Patients who desire a more androgynous presentation or less vigorous masculinization may be treated with low doses or limited courses of testosterone prostate cancer krishnadasan et al 2007 purchase cheap confido online, but should be counseled that vocal changes prostate exam guidelines order 60 caps confido with amex, hair growth and other masculinizing efects are not easily tailored and individual patient response is not easily predicted prostate cancer back pain buy genuine confido on-line. Most healthy adults can be started on the usual adult dosage of testosterone; many providers will start at a halfdose and then quickly increase to prostate cancer 7 out of 12 buy generic confido 60 caps online a full dose at the frst follow up visit or later depending on the patient’s response and goals for treatment. Dosage should be adjusted based on cessation of menses and the progress of other masculinizing efects or side efects. Patients should avoid supraphysiologic levels, as the aromatization of excess testosterone to estradiol can cause feminizing efects. In younger patients, and in patients with lower body mass, consider starting at lower doses and increasing gradually. Anecdotal reports exist of a destabilizing efect on bipolar disorder, schizophrenia and schizoafective disorder, as well as adverse mood changes in patients with a history of psychic trauma. In these patients, providers should ensure that their psychiatric state and treatment is stabilized prior to initiating testosterone, then start at lower doses and increase gradually. Compounding pharmacies, such as Strohecker’s Pharmacy, may compound cypionate into sesame seed oil if there is any indication that the patient may have an adverse reaction to the standard cottonseed oil suspension. Consider starting patients initially on topical formulations, especially if there are concerns about the efects of fuctuations in hormone levels, or if the patient desires less vigorous and more gradual masculinization. Patients must use caution in avoiding skin to skin contact with female partners or young children or pets. If skin to skin contact is anticipated, as with intimate sexual contacts, the area of application should be washed with soap and water; the majority of the dose will be absorbed from the skin within 4 to 6 hours of application. May cause thinning or loss of other body hair and may interfere with clitoral enlargement. Topical Medication name(s) Topical testosterone applied to the clitoris Usual dose 2-4% ointment in petrolatumum base Additional comments this has been used in some FtM people to improve clitoral enlargement, though one study found no appreciable efect. Transgender Women (MtF) Feminization is achieved primarily through the use of estrogen in doses that are several times higher than those used for contraception or post-menopausal treatment in natal females. Early treatment protocols used ethinyl estradiol until this formulation was shown to be associated with an exceptionally high rate of thromboembolic disease. Transdermal estradiol has been demonstrated to be much safer in regard to the risk of venous thromboembolism. Oral conjugated estrogen (Premarin) has also been used, but now is generally more expensive and may incur a higher clotting risk; conjugated estrogens also cannot be measured in serum/blood. Estrogen itself has an anti-androgen efect, but most treatment protocols also use a medication that interferes with the synthesis and/or biologic efect of testosterone. These androgen blockers help to counteract the masculinizing efect of endogenous testosterone and allow for lower doses of estrogen to be used. Additional comments There is some study data in trans females that suggests that oral estradiol may be comparable in safety to transdermal formulation, though this is not clear. Patients should be encouraged to dissolve tablets sublingually to minimize frst-pass efect on the liver. Anecdotally, injectable estradiol might possibly provide more vigorous and early breast development comparable to treatment with oral or transdermal estradiol, however, there is no empirical data to support this claim at this time. There may be potential for an increased risk of intentional or unintentional overdosage and misuse of injectable estradiol. Therefore, injectable forms should only be used cautiously as frst-line therapy, and might be used primarily in selected patients who fail to achieve adequate feminization with oral or transdermal formulations. It is advised that all patients be started at the lowest recommended dose and that doses should be increased slowly. Spironolactone directly inhibits testosterone secretion as well as inhibiting binding to the testosterone receptor; it may also exert an estrogenic efect of its own. Additional comments Consider using in patients with male pattern baldness, in patients with heavy facial hair, or in patients who are unable to tolerate higher doses of spironolactone. Use of oral