Women's Health Articles - General Medical ProblemsBy Date of Release Topic April 2, 2000 Controlling Hypertension Without Medicine October 31, 1999 Osteoporosis in Spite of Estrogen Replacement September 19, 1999 Idiopathic Cyclic Edema September 12, 1999 Facial Hair Growth After Menopause August 15, 1999 Cholesterol and Lipid Disorders August 8, 1999 Guidelines for Healthy Weight June 13, 1999 Cellulite - Is there hope? April 18, 1999 Malignant Melanoma Skin Cancers in Women March 7, 1999 Ulcer Symptoms and Helicobacter pylori January 24, 1999 Insulin Resistance Syndrome November 29, 1998 Involuntary Weight Loss Evaluation October 18, 1998 Low Back Pain -- When is Imaging Needed? September 20, 1998 Hormones and Hip Fractures in Older Women September 13, 1998 Heart Problems Caused by Diet Pills August 30, 1998 When is High Blood Pressure Hypertension? June 28, 1998 Diabetic Tendency in Polycystic Ovary Syndrome May 3, 1998 Menstrual Migraine Headache November 16, 1997 New Diabetes Diagnostic Categories October 27, 1997 Accuracy of Echocardiography in Women
This is a condition primarily of young menstruating women in which large amounts of tissue swelling (edema) occurs in the legs and abdomen after sitting or standing for periods of time and swelling of the face and eyelids upon lying down.
It is felt to be a problem of leakage of blood fluids from capillaries into fat and skin tissue especially when gravity (standing up) is added to the pressure in the vascular system. It results in large weight gain shifts from morning to evening.
Sometimes the condition is called idiopathic orthostatic (standing upright) edema or just idiopathic edema. Other names include fluid retention syndrome and cyclical edema.
This condition can result in moderate discomfort or pain in any of the areas of excess fluid accumulation. Carpal tunnel syndrome symptoms, diffuse aching, morning stiffness and muscle and bony pains as well as headaches often accompany the swelling.
It can also masquerade as premenstrual syndrome or make existing premenstrual syndrome worse. It exacerbates the swelling, abdominal bloating and general physical discomfort but it does not usually cause irritability and depressive symptoms as classic PMS does.
Sometimes the syndrome can occur in women with eating disorders who are taking diuretics or even laxatives in order to lose weight.
Some treatments seem to worsen idiopathic cyclic edema.
While one would think that taking a "water pill" or diuretic would improve this edematous condition, it turns out that in most cases this is the wrong long term treatment. In fact chronic diuretic use will increase the secretion of the body's aldosterone which in turn produces more edema.
If the chronic use of diuretics is discontinued, the cyclical swelling disappears in most cases within about 3 weeks.
Treatments for idiopathic cyclic edema
So how should idiopathic cyclic edema be treated? There are no clear cut answers. Birth control pills have been used (progesterone). It might well be worth trying captopril and ginkgo biloba. It is evident that diuretic pills should not be used.
There is no single, accepted gold standard treatment for idiopathic cyclic edema. Several different treatments have been reported. An older report indicates that the herb ginkgo biloba may be useful in treating this condition.
An agent used for treating high blood pressure called Captopril has also been used with success. It works against a kidney hormone called aldosterone which is elevated in this condition and causes excess salt and water retention.
Progesterone has also been used in the treatment of idiopathic edema under the premise that some women with idiopathic edema either do not ovulate or have a luteal phase deficiency (5).
Facial hair growth after menopause
One of our readers asks the following question:
I have recently noticed an increase in the fine hair growth on my face extending on both sides from in front of my ears, down my face toward the chin. What is causing this and what can I do about it?
I am 50 years old and about 10 years past an early menopause. About a year ago I started taking hormone replacement therapy and about 4 months ago I switched to an estrogen skin preparation compounded by a pharmacist to my doctor's prescription.
I have been putting the hormone lotion on my face instead of my inner arms. I follow that with a moisturizer, sometimes one with alpha and beta hydroxys, sometimes one without. About two weeks ago I started putting Retin A Cream® (my son's acne medication) on my face to get rid of wrinkles.
Don't laugh! In the mornings I use moisturizer again followed by sunscreen of SPF 15. I've had this "fuz" on my face for a long time but now it is getting longer. It is not thick hair that needs to be waxed but I don't like it. I also have used a dietary supplement 2 or 3 times a week that absorbs fat. It contains polyglucosamine but I've haven't used that in the last two weeks. -- Brenda C.
Menopause and facial hair growth
Increased growth of hair on the face of women just before and just after menopause is quite a common occurrence. It is primarily because of decreased estrogens. This is not the problem in your case because you are taking replacement estrogens, but let me explain about it because most women with your complaint will fall into this category.
