Quote from: xFreya on April 04, 2016, 04:52:39 PM
So I went to endo appointment today with some blood tests, some ultrasound and EKG she requested. Only issue except low Vitamin D was my high cholesterol. about 280 total, 60 hdl, 190 ldl, and triglycerids 156 or something like that. (it is ok to share these right?) I am mtf, 21, 172 cm 69 kg, don't smoke and my parents also had high cholesterol some years ago although not as high (we don't know their current levels).
She wants me to do some changes to my diet and see a month later if it drops to more normal levels before having me start hormones, and she seemed to genuinely believe that it is necessary.
Has anyone experienced this? Is it really a big risk or is she being too wary? If it is risky, what about non trans women? If a cis woman has high cholesterol levels, would her naturally high estradiol also pose an additional risk? Should I get a second opinion from another endocrinologist? I am also considering getting the blood test done again in case they made a mistake.
I am really tired of waiting, I wanted this since 2012 or earlier, after some bad experience with another therapist and a lot of other stuff in my life, I restarted with an experienced therapist at August last year, I had to go through about 7 months of therapy that I did not really need only to get the report and now this. 
That being said I do care about my health too. What should I do? 
First, cholesterol on its own is not a powerful predictor of risk of heart disease. Rather, one must have a good cholesterol: HDL ratio (in your case, seems ok, average risk), a good LDL:HDL ratio (same, ok, average risk) and not too high triglycerides (which, in your case, is ok). Things could be better.
http://www.exrx.net/Testing/LDL%26HDL.htmlOne way to improve these markers is by eating less carbs which will reduce your triglycerides and eating more saturated fat (studies have shown no association or no causal relationship between it and heart disease) which will raise your HDL while maintaining a good ratio with LDL and cholesterol. In my case my cholesterol was VERY high, but my HDL also very high and triglycerides low so my risk remained very low.
It's not all about the cholesterol or even LDL, where size of particle matters most.
Vasc Health Risk Manag. 2009; 5: 757–765.
"Total/high-density lipoprotein (HDL) cholesterol and LDL/HDL cholesterol ratios are risk indicators with greater predictive value than isolated parameters used independently, particularly LDL."
Nature Genetics 45, 1345–1352 (2013)"These results suggest that triglyceride-rich lipoproteins
causally influence risk for CAD."
Eur Heart J. 2015 Mar 1;36(9):539-50."This study confirmed the causal role of LDL-c in CHD risk, and provides support for a causal role of TGs in CHD. The existence of a causal link between HDL-c levels and CHD is less certain, although possible."
"The findings may suggest that a treatment that lowers TGs as well as increases HDL-c levels may be beneficial in the prevention of CHD events, while only targeting TGs may not be effective. The role of HDL-c on CHD risk requires further investigation."
Nutrition & Metabolism 2006 3:24"The level of LDL cholesterol is generally considered the most clinically useful marker for cardiovascular disease (CVD) and there seems little question that reduction in LDL, especially if effected by administration of statins, is accompanied by substantial reduction in the risk of cardiovascular events. The importance of LDL as a primary marker, however, must be tempered by observations that LDL is not homogeneous and atherogenicity appears to be a function of particle size: small dense LDL particles are more atherogenic [10]."
"The atherogenicity of a greater number of small LDL particles is reflected in an increase in apolipoprotein B (apoB) since each atherogenic lipoprotein particle contains one molecule of apoB and total LDL would bias results towards lower risk. Barter et al. [11] summarized evidence that apoB is a more reliable indicator of risk than LDL and further that the apoB/apoA-I ratio is superior to conventional cholesterol ratios. Finally, circulating TAG is of considerable importance in this discussion because it is mechanistically linked to the formation of atherogenic particles, and is highly sensitive to dietary manipulation."
Lancet. 2001 Aug 4;358(9279):351-5."Only the group with low cholesterol concentration at both examinations had a significant association with mortality (risk ratio 1.64, 95% CI 1.13-2.36)."
"We have been unable to explain our results. These data cast doubt on the scientific justification for lowering cholesterol to very low concentrations (<4.65 mmol/L) in elderly people."
Int J Clin Pract Suppl. 2009 Oct;(163):1-8, 28-36."The degree to which serum cholesterol is increased by dietary cholesterol depends upon whether the individual's cholesterol synthesis is stimulated or down-regulated by such increased intake, and the extent to which each of these phenomena occurs varies from person to person. Several recent studies have shed additional light on the specific interplay between dietary cholesterol and cardiovascular health risk. It is evident that the dynamics of cholesterol homeostasis, and of development of CHD, are extremely complex and multifactorial. In summary, the earlier purported adverse relationship between dietary cholesterol and heart disease risk was likely largely over-exaggerated."
