The Scarf Dust filter is more than glimmer glass, and more than black magic, and more than pro mist. There is another quality gold element to the subtle effects on skin tone. This filter combines some of the best effects from other filters together to make something rather special.
On skin, it gives a very subtle, lovely, smoothing effect, taking the edge off of more clinical modern lenses. With a lamp in the frame, it creates a very nice glow effect, coupled with the anamorphic aspects, it then becomes a stretched out halo or veiling flare.
RevBar Glow Effects
ERT has been shown clinically to improve vasomotor symptoms and totally eradicates them in most women.56,57 If a patient is unable to take estrogen, progestins have been shown to be effective in reducing hot flushes. Oral medroxyprogesterone acetate (MPA) (20 to 40 mg/day),58 depo-MPA (150 mg given intramuscularly every 3 months),59 or megestrol acetate (40 to 80 mg/day) decreases patient distress. Other agents suggested for the treatment of vasomotor instability include clonidine, naloxone, methyldopa, and a mixture of phenobarbital, ergotamine, and belladonna (Bellergal). The most carefully studied of these other agents is clonidine.46 Large doses of clonidine of up to 400 μg daily reduce the number of objectively recorded hot flushes; however, side effects have caused 40% of women to discontinue using clonidine in controlled studies.60 Moreover, at maximal tolerated dosages, the mean rate of hot flush occurrence decreases by less than one half.
Estrogen receptors have been identified in osteoblastic cells in tissue culture.78,79 Although added estrogen increases secretion of alkaline phosphatase and α1-procollagen by such cells in vitro, it is not clear whether this is the mechanism by which estrogen affects bone loss. This is especially true in view of the diverse effects of estrogens on metabolic factors that can affect bone. Progesterone receptors are present in bone as well.80
Raloxifene was approved by the FDA for the prevention and treatment of osteoporosis. Raloxifene is a benzothiophene and belongs to a class of drugs designated as selective estrogen receptor modulators (SERMs). Two other drugs in this category are clomiphene and tamoxifen, both triphenylethelenes. These drugs have estrogen agonist effects at some end-organ sites and estrogen antagonist effects at other sites and were previously known as mixed estrogen agonist-antagonists. Tamoxifen, for example, has antiestrogenic effects at the breast and reduces breast cancer recurrence for at least 5 years of treatment. It has mildly estrogenic effects on bone, lipids, and the uterus. It is not recommended for use for longer than 5 years because any protective effect on the recurrence rate for breast therapy appears lost after this time.104 Decreased bone loss has been observed in postmenopausal women using tamoxifen as treatment for breast cancer.105 There have also been reports of an increased incidence of cancer of the uterus in women using this drug.106,107
Raloxifene has a slightly different profile. It has mildly estrogenic effects on the bone and lipid profile with no observable effect on the breast or uterus. Unlike oral estrogens, raloxifene does not increase triglycerides. It also has no apparent benefit on the symptoms of hot flushes and vaginal dryness and may increase these symptoms in some women. In a 2-year trial, raloxifene produced a 1% to 2% increase in bone mineral density at the spine and hip compared with baseline and a 2.0% to 2.4% increase compared with the placebo group.108 Side effects include a 6% incidence of leg cramps and a threefold increase in venous thromboembolic events (VTEs), an increase similar to that reported with ERT. A history of VTEs is a contraindication to using raloxifene.
Sodium fluoride has been used for many years in the treatment of osteoporosis. The drug has many proponents and opponents. It appears to increase bone density substantially;109 however, it has lost favor since the publication of data indicating marked improvement in bone density with no improvement in fracture rate110 in women being treated with fluoride. A high frequency of side effects can be encountered with use of fluoride, including gastrointestinal problems, anemia, and joint and tendon inflammation. A slow-release fluoride formulation under investigation may provide better fracture protection with fewer side effects, but at present it is advisable to limit the use of fluoride to research settings until better data are available.
There are studies that refute the reported beneficial effects of estrogen on coronary heart disease.139,140,141 In one study of incident acute myocardial infarctions occurring in a large managed care program, there was no statistically significant reduction in relative risk of myocardial infarction among current users of ERT.141 No definitive conclusions can be made regarding the beneficial or detrimental effects of estrogen on coronary disease. The preponderance of data, however, suggests that estrogen administration to postmenopausal women may reduce the incidence of death from cardiovascular disease by as much as one half; however, most of these reports were observational studies and not randomized or double-blind trials. The best data probably will come from the very large Women's Health Initiative Trial sponsored by the National Institutes of Health. Results may not be available until 2005 or later.
