tablet. Fast-forward to 1.5 weeks ago taken at 6.5 months my Testosterone is unknown as he didn't bother getting it tested but my serum estradiol jumped all the way to 151 pg/mL and that was 9 hours after my last sublingual tablet and 11 since my last spiro tablet so those are my rock bottom base levels, no clue what my peak levels would be. Guess my body made huge strides adapting/making better use of the estrogen in those 3.5 months.
Estradiol levels fluctuate.
Maturitas, 12 (1990) 171-197"When the serum concentrations of natural or synthetic sex steroids are measured
at short time-intervals after administration and repeatedly during long-term
treatment, it becomes obvious that there are large
intra-individual and interindividual
variations. This holds true for both the contraceptive steroids and the natural
oestrogens and does not apply solely to the oral route. Long-term studies
indicate that an important influence is exerted by predisposing factors, particularly
the metabolic capacity of the liver, on the pharmacokinetics of sex steroids.
Large variations in oestradiol and oestrone levels can be observed in an individual
woman from day to day or from hour to hour, even during transdermal therapy
with oestradiol"