Adv Nutr. 2013 May 1;4(3):294-302."The focus on dietary manipulation of serum cholesterol may be moot in view of numerous other factors that increase the risk of heart disease. The adverse health effects that have been associated with saturated fats in the past are most likely due to factors other than SFAs, which are discussed here. This review calls for a rational reevaluation of existing dietary recommendations that focus on minimizing dietary SFAs, for which mechanisms for adverse health effects are lacking."
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."
Nutrition. 2012 Feb;28(2):118-23."All three reports included the effect of saturated fat on low-density lipoprotein cholesterol in the evidence linking saturated fat to cardiovascular disease, but the effect on high-density lipoprotein cholesterol was systematically ignored. Both U.S. reports failed to correctly describe the results from the prospective studies. Results and conclusions about saturated fat intake in relation to cardiovascular disease, from leading advisory committees, do not reflect the available scientific literature."
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."
In respect to hormones, oral estradiol will raise HDL but also triglycerides to a certain extent. Here is a summary of other findings with HRT:
Diabetologia
June 1997, Volume 40, Issue 7, pp 843-849"Oestrogen replacement therapy is associated with a decreased risk of cardiovascular disease in postmenopausal women. Patients with non-insulin-dependent diabetes mellitus (NIDDM) have an increased cardiovascular risk."
"In a double blind randomized placebo controlled trial we assessed the effect of oral 17 β -estradiol during 6 weeks in 40 postmenopausal women with NIDDM."
"
Oestrogen replacement therapy improves insulin sensitivity in liver, glycaemic control, lipoprotein profile and fibrinolysis in postmenopausal women with NIDDM."
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. The observations that the SE group showed reduced fasting insulin and WHR suggest that supra-normal circulating concentrations of estradiol, delivered subcutaneously, may beneficially influence insulin metabolism."
Acta Endocrinol (Copenh). 1986 Mar;111(3):419-23."Lipoprotein and steroid hormone levels were measured in 61 bilaterally oophorectomised women who had been treated for 3 years with implants containing either oestradiol alone or oestradiol plus testosterone. The lipoprotein levels associated with each of the two therapy regimens were compared. In addition, lipoproteins were measured in 67 untreated bilaterally oophorectomised age-matched women and compared with those of the treated women. Despite the high oestradiol levels produced by both types of implant,
the only significant finding was a reduced LDL cholesterol in the oestrogen/testosterone treated group as compared with that of the untreated group."
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"
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 (HIGH dose)
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 levels obtained, there was no significant change found in the other parameters during and after treatment."
Drugs Aging. 2000 Nov;17(5):399-410."Unopposed estradiol therapy seems to have a favourable effect on lipid profile and glucose tolerance whereas addition of a progestogen may attenuate these favourable metabolic changes." (the type of progestogen is important. Micronized bio-identical progesterone has shown to not attenuate these changes, please refer to study above, Lipids Health Dis. 2012 Oct 9;11:133.)
"Present evidence suggests that short term unopposed oral estradiol therapy has a beneficial effect on glucose homeostasis, lipid profile"
Quote from: AnonyMs on April 04, 2016, 05:32:18 PM
I tried Vitamin D3 supplements first, but they didn't work very well on me. The injection's more convenient anyway. It needs to be D3 not the other one.
Taking D3 is also debatable as this form is the non-active form, not biologically active so that if you measure the active form, you will find you have enough so don't really need any Vitamin D. There has been no
causal relationship established between this vitamin and heart disease, or cancer.
QuoteThere's some controversy regarding statins.
I get the impression too many are taking it and it's driven mostly by money. So many really don't need it and if you eat healthy, you don't need it at all. Eating more fat, including saturated and cutting down on the refined carbs, empty calories will do a lot to improve health without having to resort to statins. Pharmaceutical companies don't want you to know this, hope you remain in the dark, as many do.
QuoteHowever I do note that in the UK deaths related to the problems its supposed to fix have dropped significantly since it was introduced.
Statins reduce risk by other mechanism not related to cholesterol. Also deaths could have dropped due to other reason, for instance, better interventions, more advanced care and technology, more people eating healthier...etc.
QuoteI think you need to watch out for side effects as well.
Yes. Lowering cholesterol too much does not appear to be healthy and can create all sorts of problems. In my opinion, more harmful than beneficial.
Thincs.org is an interesting site to explore this issue.
