Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Premenstrual syndrome afflicts millions of premenopausal women and has been described as one of the most common disorders in women. Research over the past few years suggests that a variety of nutrients may have an important role in the phase related mood and behavioral disturbances of the premenstrual syndrome. There is scientific evidence, at least for a few of these micronutrients, specifically calcium and vitamin D, supporting cyclic fluctuations during the menstrual cycle that may help explain some features of PMS. Ovarian hormones influence calcium, magnesium and vitamin D metabolism. Estrogen regulates calcium metabolism, intestinal calcium absorption and parathyroid gene expression and secretion, triggering fluctuations across the menstrual cycle. Alterations in calcium homeostasis (hypocalcemia and hypercalcemia) have long been associated with many affective disturbances. PMS shares many features of depression, anxiety and the dysphoric states. The similarity between the symptoms of PMS and hypocalcemia is remarkable. Clinical trials in women with PMS have found that calcium supplementation effectively alleviates the majority of mood and somatic symptoms. Evidence to date indicates that women with luteal phase symptomatology have an underlying calcium dysregulation with a secondary hyperparathyroidism and vitamin D deficiency. This strongly suggests that PMS represents the clinical manifestation of a calcium deficiency state that is unmasked following the rise of ovarian steroid hormone concentrations during the menstrual cycle.
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PMID:Micronutrients and the premenstrual syndrome: the case for calcium. 1076 3

Seasonal Affective Disorder (SAD) is prevalent when vitamin D stores are typically low. Broad-spectrum light therapy includes wavelengths between 280-320 nm which allow the skin to produce vitamin D. This study was designed to test the hypothesis that vitamin D deficiency might play a role in SAD. A prospective, randomized controlled trial was conducted in a group of 15 subjects with SAD. Eight subjects received 100,000 I.U. of vitamin D and seven subjects received phototherapy. At the onset of treatment and after 1 month of therapy subjects were administered the Hamilton Depression scale, the SIGH-SAD, and the SAD-8 depression scale. All subjects also had serum levels of 25-hydroxyvitamin D (25-OH D) measured before and 1 week after intervention therapy. All subjects receiving vitamin D improved in all outcome measures. The phototherapy group showed no significant change in depression scale measures. Vitamin D status improved in both groups (74% vitamin D group, p < 0.005 and 36% phototherapy group, p < 0.01). Improvement in 25-OH D was significantly associated with improvement in depression scale scores (r2=0.26; p=0.05). Vitamin D may be an important treatment for SAD. Further studies will be necessary to confirm these findings.
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PMID:Vitamin D vs broad spectrum phototherapy in the treatment of seasonal affective disorder. 1088 76

25-Hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, calcium, phosphate and parathyreoidal hormone levels were assessed in 34 patients with schizophrenia (DSM-III-R, 44% female, mean age 38.9 +/- 2.1 years), 30 patients with alcohol addiction (16% female, mean age 48.7 +/- 2.2 years), 25 patients with major depression (56% female, mean age 57.6+/- years) and 31 healthy controls. Only 25-hydroxyvitamin D3 and 1,25-dihydroxvitamin D3 levels were significantly lower in all groups of psychiatric patients than in normal controls, but not phosphate, calcium and parathyreoidal hormone levels. Significant differences in the vitamin D levels could not be found between the three psychiatric groups. These findings do not support the idea that vitamin D is specifically involved in the pathophysiology of depression. The difference in patients as compared to the healthy controls might be related to a different social background resulting in differing habits e.g. of nutrition.
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PMID:Vitamin D in schizophrenia, major depression and alcoholism. 1100 48

In general, bone loss from glucocorticoid treatment occurs rapidly within the first 6 months of therapy. Glucocorticoids alter bone metabolism by multiple pathways; however, the bone loss is greatest in areas rich in trabecular bone. Preventive measures should be initiated early. It is the author's opinion that all subjects initiating treatment with prednisone at 7.5 mg or greater require calcium supplementation (diet plus supplement) at a dose of 1500 mg and vitamin D at a dose of 400 to 800 IU/d. If the patient is going to remain on this dose of glucocorticoid for more than 4 weeks, an antiresorptive agent should be started (e.g., estrogen, bisphosphonate, raloxifene). If a patient has established osteoporosis and is either initiating glucocorticoid therapy or is chronically treated with prednisone at 5 mg d or greater in addition to calcium and vitamin D supplementation, a potent antiresorptive agent (bisphosphonate) should be started. A bone mineral density measurement of either the lumbar spine or the hip may be helpful is assessing an individual's risk of osteoporosis, may improve compliance with treatment, and can be used to monitor the efficacy of the prescribed therapy. There is no reason to withhold treatment for glucocorticoid-induced bone loss until a bone mass measurement is taken, however. In motivated patients, a weight-bearing and resistance exercise program should be prescribed to help retain muscle strength and prevent depression. If hypercalciuria develops with glucocorticoid use, either thiazide diuretics or sodium restriction may be helpful. In patients who continue to lose bone or experience fracture's despite antiresorptive therapy while on glucocorticoids, bone-building anabolic agents (e.g., hPTH 1-34 or PTH 1-84) may be available someday soon.
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PMID:An update on glucocorticoid-induced osteoporosis. 1128 98

