Medical Assessment - Oral Roberts University: Fill & Download for Free

1 BackgroundI was intending to cover this issue in my update to An eMail to A Few Friends and in a so-far unfinished and unpublished draft Answer entitled https://www.quora.com/What-are-the-economic-effects-of-longer-life-expectancies-in-the-future/draft but recent researches are so useful and relevant that I decided to communicate part of that Answer here. There is often a point in the development of medical trials developing protocols when it is no longer necessary or fair to continue with placebo studies because the volunteers on the placebo group are being damaged by not being given access to the best available medicals. That point has now been reached in the studies of the causes of dementia and Alzheimers.2 Convergent ResearchThis is one of the areas in which a great deal research has converged on producing a single very reliable finding. Most future research is likely to be like this, because statistical investigation has been massively upgraded by the Clive Granger/Robert Engels development of Granger Causation Correlation Analysis for which these economist-statisticians received a Nobel Prize in 2003.3 Disease Entry Points into the Human BodyThe twelve or so major “vectors” or routes by which diseases or medicines enter the human body are through the mouth, eyes, ears, nose and lungs, via the urinal, vaginal and anal tracts, via medical or recreational injections into the blood, or accidental blood contamination through minor wounds or cuts, and via absorbance or insect injection through the skin.A few words about each of these vectors might help illustrate their significance. Medicines are most often taken orally (by mouth) and some medicines and preventative protocols (procedures for avoiding a few diseases) are most effective taken sub-lingually (under the tongue) where small doses can have a much larger effect if the medical molecule is small enough.Some medicines are taken via-drops. Some hallucinogenic drugs may be most effective that way, but it is not a habit or a route I would recommend. The potency and purity of illegal hallucinogens is very variable and often very impure due to being cut or bulked out with fillers which may be damaging to the eyes. Talcum powders and Vim have been used as illegal drug fillers and both can damage eyesight. Tear gas and mustard gas are are the most immediately disabling eye and nose entry vectors currently available.Many people use cotton buds to clean out their ears. That’s a passable procedure providing great care is taken and a fresh cotton bud is used for each ear. But I know of several cases where minor eardrum damage has occurred and others where ear syringing has been required probably due to minor infections. The small bugs living on earwax are often transferred to both ears through the use of one cotton bud for both ears. Of course they may have been there anyway.Breathing in germs in the air due to the sneezes of a person suffering from a cold or other nasal infection is a major way that cold germs can spread.The genital diseases caused by germs entering the body via the urinal or vaginal entry-points are too well known for me to illustrate here. In my opinion most people need to know how to conduct a quick medical assessment before proceeding with any kind of close sexual encounter, but lust frequently over-rides such considerations as the attendances at VD clinics and numbers of babies born with genital diseases illustrate. During the development stage of these diseases they cannot be detected by amateur or even professional medical examinations and contact-avoiding condoms are the only way to avoid such a disease. As Spike Milligan used to joke, “Condoms should be worn on every conceivable occasion.” Sexually transmitted diseases seem to cause their sufferers to become more sexually available because that’s one of the ways these diseases spread themselves. While vaginal lubricants are advertised and commercially available, there do not seem to be any genital disinfectants which destroy germs in the way Xylitol destroys water-loving mouth germs and BHT and coconut oil destroys lipid-coated germs. One doctor to whom I made that remark many years ago said such items might mask detection. In my view the limitation of transmission is important but the lack of such medicants may be because Big Pharma as usual could not easily patent such an advance. Some items such as the carcinogenic DES (see Diethylstilbestrol - Wikipedia) is an antibacterial vaginal medication previously used but is now known to produce unwanted side effects.Medical injections are a fast way to get some essential medicines quickly into the blood.Taking anal suppositories for medical purposes or for recreational drug use are both illustrations of anal access.Minor wounds and cuts can lead to major infections and to unpleasant experiences. There are some parts of the world (such as West Africa) where flying insects can spread diseases through that entry point.Medical patches on