Lordosis is historically defined as an abnormal inward curvature of the lumbar spine. However, the terms lordosis and lordotic are also used to refer to the normal inward curvature of the lumbar and cervical regions of the human spine. Similarly,  kyphosis historically refers to abnormal convex curvature of the spine. The normal outward (convex) curvature in the thoracic and sacral regions is also termed kyphosis or kyphotic. The term comes from the Greek lordōsis, from lordos ("bent backward").Lordosis in the human spine makes it easier for humans to bring the bulk of their mass over the pelvis. This allows for a much more efficient walking gait than that of other primates, whose inflexible spines cause them to resort to an inefficient forward leaning "bent-knee, bent-waist" gait. As such, lordosis in the human spine is considered one of the primary physiological adaptations of the human skeleton that allows for human gait to be as energetically efficient as it is.Lumbar hyperlordosis is excessive extension of the lumbar region, and is commonly called hollow back, sway back, or  saddle back (after a similar condition that affects some horses). Lumbar kyphosis is an abnormally straight (or in severe cases flexed) lumbar region. Types
Lumbar lordosis
Normal lordotic curvatures, also known as secondary curvatures, result in a difference in the thickness between the front and back parts of the intervertebral disc. Lordosis may also increase at puberty, sometimes not becoming evident until the early or mid-20s.In radiology, a lordotic view is an X-ray taken of a patient leaning backward.
Overdose
Raloxifene has been studied in clinical trials across a dosage range of 30 to 600 mg/day, and was well-tolerated at all dosages. Pharmacology
Pharmacodynamics
Mechanism of action
Raloxifene is a selective estrogen receptor modulator (SERM) and hence is a mixed agonist and antagonist of the estrogen receptor (ER) in different tissues. It has estrogenic activity in some tissues, such as bone and the liver, and antiestrogenic activity in other tissues, such as the breasts and uterus. Its affinity (Kd) for the ERα is approximately 50 pM, which is similar to that of estradiol. Relative to estradiol, raloxifene has been reported to possess about 8 to 34% of the affinity for the ERα and 0.5 to 76% of the affinity for the ERβ. Raloxifene acts as a partial agonist of the ERα and as a pure antagonist of the ERβ. In contrast to the classical ERs, raloxifene is an agonist of the G protein-coupled estrogen receptor (GPER) (EC50 = 10–100 nM), a membrane estrogen receptor. Clinical effects
Raloxifene has antiestrogenic effects in the mammary glands in preclinical studies. In accordance, raloxifene reduces breast density in postmenopausal women, a known risk factor for breast cancer. It does not stimulate the uterus in postmenopausal women, and results in no increase in risk of endometrial thickening, vaginal bleeding, endometrial hyperplasia, or endometrial cancer. At the same time, raloxifene has minimal antiestrogenic effect in the uterus in premenopausal women.