Combined OCs and HRTs have similar effects, including increased risks of thrombosis and heart attacks.
Rapid response to:
Research
Main morbidities recorded in the women's international study of long duration oestrogen after menopause (WISDOM): a randomised controlled trial of hormone replacement therapy in postmenopausal women
Combined OCs and HRTs have similar effects, including increased risks of thrombosis and heart attacks.
Biological scientists must know that the actions of hormones do not
vary with the reasons for which they are given. It may be fashionable to
believe that contraceptive pills are different from HRT pills but, in
reality, the overall effects are the same including the increased risks of
vascular diseases.1
All combined contraceptive and menopausal pills are designed to act
predominantly like progesterone which is necessary to prevent endometrial
hyperplasia and endometrial cancer due to oestrogen dominance.2 The
biological power of combined pills is not obvious from the doses used as
the potency of different progestogens can vary more than 12 times.3 This
means that pill combinations with lower doses can be more powerful than
pills containing higher doses. Similar or identical doses of
norethisterone, norgestrel, levonorgestrel and medroxyprogesterone acetate
have been used for both contraception and HRT. Synthetic ethinyl
estradiol in contraceptive pills is more powerful than natural estradiol
or mares’conjugated urinary oestrogens in HRT. Therefore microgram doses
of synthetic oestrogen are used for contraception and milligram doses of
“natural” oestrogens are used for HRT pills but both will have, more or
less, the same effect.
In 3 studies the relative risk of thrombosis for oral contraceptive
users was 4.0, 4.1, and 6.0 respectively.4-6 In another 3 studies, the
relative risk of thrombosis for current HRT users was 2.1, 3.5, and 3.6.
The risks were double at 6.7- 6.9 for the first 1-12 months of use.7-9
The increased risk of myocardial infarction with oral contraceptives
for current versus past or never users was 4.65 in a World Health
Organisation study in 1997. The odds risk ratio for acute myocardial
infarction was 31 for hormone users over age 35 who did not smoke. The
risk increased massively to 400 for oral contraceptive users older than
age 35 who also smoked.10
Although the risk of thrombosis is higher for new users in their
first year, the risk also increases with longer term use. Therefore, it is
important to know the results for trial volunteers from the first time
they started to take hormones. It is unsatisfactory for randomised HRT
trials to give results from the date women were first randomised as many
would be continuing and many would be stopping long-term hormone use but
still have some residual effects. Relatively few women would be starting
first ever use. Such confusions underestimate the harmful effects of
taking hormones and have even led to spurious claims of benefit, including
prevention of heart attacks.
Thousands of genes are up or down regulated by both exogenous and
endogenous progesterone and oestrogen including many affecting blood
vessel development, vasoactive amine levels and clotting mechanisms. For
decades there has been considerable scientific and epidemiological
evidence of increases in thrombosis and heart attacks in young hormone
users long before the age of the menopause.
1 Grant ECG. Hormones, thrombosis and heart attacks. J Nutr Environ
Med 1998;8:159-167.
2 Grant ECG. Hormone balance of oral contraceptives. J Obstet
Gynaecol Br Commonwealth. 1967; 2 :75-9.
3 Dickey R P. Managing contraceptive pill patients. 1995 Essential
Medical Information Systems Inc, Durant, OK, 74702-1607, USA. pp 130-131.
4 World Health Organization Collaborative Study of Cardiovascular
Disease and Steroid Hormone Contraception (1995). Effect of different
progestagens in low oestrogen oral contraceptives on venous thromboembolic
disease. Lancet 1995; 346: 582-8.
5 Bloemenkamp KWM, Rosendaal FR, Helerhorst FM, et al. Enhancement by
factor V Leiden mutation of risk of deep-vein thrombosis associated with
oral contraceptives containing third-generation progestagen. Lancet 1995;
346: 1593±6.
6 Spitzer WO, Spitzer WO, Lewis MA, Heinemann LAJ, et al. On behalf
of the Transnational Research Group on Oral Contraceptives and the Health
of Young Women. Third generation of oral contraceptives and risk of venous
thromboembolic disorders: an international case-control study. BMJ 1996;
312: 83±8.
7 Daly E, Vessey MP, Hawkins MM, et al. Risk of venous
thromboembolism in users of hormone replacement therapy. Lancet 1996; 348:
977±80.
8 Jick H, Derby LE, Myers MW, et al. Risk of hospital admission for
idiopathic thromboembolism among users of postmenopausal oestrogens.
Lancet 1966; 348: 981±3.
9 Grodstein F, Stampfer MJ, Goldhaber SZ, et al. Prospective study of
exogenous hormones and risk of pulmonary embolism in women. Lancet 1966;
348: 983±7.