the skin to provide slow dosing of very effective pain relief have been developed and are in general use throughout the world. Bee, wasp and large ant stings injecting formic acid into the skin are usually more an irritant than life-threatening but some bee stings inside the mouth can block breathing and cause death. Standing in some puddles in some parts of Africa can result in worm eggs infecting the feet. Some early Western explorers in Africa, believing from their European experience that standing barefoot in puddles was harmless, promptly discovered that Africans knew more about that than they did.Walking with bare legs or arms through Scottish wildlife areas is a beautiful experience but can be highly damaging. There are more sheep than people in my native country and Scotland’s people and visitors should enjoy hiking and the wonderful landscape without picking up a sheep or animal tick on bare legs or arms. Careless striding through the thistles and thorns can cause skin punctures which can give people these unwelcome insect hitch-hiker attachments to the skin. I have had hundreds of visits to the Scottish highlands and lowlands and through luck and appropriate dress have avoided close encounters of the animal-tick kind. But even Scots tend to discount that possibility and sometimes suffer from the tick infection resulting from that attitude and careless behaviour. See How to Remove a Tick.Many diseases currently at a low level are likely to be made more widely available and more frequently infectious due to global warming. See Global Warming May Spread Lyme Disease4 Calling Things By Their Right Names“Empty” gasoline barrels have often produced major accidents and deaths because people have smoked or lit small fires or started barbecues near these barrels. If these had been more accurately called “explosive gas containers” perhaps smokers and picnics would have sometimes been safer.The internal connections within the head are uually called the “Ear, Nose and Throat System” and could perhaps be more accurately called “The mouth, ear, nose, throat, blood and brain system” because that’s what it is.5 Answer How To Prevent Dementia and AlzheimersRecent research has suggested that Dementia develops due to gum diseases which can be “stopped” by better oral hygiene. This is probably much more of a prevention than a cure, but prevention is often better than a cure. There is no or very limited evidence that better oral hygiene can reverse dementia, although it might possibly prevent it from getting worse.6 Partial EvidenceSee the 7.25m results at a Google search for Mouth infections and dementiaPlease read the New Scientist Summary of recent research atWe may finally know what causes Alzheimer’s – and how to stop it or the WebMD report atCan Poor Dental Health Cause Dementia? andCaregiver Alert: The Connection Between Gum Disease and Alzheimer's Disease andhttps://www.rdhmag.com/articles/print/volume-37/issue-10/contents/alzheimer-s-link-with-perio.htmlThe Connection Between Dementia and Infections and note that bladder infections also get into the blood and can effect the nervous systemAn Important Link Between Bladder Infections and Dementia - Advantage Home Care andSee 8 Great Strategies to Get a Dementia Patient to Brush Their Teeth7 Conclusions7.1 From research at Harvard University to those at the University of Central Lancashire School of Medicine and Dentistry and many others, it has been suggested that gum diseases travel into the blood and brain (through the sublingual route) and can cause dementia.7.2 Dementia and much else can be prevented by better oral hygiene - by toothbrushing or by taking small spoonfuls of the sweetener Xylitol in your morning tea or coffee. See Xylitol - Wikipedia. Xylitol “looks like” a sugar to mouth germs, which seize it in order to breed, but the Xylitol will not let the germs go, so they die from the germ equivalent of a “blocked mouth.”Xylitol is listed at that source as improving dental care, preventing ear aches, managing diabetes, and weight management.Overdosing (at more than 50g/day) can cause diarrhoea and other gut problems, but it is perfectly safe in small doses.7.3 The cheapest and most effective way to take Xylitol is by buying 1 kg packs of it and adding a teaspoon (about 4gm to 6 gm) to your morning tea or coffee or cereals. It is possible to buy sachets of 4gm xylitol but that’s a bit more expensive but very useful when you are eating out or travelling.Xylitol clears much of the mucus in the mouth, nose and throat and enables unobstructed breathing and prevents germs in the ears and throat and prevents pneumonia, as the Wikipedia entry used to accurately record. Clear respiration/ventilation is helpful throughout life.I believe that mouth germs may also be implicated in all the other CNS diseases like ALS, MND and even maybe even MS and Huntingdon’s chorea. Many of these CNS degenerations may have a genetic basis which is accelerated by gum germs and other diseases which get into the blood sublingually or via other routes.