progestin with estrogen in the Women’s Health Initiative Study on post-menopausal hormone replacement was associated with an increased risk of cardiovascular disease and breast cancer. These medications may also cause signifcant weight gain and negative mood changes. Anecdotally, progestins are reported to help improve breast development, especially development of the nipple/areola complex, but this outcome is not supported in small studies. Anecdotal increases in breast size may be due to progestin-stimulated weight gain. If prescribing oral formulations, consider dosing cyclically only 10 days per month, to minimize doses and side efects, though some patients may experience pre-menstrual like symptoms with cyclic dosing. Additional comments It has been used in study protocols in treating MtF patients and has been efective and well-tolerated. Medication name(s) Electrolysis Description Female patients frequently will use electrolysis or laser therapy to manage facial and body hair that is not adequately decreased with hormonal therapy. This is especially important for patients who have undergone any genital reconstructive surgery with gonadectomy and no longer produce endogenous sex hormones. In most cases, hormone therapy should be continued without interruption, unless there are specifc serious concerns on the part of the medical or mental health provider. The medical provider will ensure that the doses and formulations of hormonal medications are appropriate and safe for each individual patient. If the patient has been on prescribed hormone therapy for over a year, a full initial assessment of the appropriateness of hormone therapy may not be necessary. The medical provider will assess the need for appropriate monitoring examination and laboratory evaluation. The patient must still be assessed fully with a complete history, physical examination, and laboratory evaluation. Referral for behavioral health assessment and management should be made as is appropriate and necessary for each individual patient. Follow-up Care and Monitoring Patients should be seen 1 month after initiating hormone therapy to assess for side efects and, if well tolerated, to increase to usual doses. Patients who are stable on hormone regimens after 2 to 3 years and who are healthy without other medical issues may be seen every 12 months. Follow up visits may be scheduled more frequently for patients with co-occurring conditions or who are at highrisk for potential adverse efects. Procedures at follow up visits: • Ensure that patient is using medication at the recommended dose; assess injection technique for problems if using an injectable medication. Patients may require re-education on the course and timing of and the individual variation in changes. Educate on efects of testosterone in thinning the vaginal lining and advise on use of viscous lubricants or other safer sex practices to reduce tearing, as appropriate. This may be related, in part, to the size of the breast in proportion to the breadth of male chest and shoulders. Urge patients to wait for at least two years of estrogen treatment before considering surgical breast augmentation. Consider referral to support groups, case management or other services that will ensure or increase patient’s safety and adjustment. Consider referral for counseling or prescription for psychiatric medications if signifcant symptomatology. Complete/write required medical documentation letters for amendment of legal documents. Ofer pre-operative direction and guidance (See appropriate section of protocols) and ensure that patients are medically stabilized and ready for surgery. Consider monitoring to ensure that levels are not supraphsyiologic, especially in younger and physically smaller patients. Several cases of prolactinomas occurring in MtF patients on estrogen have been reported; one occurred 14 years after starting hormone therapy. Most protocols recommend only a single screening level 1 to 2 years into treatment or yearly levels for 3 years; further monitoring should be based on symptoms. Lower levels close to this range may also be tolerated if the patient is feminizing well or has been on hormone treatment for over 3 years. Health Maintenance Care Mental Health • Continue to screen for and be sensitive to possible mental health problems, depression, anxiety, and suicidal ideation.
