Quote from: Ms Grace on December 16, 2016, 03:08:17 PMAs long as your diet is low in saturated fats
A 2016 study found
Food Nutr Res. 2016 Sep 27;60:31694."Our results do not support the association between CVDs and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link CVD risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with CVDs, these findings show that current dietary recommendations regarding CVDs should be seriously reconsidered."
CVD = cardiovascular disease
Ann Intern Med. 2014 Mar 18;160(6):398-406."Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats."
Am J Clin Nutr. 2010 Mar;91(3):535-46."A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD."
CHD = coronary heart disease
BMJ 2013; 347"An influential Swedish health organisation has recommended a diet that is low in carbohydrates but not low in fat for people who are overweight or obese or have diabetes.
The advice from the Swedish Council on Health and Technology Assessment is the result of a two year review of 16 000 scientific studies of diet. The recommendation contradicts the generally held belief that people should avoid foods that are rich in fat, especially those high in saturated fat."
Am J Clin Nutr. 2016 Feb;103(2):356-65."The association between saturated fatty acid (SFA) intake and ischemic heart disease (IHD) risk is debated."
"During 12 y of follow-up, 1807 IHD events occurred. Total SFA intake was associated with a lower IHD risk (HR per 5% of energy: 0.83; 95% CI: 0.74, 0.93)."
"In this Dutch population,
higher SFA intake was not associated with higher IHD risks."
Regarding clotting, a few things worth mentioning:
- bio-identical (estradiol or estradiol valerate) is much safer and if taken non-orally, the risk is negligible and may even REDUCE.
ORAL
Exp Clin Endocrinol Diabetes. 2005 Dec;113(10):586-92."Sixty male-to-female transsexuals were treated with monthly injections of gonadotropin-releasing hormone agonist (GnRHa) and oral oestradiol-17beta valerate for 2 years to achieve feminisation until SRS."
"Two side effects were documented.
One, venous thrombosis, occurred in a patient with a homozygous MTHFR mutation. One patient was found to be suffering from symptomatic preexisting gallstones. No other complications were documented. Liver enzymes, lipids, and prolactin levels were unchanged."
1 incidence out of 60.
Estradiol levels ranged from 325-1183 pmol/L, at 12-24 months.
Average age was 38.37 yrs old (SD 11.36).
J Sex Med. 2016 Nov;13(11):1773-1777."CSHT in the United States typically includes estradiol with the antiandrogen spironolactone"
"A retrospective chart review of transgender women who had been prescribed oral estradiol at a District of Columbia community health center was performed."
"The primary outcomes of interest were deep vein thrombosis or pulmonary emboli."
"From January 1, 2008 through March 31, 2016, 676 transgender women received oral estradiol-based CSHT for a total of 1,286 years of hormone treatment and a mean of 1.9 years of CSHT per patient.
Only one individual, or 0.15% of the population, sustained a VTE, for an incidence of 7.8 events per 10,000 person-years."
Journal of Clinical & Translational Endocrinology 2 (2015) 55-60"Other compelling data suggest that the incidence of venous thromboembolism (VTE) among transgender women appears associated with the presence of a hypercoaguable risk factor, including the use of an especially thrombogenic estrogen (ethinyl estradiol) which is no longer used [3].
Gooren et al. (2008), reported no increase in VTE among 2236 male-to-female (MTF) transgender individuals on HT from 1975 to 2006 compared with controls, with the exception of those who used ethinyl estradiol, for which there was a 6-8% incidence [4]."
NON-ORAL
Fertil Steril. 2010 Mar 1;93(4):1267-72."Standard MtF cross-sex hormone therapy at our department
includes transdermal 17ß-estradiol (...), oral
cyproterone acetate (...), and oral finasteride (...) and is reduced
to the administration of transdermal 17ß-estradiol (...) after sex-reassignment
surgery."
"Activated protein C resistance was detected in 18/251 patients (7.2%), and protein C deficiency was detected in one patient (0.4%).
None of the patients developed VTE under cross-sex hormone therapy during a mean of 64.2 +/- 38.0 months. There was no difference in the incidence of thrombophilia comparing MtF and FtM transsexuals (8.0% [13/162] vs. 5.6% [5/89], respectively)."
"
VTE during cross-sex hormone therapy is rare. General screening for thrombophilic defects in transsexual patients is not recommended. Cross-sex hormone therapy is feasible in MtF as well as in FtM patients with aPC resistance."
Biochem Pharmacol. 2013 Dec 15;86(12):1627-42."There was no increase in VTE risk with the use of transdermal estrogen,
even in patients with pre-existing thrombophilia [15]."
Cancer. 2005 Feb 15;103(4):717-23."Patients with prostate
carcinoma progressing after primary hormonal therapy received TDE"
TDE = transdermal estradiol (high dose)
"The mean (+/-95% CI) serum estradiol level
increased from 17.2
pg.mL (range, 14.8-19.6 pg/mL) to 460.7 pg/mL
(range, 334.6-586.7 pg/mL)."
"No change in factor VIII activity, F 1.2, or
resistance to activated protein C was observed, whereas a modest
decrease in the protein S level was observed. CONCLUSIONS: In
patients with APIC, TDE was well tolerated and produced a modest
response rate, but
was not associated with thromboembolic
complications or clinically important changes in several coagulation
factors."
Median age of patients was 75 (49-91).J Urol. 2005 Aug;174(2):527-33; discussion 532-3.
Transdermal estradiol therapy for prostate cancer reduces
thrombophilic activation and protects against thromboembolism."Levels of VIIa and XIIa were unaffected by transdermal estradiol therapy. Although levels of TAT III were increased in some patients at 12 months, the increase was markedly less than that observed historically with equivalent doses of oral estrogens. Levels of the inhibitory and fibrinolytic factors including protein C, protein S, APC-R, TPA and PAI-1 remained stable. Reductions in F1+F2, fibrinogen and D-Dimer levels represented a normalization from increased levels to the physiological range."
"
These results suggest that transdermal estradiol reduces thrombophilic activation in men with advanced prostate cancer, and protects against the risk of thrombosis."
Prostate 1989;14(4):389-95
Estrogen therapy and liver function--metabolic effects of oral and parenteral
administration."Oral administration of synthetic estrogens has profound effects on
liver-derived plasma proteins, coagulation factors, lipoproteins, and
triglycerides, whereas
parenteral administration of native estradiol
has very little influence on these aspects of liver function."
Synthetic estrogens = estrogens that aren't bio-identical
- DVT, regardless of estrogen, will also inevitably occur, sooner or later, in a population. Cause and effect can only be established once it occurs more often than expected.
- Consider that pregnant women have levels as high as 75,000 pg/ml of estradiol and yet their risks of DVT are only 0.1% and risk of pulmonary embolism is 0.01%.
I'm not a doctor and I only report what the research has found.