Clinical trials as we understand them today are a fairly recent invention, starting with the 1947 UK Medical Research Council's study of streptomycin for tuberculosis treatment, the 1st randomized clinical trial (1).Informed consent is of even more recent vintage. Dwelling at the intersection of law and medicine, birthed by the former, imposed on the latter, informed consent and clinical medicine have had an uneasy relationship from the beginning. While landmark cases started shaping its legal doctrine already in the 19th and early 20th century, informed consent's post-WWII legal lineage in the US is easy to track, with milestone rulings starting in the 1950s through to the 1970s (2, 3, 4),The 1957 Salgo v. Leland Stanford Jr. University Board of Trustees (2) established the precedent of patient self-determination with the judge coining the phrase, informed consent, in his jury instruction, the 1st known instance of its explicit use.The 1960 Natanson v. Kline (3) established the negligence standard, as in the physician having an inherent duty to make a reasonable disclosure of risks and hazards of treatment or face possible malpractice liability.The 1972 Canterbury v. Spence (4) established the reasonable person standard, i.e., the need to disclose what any reasonable person would consider necessary and sufficient to know.According to Ruth R. Faden, Tom L. Beauchamp and Nancy M.P. King, who published the definitive text-book on it in 1986 (5), how informed consent was planted in clinical medicine, how it grew, in other words its clinical medicine lineage, that's largely lost to time. This is perhaps an unavoidable difference because medicine already walks an uneasy tightrope between patient autonomy and welfare. Absence of early peer-reviewed medical studies only emphasizes the initial reluctance with which clinical medicine incorporated informed consent, and is also emblematic of the unease with which the two co-exist. Part of the reason for this unease is the perennial existence of grey areas.Why perennially grey areas? Because the young, the elderly, the frail, the poor, the poorly educated, the intellectually impaired, and the seriously ill are a part of us, a part of us that's much more dependent and thus much more vulnerable to manipulation. As Robert Q. Marston, the then-Director of the US NIH noted in an influential speech on the subject of informed consent, 'Whether or not consent is in fact informed is admittedly difficult to assess. We often are in an uncertain situation in which inadequate information, communication problems, and the inability of the subject to comprehend-or to read-or to listen-can be misleading' (6).Pre-informed consent Clinical Medicine helps understand why it's Important, nay Critical, in Clinical TrialsAs recently as 1964-1966, a study in the US found that >50% of physicians, 53% to be exact, thought it was 'ethically appropriate for a physician not to tell a cancer patient that she had been enrolled in a double blind clinical trial of an experimental anticancer drug and was currently receiving a placebo' (5, page 89).Two of the most prominent egregious abuses in human medical research, namely, Nazi human experimentation during the Holocaust and the Tuskegee Syphilis Study* certainly cast a long shadow, necessitating clear, formal, legally binding guidelines for human experimentation. While case law verdicts helped shape the legal framework for informed consent, the cultural framework, at least in the US, arose from several other cases that drove public debate, illuminated gaps in physician understanding of informed consent, and highlighted the roles and responsibilities of research committees and funders. Careful examination of the details and circumstances of some of these prominent cases helps drive home why informed consent is not only important but indeed critical. Two of several prominent US examples that were crucial in fleshing out informed consent as it exists today are elaborated here.The Jewish Chronic Disease Hospital CaseConducted at the Jewish Chronic Disease Hospital (JCDH) in Brooklyn, New York, and funded by Sloan-Kettering Institute for Cancer Research, the American Public Health Service and the American Cancer Society. With 10 years of research on anti-cancer immune responses under his belt, in July 1963, chief investigator Dr. Chester M. Southam convinced the hospital medical director Emmanuel E. Mandel to permit injection of a suspension of foreign, live cancer cells into 22 JCDH patients.The research question? Do cancer patients reject cancer transplants or not? Obviously comparison with response of cancer-free patients, the controls, was also required.The informed consent aspect? Some were informed orally they were involved in an experiment, but not that they would be injected with live cancer cells. No written informed consent.The final insult to injury, some patients were incompetent to give informed consent.The non-cancer patients, i.e., the controls, weren't informed either that they were getting injected with live cancer cells.The grounds? Might unnecessarily agitate the participants.The defense? That it was customary in medical research that consent 'not be documented even in far more dangerous research' (5, page 161), something that sounds utterly indefensible in the year 2015.As the New York Post reported in 2013, three young physicians, Drs. Avir Kagan, David Leichter and Perry Fersko, courageously went against the prevailing status quo and refused to participate in this study (7). They also brought it to the attention of attorney William Hyman, one of JCDH's Board of Directors, who filed a suit to access hospital records to learn more about the study (8). Hyman's concerns ranged from potential patient abuse, potential reputation damage to the hospital and its possible liability. The Hyman-driven review revealed (5, page 162),The study wasn't presented to the hospital's' research committee.Physicians directly responsible for patient care of subjects involved in the research weren't consulted about the cancer cell injections.Three physicians who had been consulted by Dr. Mandel were against the research arguing 'subjects were incapable of giving appropriate consent'.In 1966, the Board of Regents of the State University of New York censured Drs. Southam and Mandel, finding them guilty of deceit, fraud and unprofessional conduct, writing in its judgment (5, page 162, 9, see Regent' decision from 10 below),'A physician has no right to withhold from a prospective volunteer any fact which he knows may influence the decision. It is the volunteer's decision to make. . . . There is evidenced in the record in this proceeding an attitude on the part of some physicians . . . that