Another form of vitamin E like the Gamma tocopherol has been shown to prostate oncology associates buy confido visa improve inflammation man health about inguinal hernia men buy confido us, oxidative stress androgen hormone order discount confido, and apoptosis in diabetic wounds by nuclear factor kappa B prostate oncology hematology order confido 60 caps amex, nuclear factor (erythroid-derived 2)-like 2, and sirtuin-1 . In contrast, menaquinone is a product of bacterial from the gut or conversion of phylloquinone derived from the diet. Ascorbate is a powerful antioxidant with the ability to mop up free radicals within, and outside the cell which is by acting directly on peroxyl radicals or indirectly by boosting the antioxidant properties of vitamin E, this helps to control lipid peroxidation of cellular membranes and nuclear materials of the cell. Ascorbate also prevents the formation of nitrosamine, which produces reactive nitrogen species . Vitamin C, in combination with L-carnitine, was reported to improve cisplatin-induced nephrotoxicity due to their antioxidant and anti-inflammatory property . Vitamin C has also been reported to generate ascorbate radicals and Hydrogen peroxide in pharmacological doses . Therefore, Ascorbic acid in high doses has been suggested to kill cancer cells by inducing pro-oxidant effects selectively. One of the mechanisms suggested for its anti-cancer effect is through the induction of hydrogen peroxide in cell and depleting Nicotinamide Adenine Dinucleotide . Riboflavin can be regarded as one of the neglected antioxidant nutrients, because primarily, vitamin C, E, and Carotenoids are mainly known to be antioxidants. Riboflavin possesses some antioxidant property as a result of the glutathione redox cycle and its conversion from reduced riboflavin to its oxidised form . Reduced glutathione acts as an antioxidant in the intracellular milieu by deactivating reactive oxygen species during the conversion to its oxidised form . Glutathione is crucial to its ability to deactivate peroxides, especially hydroperoxides . Therefore it is expected that riboflavin deficiency may increase lipid peroxidation. Several animal studies indicated the negative effects of riboflavin deficiency on lipid metabolism as well as the desired effect of riboflavin administration [89-93]. A similar study reported reduced lipid peroxides like malondialdehyde and protein carbonyls in diabetic rats after riboflavin administration . Pyridoxine possesses some antioxidant property, even though it is not a classical antioxidant compound. An in-vitro study reported that vitamin B6 prevented the generation of oxygen radicals and lipid peroxidation in U937 monocytes, which may occur via alteration of mitochondrial function , Vitamin B6 deficient rats developed peroxidative stress because of increased thiobarbituric acid activity in the rat liver and heart  suggesting a pivotal role for pyridoxine in preventing peroxidation. Deficiency of vitamin B6 has a connection with atherogenesis by influencing the biosynthesis of long-chain polyunsaturated fatty acids, increase lipid peroxidation, and affect antioxidant defence . A theoretical study of the scavenging capacity of pyridoxine on different reactive oxygen species viz. Cobalamin may possess some antioxidant property due to some evidence from in-vitro studies. Some authors suggest that vitamin B12 possess a direct super-oxide scavenger mechanism [6, 100]. Administration of cyanocobalamin on human aortic cells lowered the level of superoxide in the intracellular fluid and mitochondrion . Furthermore, some in-vivo studies have also reported results with a reduced superoxide burst in the ganglion cells of the retina after vitamin B12 administration . Vitamin B12 stimulates the conversion of homocysteine to methionine, and a deficiency of vitamin B12 will imply increase homocysteine levels . Homocysteine is readily oxidised to hydrogen peroxide, thereby increasing reactive oxygen species in the body [104, 105]. Therefore, it indirectly protects against oxidative stress due to its role in homocysteine metabolism. Subclinical deficiency of vitamin B12 causes the generation of reactive oxygen species, which in turn impairs the uptake of vitamin B12. Oxidative stress can contribute to the formation of advanced glycated end products, which could reduce vitamin B12 uptake [106, 107]. A study on the possible beneficial effect of Niacin administration in rats exposed to methyl mercury demonstrated that niacin ameliorated the adverse effect produced by methyl mercury, the mechanism behind its useful role was suggested to relate to the inherent antioxidant potential of Niacin . Administration of pantothenic acid has been reported to significantly reduce oxidative stress and improved damage to the brain in gamma-irradiated rats . However, folates may have a direct antioxidant effect invivo, which has no connection to its homocysteine-lowering effect . The reduced forms of folic acid were found to have a comparable antioxidant property with vitamin C and vitamin E . The protective role of folates in these diseases was suggested to be due to its antioxidant property [117, 128]. Cabbage, eggplant, romaine lettuce, precursor of some key enzymes of mushrooms, navy beans, black beans, barley, carbohydrate metabolism . It also helps in the structural Also, we have lima beans, oats, sesame development of brain cells , and it seeds, kidney beans, peanuts, sweet potato, is involved in the detoxification of tofu, tuna, pineapple, oranges, broccoli, alcohol . It also