Estrogens that a woman normally produces during her reproductive years stimulates a blood protein called sex hormone binding globulin (SHBG). This protein absorbs and holds any male hormones such as testosterone or DHEA which circulate in small amounts in all women.
These male hormones called androgens will stimulate hair to grow in a male pattern with beard, mustache, and abdominal hair growing up from the pubic area toward the navel and stimulate the growth of acne in the skin. When sex hormone binding globulin is high, it deactivates the androgens so that women do not have these male hair problems or acne. In fact the birth control pills that decrease acne do so because the estrogen in the pill increases SHBG.
Before menopause, when the ovaries do not ovulate regularly, estrogen levels drop and androgen levels are more free to stimulate hair growth and acne. That is why most menopausal and some perimenopausal women will notice increased facial hair growth.
In addition to requiring more free testosterone to have increased hair growth, there is another step in the process. The testosterone has to be converted in the skin to dihydrotestosterone by an enzyme called 5-alpha reductase. Dihydrotestosterone is really the culprit.
Therefore another mechanism that explains increased facial hair is if something stimulates 5 alpha reductase. I think in your case, that is what is going on. Let me further explain.
Two types of hair
The pattern of hair growth and the number of hair follicles is determined by time of birth. No new hair follicles develop after you are born; thus if a hair and its follicle is totally removed, it will not return. There are basically two types of hair, soft lanugo hair called vellus hair and a thicker, coarser hair called a terminal hair.
Vellus hair is all over the body except for the palms and soles. If vellus hair is stimulated, it is called "hypertrichosis". It sounds as if that is the problem you are describing. If vellus hair is changed to thick, coarse terminal hair, usually by "male hormone excess" (androgens), this is called hirsutism. Unless you are having a mustache or beard, it is unlikely that the problem is an increased level of testosterone.
Causes of hypertrichosis
As opposed to being born with an increased tendency toward faster hair growth, newly acquired hypertrichosis is most commonly due to medications. Hormonal substances such as testosterone, danazol, corticotrophin (ACTH), metyrapone, anabolic steroids (testosterone, DHEA) and glucocorticoids such as prednisone cause increased vellus and terminal hair growth as well as conversion of vellus to terminal hairs.
Hypertrichosis is a common adverse effect of cyclosporin, a chemotherapy drug, and minoxidil and diazoxide used for the treatment of hypertension. In fact minoxidil (Rogaine®) is the medication actively being sold to men who are balding. Retinoic acid (Retin A®) also stimulates hair growth similar to minoxil. It probably causes a skin irritation that stimulates 5 alpha reductase which governs sensitivity of the hair follicle to circulating androgens.
I could not find any evidence that polyglucosamine (chitosan) caused abnormal hair growth. I did however find a study that says it does not work to prevent fat absorption and to cause weight loss as it is being marketed to do.
Alpha and beta hydroxys refer to skin protein kinase C (PKC) isoforms. Apparently PKC alpha stimulates hair growth but if you could find a lotion with protein kinase C gamma in it, it might decrease hair growth.
Sunscreen often contains titanium dioxide and sometimes zinc oxide. I did not find evidence that sunscreens induced increased hair growth except it is important to keep in mind that any chemical that produces a skin irritation can stimulate the enzyme (5 alpha reductase) that makes thin vellus hair become thicker and grow faster.
While it is unlikely that you have any serious disease going on, there is a rare medical condition called porphyria cutanea tarda, a metabolic disorder of heme (hemoglobin) biosynthesis, that is characterized by hyperpigmentation of the skin, facial hypertrichosis, and dark urine.
It has been associated with excess alcohol ingestion, estrogen administration, iron overload, and several environmental liver toxins. Also, even rarer, internal metastatic cancer can be associated with an acquired hypertrichosis. If you were to notice your urine become very dark, or you have any general weight loss or increased fatigue, you should see your doctor to be checked out.
Effect of estrogens and progesterones on hair
Estrogens alone act the opposite of androgens. They slow the rate of growth and lead to finer, less pigmented and slower growing hair. Progestins or progesterones have very minimal direct effect on hair growth.
However when estrogen and progesterone are at very high levels such as during pregnancy, there is an increase in the hair growth becoming synchronous (all in the same phase together) so that there seems to be an increased growth followed months later by shedding of hair all at once as most of the follicles go into a resting phase.
In your case the estrogen skin lotion you use may make the hairs finer but it should not be stimulating growth.
My recommendation would be to stop the Retin A®. It is the most likely culprit. You should feel guilty for "borrowing" your son's medication. Also discontinuing use of the cream with the alpha and beta hydroxys would be wise and then after about 6 months, if the growth stops, you could try it again to see if it has much of an effect.