Estrogen also has an effect on liver function. The effects are influenced by the dose, the route of administration, and the type of estrogen used. The usual estrogen replacement dose, 0.625 mg of conjugated equine estrogen daily, is about one fifth as potent as one dose commonly used in low-dose oral contraceptives, 30 μg of ethinyl estradiol. The synthetic estrogens used in oral contraceptives, unlike the natural estrogens used for estrogen replacement, significantly increase globulins produced in the liver, including renin substrate (angiotensinogen), causing elevated blood pressure in some women.143 Natural estrogens also stimulate hepatic synthesis of renin substrate but to a much lesser extent. Blood pressure is unaffected by postmenopausal ERT,144,145 except for the 5% to 8% of such women who develop an idiosyncratic elevation.146 Several observational and prospective reports have indicated an increased risk of VTEs with use of ERT.147,148,149,150,151,152 The increase in relative risk was 2.0 to 3.6. The absolute risk is small because of the overall low incidence of these events (less than 1 in 10,000). However, because of the potential serious and life-threatening sequelae of VTEs caution should be exercised in assessing the risk to benefit ratio in individuals deemed to be at increased risk of VTEs.
Several small studies of different progestins suggest that the synthetic progestins commonly used together with estrogen for replacement therapy have an adverse effect on lipoprotein metabolism, causing a substantial increase in LDL cholesterol and a significant decrease in HDL cholesterol.153 In contrast, data from the prospective Postmenopausal Estrogen-Progestin Intervention Trial showed that micronized progesterone did not adversely affect the beneficial effects on lipids of conjugated equine estrogens.151 The effects of progestins on lipoproteins are greater with the 19-nortestosterone derivatives and appear to be dose dependent.154 During the phase of the treatment cycle when estrogen and progestin are given together, it appears that the beneficial effects of estrogen on lipoprotein cholesterol levels are negated at least in part.155,156,157 These findings have led to the common recommendation that progestogens, if prescribed, should be given in the lowest possible dose needed to achieve the desired histologic changes in the endometrium and should not be given to women who have undergone hysterectomy. The clinical significance of the effect of progestins on the lipid profile is not known. Early research on cardiovascular health and HRT focused on the beneficial effect of HRT on the lipid profile.
Estrogen interacts with the cardiovascular system in many ways. Documented effects of estrogen include a decrease in fibrinogen, lipoprotein a, plasminogen activator inhibitor, fasting glucose, collagen formation, and neointimal proliferation.158,159,160,151 Estrogen appears to enhance vasodilation and collateral vessel formation161 The effects of estrogens on lipids may be of little added benefit to their apparently beneficial cardiovascular effects. Several groups have attempted to estimate the effects of estrogen alone and estrogen given with a progestin to postmenopausal women for HRT.162,163 More studies are needed to define the benefits of estrogens on cardiovascular disease and to determine the optimal way in which estrogens and progestins should be administered.
Several studies reported that estrogen-induced hyperplasia and carcinoma of the endometrium can be prevented by the addition of a progestin.173,174,175 However, one study indicated twice the rate of hyperplasia in women using cyclic estrogen and progestin an average of 4 years compared with nonusers.176 Progestins block estrogen receptor synthesis,177 induce estradiol dehydrogenase (the enzyme that converts estradiol to estrone),178 and increase the rate of sulfation of estrogen in the endometrium.179 These actions limit the effect estrogen has on the endometrium, thereby preventing endometrial proliferation. Norethindrone (350 μg) or norgestrel (150 μg) can decrease receptor DNA activity in women on 0.625 mg of conjugated estrogen to the level normally seen in the secretory phase of the menstrual cycle. Although dosages of MPA less than 10 mg have not been proved to eliminate the risk of endometrial carcinoma, they decrease the receptor activity and may be protective if given for more than 12 days. Some data suggest that duration of therapy may be more important than dose with regard to hyperplasia;180 however, results of long-term use of low-dose progestins have not been reported, and one very large short-term study involving 1385 women on four different regimens of estrogen and MPA found hyperplasia only in the two groups using the lowest amount of MPA.181 The maximal effects of progestins are not seen until after 6 days of continuous therapy, and hyperplasia is usually inhibited when these agents are given for 12 or more days.182 2ff7e9595c
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