promotes iron greens, soybeans, yogurt, almonds, turkey, metabolism and its deficiency green peas, sweet potato, sardines, tuna, increases the risk of anaemia as iron is carrots and cabbage  an essential element for red blood cell production . Vitamin B3 They are primarily involved in the Mushrooms, cauliflower, sweet potato, Niacin production of energy from dietary broccoli, beet greens, asparagus, turnip Nicotinamide proteins, carbohydrates, and fats . Vitamin B6 Vitamin B6 is involved in red blood Tuna, spinach, cabbage, bell peppers, turnip Pyridoxine cell production, carbohydrate greens, garlic, cauliflower, turkey, beef, metabolism, liver detoxification, brain chicken, salmon, sweet potato, potatoes, and nervous system health . Vitamin B12 It plays an essential role in energy sardines, salmon, tuna, cod, lamb, scallops, Cobalamin metabolism shrimps, beef, yoghurt, cow’s milk, eggs, Vitamin B12 needed for erythrocyte turkey, chicken, cheese, mushrooms and maturation during the production of breakfast cereals. Vitamin B12 also maintains bone health as the incidence of osteoporosis is increased with deficiency of this vitamin 12. Also, Vitamin C is needed asparagus, sea vegetables, fennel, and sweet for collagen production, which is a potatoes . The synthesis of certain neurotransmitters is also dependent on vitamin C, especially neurotransmitters involved in signalling of feelings, thoughts, and commands throughout the brain and nervous system. Vitamin C is also prerequisite for the synthesis of serotonin, a hormone needed for the proper functioning of the endocrine system, nervous system, digestive system and immune system. Conclusion this review discusses both in-vivo and in-vitro studies on the antioxidant properties of vitamins. It has also been able to call attention to other vitamins (Vitamin K, Vitamin D, Niacin, Pyridoxine and Riboflavin) asides classical antioxidants (Vitamin C, E and carotenoids) which play vital roles in defending the body against free radicals by potentiating enzyme antioxidants, acting as co-enzymes, in their reduced physiological forms or by directly attacking free radicals. More studies using improved techniques should be carried out on these vitamins to delineate their role to allow their incorporation as nutritional supplementation for the management and prevention of human diseases. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular diseasefi Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons. The Journal of Neuroscience: the Official Journal of the Society for Neuroscience 23 (2003): 5816-5826. Cobalamin-associated superoxide scavenging in neuronal cells is a potential mechanism for vitamin B12-deprivation optic neuropathy. Characterisation of endoperoxide and hydroperoxide intermediates in the reaction of pyridoxine with singlet oxygen. Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases. Oxidative Stress and Its Significant Roles in Neurodegenerative Diseases and Cancer. Potential role of nutrients on immunity; International Food Research Journal 23 (2015): 464-474. The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomised controlled trial. Vitamin D in the prevention of acute respiratory infection: a systematic review of clinical studies. Vitamin E and immune response in the aged: molecular mechanisms and clinical implications. Menadione (vitamin K3) is a catabolic product of oral phylloquinone (vitamin K1) in the intestine and a circulating precursor of tissue menaquinone-4 (vitamin K2) in rats.
But the notion of the “cure” as the singular solution to prostate cancer level 7 discount confido 60 caps cancer had degenerated into a sclerotic dogma prostate gland histology cheap confido 60 caps without a prescription. Bailar and Smith noted prostate oncology zanesville order confido cheap, “A shift in research emphasis prostate health purchase confido 60caps amex, from research on treatment to research on prevention, seems necessary if substantial progress against cancer is to be forthcoming. Past disappointments must be dealt with in an objective, straightforward and comprehensive manner before we go much further in pursuit of a cure that always seems just out of reach. In Georgian England, sweeps and climbing-boys were regarded as general cesspools of disease—dirty, consumptive, syphilitic, poxridden—and a “ragged, ill-looking sore,” easily attributed to some sexually transmitted illness, was usually treated with a toxic mercury-based chemical and otherwise shrugged off. If a sexual “sore,” then why would it get “exasperated” by standard emollient drugsfi He recorded that minute, invisible particles of soot could be found lodged under their skin for days, and that scrotal cancer typically burst out of a superficial skin wound that tradesmen called a soot wart. Sifting through these observations, Pott eventually pinned his suspicion on chimney soot lodged chronically in the skin as the most likely cause of scrotal cancer. If soot, and