The prevalence of osteoporosis is rising as the population of the United States and other developed countries ages. These increasing numbers of people have motivated pharmaceutical companies to develop and market several antiresorptive medications that can slow down the bone loss associated with osteoporosis. Although these are not cures for this disease, they are an important first step in a vital ongoing public health effort to prevent osteoporosis in the future and to manage osteoporosis now. We cannot expect to remediate the problems caused by this disease if we attend only to its skeletal implications. Like any other chronic disease, osteoporosis has significant psychologic and social consequences. From anxiety and depression to social withdrawal and isolation, if these problems are left unresolved, they can have a significant negative impact not only on health issues but also on overall quality of life. No quick fixes exist for the numerous ways in which osteoporosis can transform an autonomous person into a dependent and hopeless patient. In part, responsibility for helping this patient rests with the medical community. Referrals to appropriate providers can improve a patient's physical and emotional well-being. Physician specialists can help the patient manage comorbid conditions. Physical and occupational therapists can teach exercises, home safety, and safe movement. Social workers can provide a framework for coping that enables individuals to improve their interpersonal interactions and minimize stress in their lives. Nutritionists, pharmacists, nurses, and other health care professionals can make major contributions to the quality of life of people with osteoporosis and should be encouraged to do so. Unfortunately, managed care has set policies that deprive patients with osteoporosis of the kinds of care that would be most useful to them. As we have advocated for the last 15 years, a multidisciplinary approach offers patients the most positive overall way to manage osteoporosis. Therefore, new alternatives need to be examined, alternatives that provide both low-cost and high-quality care. In the long run, patients who practice self-management, that is, those who take responsibility for their own calcium and vitamin D intake, are compliant with medications, exercise, and practice home safety, and who have a healthy outlook, can control their osteoporosis. The most effective intervention for the future may be to teach individuals how to use self-management strategies so that they can take charge of their osteoporosis and positively influence their quality of life.
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PMID:The nonskeletal consequences of osteoporotic fractures. Psychologic and social outcomes. 1128 99

Pruritus, fatigue and metabolic bone disease represent three major extrahepatic manifestations of chronic cholestatic liver disease that considerably affect the patient's quality of life. The present article reviews pathogenetic aspects of and current therapeutic approaches to extrahepatic manifestations of cholestatic liver disease. Pathogenesis of pruritus of cholestasis remains poorly understood. The involvement of putative peripherally acting pruritogens, such as bile acids or endogenous opioids, is being discussed. More recently, central mechanisms, including an increased central opioidergic tone and pertubations in the serotonergic system have been proposed. Treatment of the underlying disease is beneficial also for the control of cholestasis-associated pruritus. Current therapeutic recommendations include ursodeoxycholic acid, cholestyramine, rifampicin and opioid antagonists. Liver transplantation may be indicated when severe pruritus is refractory to medical treatment. Fatigue is being recognized as the most frequent and one of the most disabling complaints in chronic cholestasis. Fatigue is presumably of central origin and its association with other neuropsychiatric disorders (e.g. depression, obsessive-compulsive disorders) is consistent with defective central neurotransmission. No specific therapies are currently available and a healthy lifestyle, regular sleep and avoidance of unnecessary stress and other precipiting factors are recommended. Antidepressant therapy may be warranted in selected patients. Osteopenia and osteoporosis are common in chronic cholestatic liver disease, whereas osteomalacia is rare. The pathophysiology of cholestasis-associated metabolic bone disease is regarded as multifactorial. Therapeutic recommendations include regular exercise, calcium and vitamin D supplementation in late stage disease, hormone replacement therapy in postmenopausal women and bisphosphonates.
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PMID:Extrahepatic manifestations of cholestasis. 1216 13

