Also see:
Heart Arrhythmia
Thyroid Status and Cardiovascular Disease
Hypothyroidism and Shift in Death Patterns
A Cure for Heart Disease
Unsaturated Fats and Heart Damage
Oral Contraceptives, Estrogen, and Clotting
Estrogen Dominance and Magnesium Deficiency
Quote by Ray Peat, PhD:
“A basic property of the heart muscle is that when it beats more frequently, it beats more strongly. This is called the staircase effect, from the way a tracing of it motion rises, beat by beat, as the rate of stimulation is increased. This is a logical way to behave, but sometimes it fails to occur: In shock, and in heart failure, the pulse rate increases, without increasing the volume of blood pumped in each contraction.
Szent-Gyorgyi found that estrogen treatment decreased the staircase effect, while progesterone treatment increased the staircase. He described the staircase as a situation in which function (the rate of contraction) builds structure (the size of contraction). Progesterone allowed “structure” to be built by the contraction, and estrogen prevented that.”
“Estrogen (which is increased in men who have had heart attacks) is another factor which decreases the heart’s stroke volume, and estrogen is closely associated with the physiology of the free unsaturated fatty acids.”
“Estrogen itself intensifies all of these changes of hypothyroidism, increasing permeability and edema, and decreasing the force of the heart-beat, impairing the diastolic relaxation. Besides its direct actions, and synergism with hypothyroidism, estrogen also chronically increases growth hormone, which causes chronic exposure of the blood vessels to higher levels of free fatty acids (with a bias toward unsaturated fatty acids), and promotes edema and vascular leakage. Hyperestrogenism, like hypothyroidism, tends to produce dilution of the body fluids, and is associated with increased bowel permeability, leading to endotoxemia; both dilution of the plasma and endotoxemia impair heart function.
Progesterone’s effects are antagonistic to estrogen’s:. Progesterone decreases the formation of nitric oxide, decreasing edema; it strengthens the heart beat, by improving venous return and increasing stroke volume, but at the same time it reduces peripheral resistance by relaxing arteries (by inhibiting calcium entry but also by other effects, and independently of the endothelium) and decreasing edematous swelling.
…
During the years that men are beginning to have a considerable risk of heart attacks, with declining thyroid function indicated by lower T3, their testosterone and progesterone are declining, while their estrogen is rising. Men who have heart attacks have much higher levels of estrogen than men at the same age who haven’t had a heart attack.
Whether the issue is free radical damage, vascular permeability with fat deposition, vascular spasm, edema, decreased heart efficiency, or blood clotting, the effects of chronic estrogen exposure are counter-adaptive. Progesterone, by opposing estrogen, is universally protective against vascular and heart disease.
So far, the rule in most estrogen/progesterone research has been to devise experiments so that claims of benefit can be made for estrogen, with the expectation that they will meet an uncritical audience. In some studies, it’s hard to tell whether idiocy or subterfuge is responsible for the way the experiment was designed and described, for example when synthetic chemicals with anti-progesterone activity are described as “progesterone.” Since one estrogen-funded researcher who supposedly found progesterone to be ineffective as treatment for premenstrual syndrome practically admitted to me in conversation an intent to mislead, I think it is reasonable to discount idiocy as the explanation for the tremendous bias in published research.With the vastly increased resources in the estrogen industry, resulting from the product promotion “for the prevention of heart disease,” I think we should expect the research fraud to become increasingly blatant.
Rather than being “heart protective,” estrogen is highly heart-toxic, and it is this that makes its most important antagonist, progesterone, so important in protecting the heart and circulatory system.” -Ray Peat, PhD
Arteriosclerosis. 1986 Jul-Aug;6(4):418-21.
Sex hormone levels in young Indian patients with myocardial infarction.
Sewdarsen M, Jialal I, Vythilingum S, Desai R.