not some mystical, numinous humor (a la Galen), caused scrotal cancer, then two facts had to be true. Orphans, often as young as four and five years old, were “apprenticed” to master sweeps for a small price. By the late eighteenth century, the embarrassing plight of London’s climbing-boys was publicly exposed, and social reformers in England sought to create laws to regulate the occupation. Pott did not live to see the changes—he contracted pneumonia and died in 1788—but the man-made epidemic of scrotal cancer among sweeps vanished over several decades. In 1761, more than a decade before Pott had published his study on soot cancer, an amateur scientist and apothecary in London, John Hill, claimed that he had found one such carcinogen concealed in another innocuous-seeming substance. While Pott’s august monograph on soot cancer circulated through the medical annals of England drawing admiration and praise, Hill’s earlier pamphlet, written in colorful, colloquial language and published without the backing of any medical authority, was considered a farce. In pubs, smoking parlors, and coffeehouses—in “close, clouded, hot, narcotic rooms”—men in periwigs, stockings, and lace ruffs gathered through the day and night to pull smoke from pipes and cigars or sniff snuff from decorated boxes. It was a relatively minor innovation—the addition of a piece of translucent, combustible paper to a plug of tobacco—that further escalated tobacco consumption. The story is likely apocryphal, and the idea of packing tobacco in paper was certainly not new. When these soldiers returned from the war, they brought their habits, like viruses again, to their respective homelands with them. In the Soviet gulags, it became an informal currency; among English suffragettes, a symbol of rebellion; among American suburbanites, of rugged machismo, among disaffected youth, of generational rift. The cigarette offered its equal and opposite salve: camaraderie, a sense of belonging, and the familiarity of habits. It was precisely this rapid, viral ascendancy of tobacco that made its medical hazards virtually invisible. Pott, for instance, had discovered the link between scrotal cancer and chimney sweeping because chimney sweeping (the profession) and scrotal cancer (the disease) were both uncommon enough that the juxtaposition of the two stood out starkly like a lunar eclipse—two unusual occurrences in precise overlap. And when a risk factor for a disease becomes so highly prevalent in a population, it paradoxically begins to disappear into the white noise of the background. As the Oxford epidemiologist Richard Peto put it: “By the early 1940s, asking about a connection between tobacco and cancer was like asking about an association between sitting and cancer. Even surgeons, who encountered lung cancer most frequently, could no longer perceive any link. By the time the cigarette returned to visibility as arguably the world’s most lethal carrier of carcinogens, it would be far too late. The lung cancer epidemic would be in full spate, and the world would be deeply, inextricably ensconced, as the historian Allan Brandt once characterized it, in “the cigarette century. The sentence, although couched in characteristic English understatement, was strong enough to provoke a response. In February 1947, in the midst of a bitterly cold winter, the ministry asked the Medical Research Council to organize a conference of experts on the outskirts of London to study this inexplicable rise of lung cancer rates and to hunt for a cause. One expert, having noted parenthetically that large urban towns (where cigarette consumption was the highest) had much higher rates of lung cancer than villages (where consumption was the lowest), concluded that “the only adequate explanation” was the “smokiness or pollution of the atmosphere. Befuddled by this variance in opinions, the council charged Austin Bradford Hill, the eminent biostatistician who had devised the randomized trial in the 1940s, to devise a more systematic study to identify the risk factor for lung cancer. Across the Atlantic, too, the link between smoking and cancer was seemingly visible only to neophytes—young interns and residents “uneducated” in surgery and medicine who seemed to make an intuitive connection between the two. In the summer of 1948, Ernst Wynder, a medical student on a surgical rotation in New York, encountered an unforgettable case of a forty-two-year-old man who had died of bronchogenic carcinoma—cancer of the airways of the lung. The man had been a smoker, and as in most autopsies of smokers, his body had been scarred with the stigmata of chronic smoking: tar-stained bronchi and soot-blackened lungs. Since nothing had been proved there exists no reason why experimental work should be conducted along this line. Graham also reasoned the trial would teach Wynder about the complexities and nuances of study design and allow him to design a trial to capture the real risk factor