Osteoporosis or osteopenia occurs in about 44 million Americans, resulting in 1.5 million fragility fractures per year. The consequences of these fractures include pain, disability, depression, loss of independence, and increased mortality. The burden to the healthcare system, in terms of cost and resources, is tremendous, with an estimated direct annual USA healthcare expenditure of about $17 billion. With longer life expectancy and the aging of the baby-boomer generation, the number of men and women with osteoporosis or low bone density is expected to rise to over 61 million by 2020. Osteoporosis is a silent disease that causes no symptoms until a fracture occurs. Any fragility fracture greatly increases the risk of future fractures. Most patients with osteoporosis are not being diagnosed or treated. Even those with previous fractures, who are at extremely high risk of future fractures, are often not being treated. It is preferable to diagnose osteoporosis by bone density testing of high risk individuals before the first fracture occurs. If osteoporosis or low bone density is identified, evaluation for contributing factors should be considered. Patients on long-term glucocorticoid therapy are at especially high risk for developing osteoporosis, and may sustain fractures at a lower bone density than those not taking glucocorticoids. All patients should be counseled on the importance of regular weight-bearing exercise and adequate daily intake of calcium and vitamin D. Exposure to medications that cause drowsiness or hypotension should be minimized. Non-pharmacologic therapy to reduce the non-skeletal risk factors for fracture should be considered. These include fall prevention through balance training and muscle strengthening, removal of fall hazards at home, and wearing hip protectors if the risk of falling remains high. Pharmacologic therapy can stabilize or increase bone density in most patients, and reduce fracture risk by about 50%. By selecting high risk patients for bone density testing it is possible to diagnose this disease before the first fracture occurs, and initiate appropriate treatment to reduce the risk of future fractures.
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PMID:Management of osteoporosis. 1525 71

Synthetic corticosteroids have variable glucocorticoid and mineralocorticoid potencies. Depending on their galenic form they can be administered either by intravenous, oral, intraarticular, intramuscular, inhalative or topic route. A local application is preferable over a systemic administration to avoid side effects. An initially high dose should always be tapered to the lowest possible effective dose. Among the side effects some have substantial clinical implications: Osteoporosis (to be treated during any long-term steroid application with calcium, vitamin D and eventually bis-phosphonates), immunodeficiency and a risk for often atypical infections, diabetes mellitus and psychiatric disorders such a depression and psychosis. A long-term glucocorticoid treatment can lead to a permanent adrenal insufficiency (M. Addison), which must be recognized and properly managed.
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PMID:[Corticosteroid therapy]. 1577 40

The correction of a subtle nutritional deficiency that may reduce the risk of a future chronic disease is indeed a challenge. However, some specific examples in the past, such as the addition of folic acid to prevent neural tube defects and calcium and vitamin D to prevent osteoporosis, should provide some encouragement that some conditions can be prevented with the appropriate addition of a deficient compound. One of the most intriguing current and future impacts on public health may come from a greater intake of omega-3 fatty acids such as alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). The omega-3 fatty acids continue to accumulate research that suggests that may prevent a variety of diverse chronic diseases and potentially some acute clinical scenarios. In Part 1 of this manuscript the potential for these compounds to prevent certain cardiovascular conditions are discussed. In Part 2 the potential for an impact in arthritis, numerous areas of cancer research, depression, maternal and child health, neurological diseases, osteoporosis, and other medical disciplines are also briefly covered. The future appears bright for these agents, but specifically which conditions, who qualifies, testing, frequency, adequate sources, future trials and numerous other questions need to be addressed and answered before the potential impact can catch up to the recent hype.
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PMID:An introduction to dietary/supplemental omega-3 fatty acids for general health and prevention: part I. 1588 81

The correction of a subtle nutritional deficiency that may reduce the risk of a future chronic disease is indeed a challenge. However, some specific examples in the past, such as the addition of folic acid to prevent neural tube defects and calcium and vitamin D to prevent osteoporosis, should provide some encouragement that some conditions can be prevented with the appropriate addition of a deficient compound. One of the most intriguing current and future impacts on public health may come from a higher intake of omega-3 fatty acids, such as alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). The omega-3 fatty acids continue to accumulate research that suggests that they may prevent a variety of diverse chronic diseases and potentially some acute clinical scenarios. In the first part of this article, the potential for these compounds to prevent certain cardiovascular conditions are discussed. In the second part, the potential for an impact in arthritis, numerous areas of cancer research, depression, maternal and child health, neurologic diseases, osteoporosis, and other medical disciplines are also briefly covered. The future appears bright for these agents, but specifically which conditions, who qualifies, testing, frequency, adequate sources, future trials, and numerous other questions need to be addressed and answered before the potential impact can catch up to the recent hype.
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PMID:An introduction to dietary/supplemental omega-3 fatty acids for general health and prevention: part II. 1588 82


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