10 WHO Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Acute myocardial infarction and combined oral
contraceptives: results of an international case control study. Lancet
1997; 349: 1202±9.
Rapid Response:
Combined OCs and HRTs have similar effects, including increased risks of thrombosis and heart attacks.
Biological scientists must know that the actions of hormones do not
vary with the reasons for which they are given. It may be fashionable to
believe that contraceptive pills are different from HRT pills but, in
reality, the overall effects are the same including the increased risks of
vascular diseases.1
All combined contraceptive and menopausal pills are designed to act
predominantly like progesterone which is necessary to prevent endometrial
hyperplasia and endometrial cancer due to oestrogen dominance.2 The
biological power of combined pills is not obvious from the doses used as
the potency of different progestogens can vary more than 12 times.3 This
means that pill combinations with lower doses can be more powerful than
pills containing higher doses. Similar or identical doses of
norethisterone, norgestrel, levonorgestrel and medroxyprogesterone acetate
have been used for both contraception and HRT. Synthetic ethinyl
estradiol in contraceptive pills is more powerful than natural estradiol
or mares’conjugated urinary oestrogens in HRT. Therefore microgram doses
of synthetic oestrogen are used for contraception and milligram doses of
“natural” oestrogens are used for HRT pills but both will have, more or
less, the same effect.
In 3 studies the relative risk of thrombosis for oral contraceptive
users was 4.0, 4.1, and 6.0 respectively.4-6 In another 3 studies, the
relative risk of thrombosis for current HRT users was 2.1, 3.5, and 3.6.
The risks were double at 6.7- 6.9 for the first 1-12 months of use.7-9
The increased risk of myocardial infarction with oral contraceptives
for current versus past or never users was 4.65 in a World Health
Organisation study in 1997. The odds risk ratio for acute myocardial
infarction was 31 for hormone users over age 35 who did not smoke. The
risk increased massively to 400 for oral contraceptive users older than
age 35 who also smoked.10
Although the risk of thrombosis is higher for new users in their
first year, the risk also increases with longer term use. Therefore, it is
important to know the results for trial volunteers from the first time
they started to take hormones. It is unsatisfactory for randomised HRT
trials to give results from the date women were first randomised as many
would be continuing and many would be stopping long-term hormone use but
still have some residual effects. Relatively few women would be starting
first ever use. Such confusions underestimate the harmful effects of
taking hormones and have even led to spurious claims of benefit, including
prevention of heart attacks.
Thousands of genes are up or down regulated by both exogenous and
endogenous progesterone and oestrogen including many affecting blood
vessel development, vasoactive amine levels and clotting mechanisms. For
decades there has been considerable scientific and epidemiological
evidence of increases in thrombosis and heart attacks in young hormone
users long before the age of the menopause.
1 Grant ECG. Hormones, thrombosis and heart attacks. J Nutr Environ
Med 1998;8:159-167.
2 Grant ECG. Hormone balance of oral contraceptives. J Obstet
Gynaecol Br Commonwealth. 1967; 2 :75-9.
3 Dickey R P. Managing contraceptive pill patients. 1995 Essential
Medical Information Systems Inc, Durant, OK, 74702-1607, USA. pp 130-131.
4 World Health Organization Collaborative Study of Cardiovascular
Disease and Steroid Hormone Contraception (1995). Effect of different
progestagens in low oestrogen oral contraceptives on venous thromboembolic
disease. Lancet 1995; 346: 582-8.
5 Bloemenkamp KWM, Rosendaal FR, Helerhorst FM, et al. Enhancement by
factor V Leiden mutation of risk of deep-vein thrombosis associated with
oral contraceptives containing third-generation progestagen. Lancet 1995;
346: 1593±6.
6 Spitzer WO, Spitzer WO, Lewis MA, Heinemann LAJ, et al. On behalf
of the Transnational Research Group on Oral Contraceptives and the Health
of Young Women. Third generation of oral contraceptives and risk of venous
thromboembolic disorders: an international case-control study. BMJ 1996;
312: 83±8.
7 Daly E, Vessey MP, Hawkins MM, et al. Risk of venous
thromboembolism in users of hormone replacement therapy. Lancet 1996; 348:
977±80.
8 Jick H, Derby LE, Myers MW, et al. Risk of hospital admission for
idiopathic thromboembolism among users of postmenopausal oestrogens.
Lancet 1966; 348: 981±3.
9 Grodstein F, Stampfer MJ, Goldhaber SZ, et al. Prospective study of
exogenous hormones and risk of pulmonary embolism in women. Lancet 1966;
348: 983±7.
10 WHO Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Acute myocardial infarction and combined oral
contraceptives: results of an international case control study. Lancet
1997; 349: 1202±9.
Competing interests:
None declared
Competing interests: No competing interests