The finding of abnormal levels of sex hormones in men with coronary artery disease has led to the hypothesis that alterations in sex hormones may represent an important risk factor for myocardial infarction. In this study, the sex hormone profile of 28 young men (aged less than 40 years) with myocardial infarction was compared with 28 age- and weight-matched normal men. Although the mean total serum estradiol levels and the free estradiol index of the patients and controls were similar, the mean serum total testosterone level and the free testosterone index were significantly lowered in the patients with myocardial infarction (p less than 0.01). The ratio of serum estradiol to testosterone was significantly increased in the patients (p = 0.0005) and correlated with serum cholesterol, triglycerides, and plasma glucose. A significant inverse correlation was also demonstrated between total testosterone and serum cholesterol and triglycerides. Hence, the results of this study support the hypothesis that low plasma testosterone and an increased estradiol-to-testosterone ratio may be important risk factors for myocardial infarction.
Atherosclerosis. 1990 Aug;83(2-3):111-7.
Abnormalities in sex hormones are a risk factor for premature manifestation of coronary artery disease in South African Indian men.
Sewdarsen M, Vythilingum S, Jialal I, Desai RK, Becker P.
The relation between sex hormone levels and myocardial infarction was studied in a case-control study among 117 Indian men with myocardial infarction aged 30-60 years and in 107 healthy Indian male controls. The patients and controls were further divided into subsets defined by age in decades. In the total patient population, testosterone concentration was significantly lower than in the controls (P less than 0.01), whilst oestradiol (P less than 0.0005) and the oestradiol to testosterone ratio (P less than 0.0005) were significantly higher. Multivariate stepwise logistic regression analyses demonstrated that free testosterone index, the free oestradiol index, and the oestradiol to testosterone ratio were significantly associated with myocardial infarction, and that this association was independent of age, body mass index, smoking and serum lipids. Further analyses according to age subsets revealed that compared to respective control groups, patients in the 4th decade had both significant hypotestosteronaemia and hyperoestrogenaemia, whereas in patients of the 5th decade significant differences in total and in the calculated free oestradiol index were noted, and in the 6th decade a significant difference was detected only in the free oestradiol index. Hence, we conclude that aberrations in endogenous sex hormones are significantly associated with myocardial infarction, and that this association appears to be strongest in young men and diminishes with age, suggesting that these disturbances in sex hormones may be associated with premature manifestation of coronary artery disease.
Am J Med. 1982 Dec;73(6):872-81.
Serum estrogen levels in men with acute myocardial infarction.
Klaiber EL, Broverman DM, Haffajee CI, Hochman JS, Sacks GM, Dalen JE.
Serum estradiol and serum estrone levels were assessed in 29 men in 14 men in whom myocardial infarction was ruled out; in 12 men without apparent coronary heart disease but hospitalized in an intensive care unit; and in 28 men who were not hospitalized and who acted as control subjects. (The 12 men who were hospitalized but who did not have coronary heart disease were included to control for physical and emotional stress of a severe medical illness.) Ages ranged from 21 to 56 years. Age, height, and weight did not differ significantly among groups. Blood samples were obtained in the patient groups on each of the first three days of hospitalization. The serum estrone level was significantly elevated in all four patient groups when compared with that in the control group. Estrone level, then, did not differentiate patients with and without coronary heart disease. Serum estradiol levels were significantly elevated in the groups with myocardial infarction, unstable angina, and in the group in whom myocardial infarction was ruled out. However, estradiol levels were not significantly elevated in the group in the intensive care unit without coronary heart disease when compared to the level in the normal control group. Serum estradiol levels, then, were elevated in men with confirmed or suspected coronary heart disease but were not elevated in men without coronary heart disease even under the stressful conditions found in an intensive care unit. Serum estradiol levels were significantly and positively correlated (p less than 0.03) with serum total creatine phosphokinase levels in the patients with myocardial infarction. The five patients with myocardial infarction who died within 10 days of admission had markedly elevated serum estradiol levels. The potential significance of these serum estradiol elevations is discussed in terms of estradiol’s ability to enhance adrenergic neural activity and the resultant increase in myocardial oxygen demand.
Lancet. 1976 Jul 3;2(7975):14-8.
Evidence for hyperoestrogenaemia as a risk factor for myocardial infarction in men.
Phillips GB.