for lung cancer in the future. Lung cancer patients and a group of control patients without cancer were asked about their history of smoking. This setup (called a case-control study) was considered methodologically novel, but the trial itself was thought to be largely unimportant. When Wynder presented his preliminary ideas at a conference on lung biology in Memphis, not a single question or comment came from the members of the audience, most of whom had apparently slept through the talk or cared too little about the topic to be roused. In contrast, the presentation that followed Wynder’s, on an obscure disease called pulmonary adenomatosis in sheep, generated a lively, half-hour debate. Just a few steps away, on the gilded railings of the London School of Tropical Medicine, the seminal epidemiological discoveries of the nineteenth century—the mosquito as the carrier for malaria, or the sand fly for black fever—were celebrated with plaques and inscriptions. But many epidemiologists argued that such cause-effect relationships could only be established for infectious diseases, where there was a known pathogen and a known carrier (called a vector) for a disease—the mosquito for malaria or the tsetse fly for sleeping sickness. The notion that a chronic disease such as lung cancer might have a “carrier” of its own sort, to be gilded and hung like an epidemiological trophy on one of those balconies, was dismissed as nonsense. They were an odd couple, the younger Doll formal, dispassionate, and cool, the older Hill lively, quirky, and humorous, a pukka Englishman and his puckish counterpart. Patients with lung cancer (“cases”) versus patients admitted for other illnesses (“controls”) were culled from twenty hospitals in and around London and interviewed by a social worker in a hospital. The survey included questions about the proximity of gasworks to patients’ homes, how often they ate fried fish, and whether they preferred fried bacon, sausage, or ham for dinner. As more interviews poured in week after week, the statistical association strengthened. Even Doll, who had personally favored road-tar exposure as the cause of lung cancer, could no longer argue with his own data. It is tempting to suggest that Doll, Hill, Wynder, and Graham had rather effortlessly proved the link between lung cancer and smoking. In an often-quoted statistical analogy, this is akin to asking car accident victims whether they had been driving under the influence of alcohol—but interviewing them after their accident. But it does not tell a drinker his or her actual chances of being involved in an accident. What if drivers tend to overestimate (or underestimate) their intoxication at the time of an accidentfi If a cohort of people could be randomly assigned to two groups, and one group forced to smoke cigarettes and the other forced not to smoke, then one could follow the two groups over time and determine whether lung cancer developed at an increased rate in the smoking group. Random assignment aside, the problem with the Doll and Hill study thus far was that it had estimated risk retrospectively. Could an epidemiologist watch a disease such as lung cancer develop from its moment of inception, much as an embryologist might observe the hatching of an eggfi In the early 1940s, a similar notion had gripped the eccentric Oxford geneticist Edmund Ford. A firm believer in Darwinian evolution, Ford nonetheless knew that Darwin’s theory suffered from an important limitation: thus far, the evolutionary progression had been inferred indirectly from the fossil record, but never demonstrated directly on a population of organisms. The trouble with fossils, of course, is that they are fossilized—static and immobile in time. But this proof is retrospective and indirect; that three evolutionary stages exist suggests, but cannot prove, that one fossil had caused the genesis of the next.
Overall prostate cancer- yahoo news search results proven confido 60 caps, in the studies with available data androgen hormone 411 order confido 60 caps without prescription, general adult population had approximately 50% of non-White participants mens health meal plan order confido. Finally prostate cancer early stages buy generic confido 60 caps on-line, the combined reviews for older adults included 53 studies for psychotherapies and medication (Cuijpers, Karyotaki, Pot, et al. The samples within the reviews included adults ages 50 and older with approximately 83% females across all studies. Of the studies in the reviews with reported data, the sample included only a range of 44 6. The reviews for depression in children and adolescents did not exclude comorbid psychiatric disorders. Regarding the review that assessed the efficacy of interpersonal psychotherapy versus cognitive-behavioral therapy in the treatment of child/adolescent depression, Zhou and colleagues (2015) found that the studies 45 that recruited patients with comorbid psychiatric disorders