Muscle and bone
There is a significant decrease in hip fracture risk during treatment that to a lesser degree persists after HRT is stopped. It also helps collagen formation, which in turn improves intervertebral disc and bone strength.Hormone replacement therapy in the form of estrogen and androgen can be effective at reversing the effects of aging on muscle. Lower testosterone is associated with lower bone density and higher free testosterone is associated with lower hip fracture rates in older women. Testosterone therapy, which can be used for decreased sexual function, can also increase bone mineral density and muscle mass. Side effects
Side effects in HRT occur with varying frequency and include:

Contraindications
The following are absolute and relative contraindications to HRT:

Absolute contraindications
Undiagnosed vaginal bleeding
Severe liver disease
Pregnancy
Severe coronary artery disease
Aggressive breast, uterine or ovarian cancer

Relative contraindications
Migraine headaches
History of breast cancer
History of ovarian cancer
Venous thrombosis
History of uterine fibroids
Atypical ductal hyperplasia of the breast
Active gallbladder disease (cholangitis, cholecystitis)
Well-differentiated and early endometrial cancer – once treatment for the malignancy is complete, is no longer an absolute contraindication. History and research
The extraction of CEEs from the urine of pregnant mares led to the marketing in 1942 of Premarin, one of the earlier forms of estrogen to be introduced. From that time until the mid-1970s, estrogen was administered without a supplemental progestogen. Beginning in 1975, studies began to show that without a progestogen, unopposed estrogen therapy with Premarin resulted in an eight-fold increased risk of endometrial cancer, eventually causing sales of Premarin to plummet.
Sulindac is a nonsteroidal anti-inflammatory drug (NSAID) of the arylalkanoic acid class that is marketed as Clinoril. Imbaral (not to be confused with mebaral) is another name for this drug. Its name is derived from sul(finyl)+ ind(ene)+ ac(etic acid)
It was patented in 1969 and approved for medical use in 1976. Medical uses
Like other NSAIDs, it is useful in the treatment of acute or chronic inflammatory conditions. Sulindac is a prodrug, derived from sulfinylindene, that is converted in the body to the active NSAID. More specifically, the agent is converted by liver enzymes to a sulfide that is excreted in the bile and then reabsorbed from the intestine. This is thought to help maintain constant blood levels with reduced gastrointestinal side effects. Some studies have shown sulindac to be relatively less irritating to the stomach than other NSAIDs except for drugs of the COX-2 inhibitor class. The exact mechanism of its NSAID properties is unknown, but it is thought to act on enzymes COX-1 and COX-2, inhibiting prostaglandin synthesis. Its usual dosage is 150-200 milligrams twice per day, with food. It should not be used by persons with a history of major allergic reactions (urticaria or anaphylaxis) to aspirin or other NSAIDs, and should be used with caution by persons having pre-existing peptic ulcer disease. Sulindac is much more likely than other NSAIDs to cause damage to the liver or pancreas, though it is less likely to cause kidney damage than other NSAIDs.