Fifteen men who had had a myocardial infarction between the ages of 32 and 42 years were compared with fifteen age-matched healthy men. Seven of the patients had a strikingly slow rate of beard growth, three had evidence of gynaecomastia, and three had a loss of libido. The slow beard growth and decreased libido, and possibly the gynaecomastia, preceded the myocardial infarction. Mean serum oestradiol and oestrone concentrations were significantly increased in the patients, 43.5 +/- 8.8 (standard deviation) and 50.7 +/- 9.5, respectively, compared wth 33.5 +/- 5.5 and 37.5 +/- 5.8 pg/ml in the controls (p less than 0.001). Mean serum testosterone and dihydrotestosterone concentrations were not significantly different in the two groups. Serum oestradiol and oestrone concentrations were directly proportional to each other as were those of testosterone and dihydrotestosterone. These results suggest that the hyperoestrogenaemia preceded the myocardial infarction and that hyperoestrogenaemia may be an important risk factor for myocardial infarction in men.
Arch Intern Med. 1982 Jan;142(1):42-4.
Relationship between sex hormones, myocardial infarction, and occlusive coronary disease.
Luria MH, Johnson MW, Pego R, Seuc CA, Manubens SJ, Wieland MR, Wieland RG.
An alteration in sex hormones has been considered a risk factor for myocardial infarction. In this study, estradiol (E2) and testosterone (T) levels were evaluated in healthy firefighters, patients with myocardial infarction acutely and during their convalescence, patients with no evidence of occlusive coronary artery disease on arteriography, and patients with chronic angina pectoris in whom there was at least one vessel that indicated 50% occlusive coronary artery disease. Although T levels were similar in all groups, E2 levels were substantially higher in patients with myocardial infarction and in patients with chronic angina pectoris. These results support the hypothesis that elevated estrogen levels may be a risk factor for myocardial infarction and coronary artery disease, possibly by promoting clotting or coronary spasm.
Arteriosclerosis, Thrombosis, and Vascular Biology. 1996; 16: 1383-1387
The Association of Hyperestrogenemia With Coronary Thrombosis in Men
Gerald B. Phillips; Bruce H. Pinkernell; Tian-Yi Jing
Both hyperestrogenemia and hypotestosteronemia have been reported in association with myocardial infarction (MI) in men. It was previously observed that the serum testosterone concentration correlated negatively with the degree of coronary artery disease (CAD) in men who had never had a known MI. The present study investigated the relationship of sex hormone levels to the thrombotic component of MI by comparing these levels in 18 men who had had an MI (ie, thrombosis) and 50 men with no history of MI (ie, no thrombosis) whose degree of CAD was in the same range. The mean degree of CAD, age, and body mass index in these two groups was not significantly different. The mean serum estradiol level in the men who had had an MI (38.5±8.8 pg/mL) was higher (P=.002) than the level in the men who had not had an MI (31.9±7.1 pg/mL). The mean levels of testosterone, free testosterone, sex hormone–binding globulin, insulin, dehydroepiandrosterone sulfate, cholesterol, HDL cholesterol, and systolic and diastolic blood pressure did not differ significantly. Estradiol was the only variable measured that showed a significant relationship to MI (P<.003 by multivariate logistic regression). These findings suggest that hyperestrogenemia may be related to the thrombosis of MI.
Am J Med. 1983 May;74(5):863-9.
Association of hyperestrogenemia and coronary heart disease in men in the Framingham cohort.
Phillips GB, Castelli WP, Abbott RD, McNamara PM.
The serum levels of estradiol and testosterone as well as established risk factors for coronary heart disease were estimated in 61 men (mean age 70.0 +/- 6.4 [SD] years) with coronary heart disease and in 61 matched control subjects enrolled in the Framingham Heart Study. The mean serum estradiol level was significantly higher in the subjects with coronary disease (p = 0.011). This difference in estradiol level increased with the exclusion of subjects older than 75 years (p less than 0.001). The mean serum testosterone level was not significantly different. None of the established risk factors for coronary heart disease was different between subjects with coronary disease and control subjects except blood glucose level, which was higher in the subjects with coronary disease (p = 0.025). We conclude that hyperestrogenemia is an important correlate of coronary heart disease in men.