had lower effect sizes. The authors emphasized the need for more research on the efficacy of interpersonal psychotherapy and cognitive-behavioral therapy in patients with comorbid psychiatric disorders due to the small samples sizes that may have contributed to this finding (Zhou et al. While Cipriani and colleagues (2016) included pharmacological studies that recruited children and adolescents with comorbid psychiatric disorders, they excluded studies that recruited “participants with treatmentresistant depression, with treatment duration of less than 4 weeks, or with an overall sample size of fewer than ten patients” (p. Four out of the six reviews of depression in the general adult population did not exclude comorbid psychiatric and medical disorders (Cuijpers, Driessen, et al. While Gartlehner and colleagues (2015) searched for studies that had comorbidity as an inclusion criterion, they noted the paucity of high-quality studies that included patients with comorbid psychiatric and medical disorders in most of the studies. However, Cuijpers, Karyotaki, Pot, and colleagues (2014a) as well as Wilkinson and Izmeth (2012)47 were unable to find studies that included older adults with depression as well as comorbid medical and psychiatric disorders in clinical trials. Both reviews emphasized the need for future research to include comorbid disorders in assessing treatment efficacy for depression in older adults. Defining Efficacy and Comparative Effectiveness In this guideline, the term efficacy refers to the impact of a treatment compared with an inactive control. The term comparative effectiveness refers to the benefit of one active treatment compared with another. The type of comparison (control) group used by studies varied across the systematic reviews/meta-analyses. Broadly, however, control groups used by studies included both active and nonactive controls. An example of an often-used active control was treatment as usual (whose exact definition varies by study). The evidence profiles were summaries of data included in the systematic reviews and include, for each outcome, the number of studies, absolute effect sizes, confidence intervals (when available), and strength of evidence ratings. For adults, evidence profiles were provided in the report “Nonpharmacological Versus Pharmacological Treatments for Adult Patients With Major Depressive Disorder,” (Gartlehner et al. The panel worked with data directly from the report for the remainder of the systematic reviews and metaanalyses. So, in some cases the panel had additional quality information for particular outcomes included in the evidence profiles but did not have that data for all interventions and outcomes. Decision tables and grids are documents developed and then used by panel members to summarize and evaluate the evidence generated in the systematic review or meta-analyses, along with any supplemental information. Panel ratings and judgments were documented on the decision tables and grids to aid in the formulation of recommendations (Treweek et al. These tables allow panel members to document decisions, compare consistency across decisions, and give transparency to reviewers and users of the guideline document. The four main domains of decision-making are documented as follows: (1) strength of evidence; (2) treatment outcomes and the balance of benefits vs. Only for interventions that had at least low strength of evidence for one of the outcomes were decision tables or grids completed. As the panel progressed with its work, they decided that the creation and review of evidence in decision tables resulted in redundancy as the same information concerning possible harms and burdens or patient values and preferences was considered repeatedly for different bodies of outcome evidence. To facilitate decision making yet maintain consistency and transparency, a revised “grid” process was created that included distinct columns for separate questions and outcomes and individual decision-making regarding efficacy but allowed consideration of the same data for harms and burdens across those columns. This greatly increased the efficiency of the evidence review while keeping consistency and transparency. Although some have questioned the applicability of some randomized trials due to potential differences between sample characteristics or treatment settings and the “real world” application (Shean, 2016), the panel decided to not supplement the randomized trials included in the reviews with observational. Panel members made two significant exceptions to this decision when it became clear that data were lacking in randomized trials findings on two outcomes: (1) harms and burdens of psychological treatments and (2) patient values and preferences regarding particular treatments. In response, the panel decided there was a need to gather and review more information on these topics. Concerning harms, panel members decided to review those observational studies