It may, according to animal evidence, but I would guess it would not cause nearly as much hair growth as the Retin A® which has actually been used to stimulate hair growth in those with abnormal hair loss.
top of page
Everyone tells us to watch our fat and cholesterol intake but it is apparent that some women are more genetically predisposed to have higher serum cholesterol values than others. Arteriosclerosis is caused by deposition of cholesterol in the wall of arteries but it is a combination of several lipoproteins (lipids) involved in the process including very low density lipoprotein (VLDL), remnant lipoprotein, and low density lipoprotein (LDL). There probably needs to be some injury to the blood vessel wall to facilitate this lipid deposition but basically the more lipid floating around in the bl
ood stream, the more that gets deposited in blood vessels. High density lipoprotein (HDL) carries away cholesterol from the arterial walls so it is called a "good" cholesterol. This is the cholesterol that is increased by postmenopausal estrogen replacement and that is naturally higher in women during their reproductive years before menopause.
Most of the time lipid levels can be kept in normal range by a reasonable diet, but some women will continue to have high cholesterol levels even when they stick to a low fat diet because they have a familial tendency to lipid disorders. A recent article, Knopp RH: Drug treatment of lipid disorders. N Engl J Med. 1999;341 (7):498-511, reviewed when high lipid levels should be treated with medical therapy in addition to diet.
What are the causes of hyperlipidemia?
There are several familial (genetic) conditions that lead to primary lipoprotein disorders.
|Familial combined hyperlipidemia||coronary artery disease,peripheral vascular disease, stroke|
|Remnant removal disease (familial dysbetalipoproteinemia)||coronary artery disease,peripheral vascular disease, stroke|
|Familial or polygenic hypercholesterolemia||coronary artery disease, occasionally peripheral vascular disease, stroke|
|Familial hypoalphalipoproteinemia (low HDL syndrome)||coronary artery disease, peripheral vascular disease, (may be associated with hypertriglyceridemia|
There are also many secondary causes for elevated cholesterol and if you have a high serum cholesterol value, these conditions should be treated or changed, if they can, prior to taking any lipid lowering medication.
- diabetes or insulin resistance
- nephrotic syndrome (kidney disease)
- alcohol ingestion
- antihypertensives (beta adrenergic antagonists)
- thiazide diuretics
- steroid medications
- acne treatment (isotretinoin)
- sertraline (Zoloft®) therapy
- Age, postmenopausal
- hypertension (even if treated)
- diabetes mellitus
- history of cardiovascular disease in first degree relatives (less than 65 years for women, male relatives less than 55 years of age)
- serum HDL cholesterol concentration less than 35 mg/dl
|Category||Dietary Therapy Threshold||Drug Therapy Threshold|
|Total cholesterol||LDL cholesterol||Total cholesterol||LDL cholesterol|
|0 or 1 risk factor for cardiovascular disease||240 mg/dl||160 mg/dl||275 mg/dl||190 mg/dl|
|2 or more risk factors for cardiovascular disease||200 mg/dl||130 mg/dl||240 mg/dl||160 mg/dl|
|existing cardiovascular disease||160 mg/dl||100 mg/dl||200 mg/dl||130 mg/dl|
What kind of diet is recommended as treatment for hyperlipidemia?
Low cholesterol diets have been divided into low (Step I diet) and lower (Step II diet). They can be begun sequentially or if conditions are bad enough to warrant drug therapy, you can go directly to Step II when treatment is begun. Step I diet contains no more than 30 percent of calories from fat, less than 10% of calories from fatty acids, and less than 300 mg of cholesterol per day.
A Step II diet restricts further by limiting the calories from saturated fatty acids to less than 7% a day and the cholesterol to less than 200 mg per day. This diet decreases LDL cholesterol concentrations 8-15%.
Why not just take medication to lower my cholesterol in case my diet plan is less than perfect?
Different drugs are used as treatment for hyperlipidemia but the most common ones are in a class called "statins". They are similar to building blocks of cholesterol and act as competitors so that real cholesterol is not manufactured.
These would include: lovastatin (Mevacor®), pravastatin (Pravachol®), simvastatin (Zocor®), atorvastatin (Lipitor®), fluvastatin (Lescol®), and cerivastatin (Baycol®). When given alone for the prevention of heart disease, these drugs can reduce coronary artery disease by 25-60% and reduce the risk of death from any cause by 30%. They can have serious side effects, however, so they are not routinely given for only slightly elevated cholesterol levels
Adverse side effects of statins
- gastrointestinal upset
- muscle aches
- muscle disease
- peripheral nerve inflammation
- lupus-like syndrome
It is to your advantage to learn the most about cholesterol that you can. It can play a role in heart disease which is a frequent cause of death and disability in women.
top of page