that gave attention to the assessment of harms that were identified in the reviews. Details of the search process methodology for both of these supplemental sources of information are described below. The findings of these additional reviews along with input from clinicians and consumers on the panel were used to make the treatment recommendations more comprehensive with regard to the risk of harm or adverse events associated with various interventions for depression (determined to be a critical outcome) and patient values and preferences. Each panel member received an explicit opportunity to raise any questions or concerns about the process of completing each decision table or the grid. The panel as a group reviewed each decision table and grid to identify any questions or concerns that users of the guideline (including patients, clinicians, scientists, and administrators) might raise. For purposes of consistency across all clinical practice guidelines, the Advisory Steering Committee established voting procedures that can be found in Appendix F. The four domains below formed the basis on which each treatment recommendation and its strength were decided. For each recommendation, text description and a justification for the recommendation were included on the decision table and grid (see Appendix C as well as additional appendices links). For each of the decision tables and grids, aggregate/global strength of evidence was based on the strength of evidence from the review for the two critical outcomes, namely, response to treatment (reduction in depressive symptoms) and serious adverse events. For example, if one critical outcome had “high” strength of evidence but the other critical outcome had “low” strength of evidence, the global quality of evidence for that particular decision table or column in the grid would be low, because that is the lowest strength of evidence for an individual critical outcome. The strength of evidence for serious harms, one of the panel’s critical outcomes, was insufficient/very low, for all interventions for which decision tables and grid columns were completed. This explains why the global strength of evidence was insufficient/very low for all interventions, despite low, moderate, or high strength of evidence for the critical outcome of response to treatment. One of the key components of the decision-making process for the guideline developmental panel was assessment of the balance between benefits and harms. Quantification of benefits was based on data from the quantitative meta-analyses for each of the important and critical outcomes that the panel had selected at the start of the guideline development panel process for those interventions that had at least low quality of evidence for the critical outcome, response to treatment. For each of the outcomes on the decision tables, magnitude of benefits and harms/burdens was rated on a five-point scale: (1) 48 49 large/modest benefit; (2) small benefit; (3) no effect; (4) small harm; and (5) modest /large 50 51 harm. On the grids, the panel rated the magnitude of benefits as large, modest, or small benefit of Treatment 1 relative to Treatment 2 and the reverse or No difference in effect or Unable to rate. Because “serious adverse events” was one of the two critical outcomes of treatment decided on by the panel, these needed more precise specification and definition. Ultimately, panel members considered events such as the need for hospitalization secondary to suicidality as a serious adverse event and then identified additional harms such as medication side effects. Harms were differentiated from burdens that were identified as disruptions associated with treatment. As discussed earlier, the review of the treatment literature did not generate sufficient data on harms and burdens of interventions because, unfortunately, this information is not routinely reported in studies of psychosocial interventions and not reported in detail in many studies of psychopharmacological interventions. For the older adult review, the same data extraction was also conducted on those studies identified but excluded from the systematic review because of high risk of bias to expand the available pool of information. Some of the search terms used included: “depression,” “treatment,” and “older adults. It was from these studies that the panel had additional information on possible harms or burdens associated with the interventions under consideration. Further, as described in more detail below, physician members of the panel provided information on potential harms/burdens of medications. Moreover, panel members consulted with a prominent expert in child psychiatry regarding the panel’s recommendations pertaining to medication in children/adolescents to review and assess for any potential concerns. Consumer members reported on both their own and peer experiences with various interventions.
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