the patient's consent is an empty formality. Deliberate nondisclosure of the material fact is no different from deliberate misrepresentation of such a fact. . . . The alleged oral consents that they obtained after deliberately withholding this information were not informed consents and were, for this reason, fraudulently obtained'.The Willowbrook State School CaseAn institution on Staten Island, New York, it was then classified in a manner unthinkable today, a mere 60 years later, namely, as a place for 'defective children'. Originally designed to house 3000, by 1963 it housed >6000. With the children's severe developmental impairments amplified by poor oversight, large numbers weren't even properly toilet trained. Unsurprisingly, such conditions not just predisposed to but also facilitated easy spread of fecal-borne infections. For example, in 1954, many children contracted hepatitis (presumably hepatitis A) within 6 to 12 months of living at Willowbrook.In 1956, Saul Krugman and colleagues started a series of experiments to develop an effective prophylactic. Funded by the US Armed Forces Epidemiological Board, the US Army Medical Research and Development Command, the Health Research Council of the City of New York, and several committees at New York University School of Medicine, including its Committee on Human Experimentation, they deliberately infected newly admitted patients with isolated hepatitis virus strains. Of the 10,000 children admitted to Willowbrook after 1956, ~ 750 to 800 were sent to Krugman's special hepatitis unit. Wards of the state never included in the studies, the children's parents had given written consent. At first, parents were informed by either letter or personal interview. Later, informed consent entailed groups discussions with parents of prospective parents.From the beginning, these studies were on the radar of Henry K. Beecher. With a decidedly murky ethical background himself, nevertheless, by the 1960s he'd emerged a pioneer of informed consent with his publication in 1959 of 'Experimentation in Man'. Beecher first listed the Willowbrook study in 1966 as one of 22 'ethically dubious' experiments. His repeat highlighting of this study in his 1970 book, Research and the Individual, brought the matter to the public's attention. Criticism gained momentum with the theologian Paul Ramsey joining in and with Stephen Goldby publishing a sharply critical letter in the Lancet in April 1971 (11), with the full support of the Lancet editors who publicly apologized for having previously overlooked the issue of informed consent.Such public scrutiny forced the researchers to defend themselves in the public arena. Their defense? Since most of the children recruited in the study would contract hepatitis anyway, they weren't placed in greater danger compared to the other institutionalized children. Optimal isolation, better attention, administered the best available anti-hepatitis therapy then available, the researchers asserted that their attempt to give the selected children sub-clinical hepatitis infections would immunize them against specific hepatitis viruses (12). That's not all. Influential editors of several prestigious medical journals, namely JAMA, NEJM, Journal of Infectious Diseases, agreed with this defense, arguing such research was valuable for understanding hepatitis, had potential value to such institutionalized children, had sufficient consent provisions, didn't expose the children to unnecessary risks and was performed by competent investigators (13).The rebuttal? The studyIncreased the children's later life risk for chronic liver disease.Unlike other Willowbrook residents, study children didn't receive protective doses of gamma globulin (14).Both process and legitimacy of consent obtained for the study were also easy to challenge. Consent forms used suggested the children would receive a vaccine against the virus, some parents were only contacted by letter. A key change happened in late 1964. Willowbrook became so overcrowded that new patient admissions ceased while Krugman's special research unit continued accepting children whose parents 'volunteered' them for the study, suggesting implicit coercion into the study as a means for parents getting their children admitted to Willowbrook (15). Study reviewers and we ourselves could easily conclude that social pressures under which such parents gave their consent, especially post-1964, undermined their ability to act in the best interests of their children.As Faden, Beauchamp and King note in their book (5, page 164), while Krugman's research unit was eventually closed, debate about the ethics of the Willowbrook study never resolved satisfactorily (16) and we see remarkable parallels regarding the ethics of informed consent issues here and in the 2009 PATH-ICMR HPV (Human Papilloma Virus) clinical trial**, ***. In both, the subjects of research were minors and parents/guardians offered informed consent on their behalf, one of the perennial grey areas I referenced earlier.The Road to Today's Informed Consent Becomes ClearerWith such recent examples of egregious medical research abuses as the backdrop, in 1973, Robert Q. Marston, the then-Director of the US NIH made an influential speech (6) that highlighted the central role of informed consent in clinical trials, 'That the committee determine that the rights and welfare of the subjects involved are adequately protected, that the risks of an individual are outweighed by the potential benefits to him or by the importance of the knowledge to be gained, and that informed consent is to be obtained by methods that are adequate and appropriate', and that 'if, in a specific case, I were forced to choose between the individual and the general welfare of society, I would choose to protect the individual'.He emphasized (6) that review committees that oversee human experimentation needed to strictly adhere to three basic criteria, namely,' Protection of the rights and welfare of the subjects.Weighing of risks against benefits.Determination that informed consent is to be obtained by methods that are adequate and appropriate.'In the US, it was in 1981 that the Judicial Council of the American Medical Association (AMA) first took an explicit stance on Informed Consent (5, page 96),'INFORMED CONSENT.The patient's right of self-decision can be effectively exercised only if the patient possesses enough information to enable an intelligent choice. The patient should make his own determination on treatment. Informed consent is a basic social policy for which exceptions are permitted (1) where the patient is unconscious or otherwise incapable of consenting and harm from failure to treat is imminent; or (2) when risk-disclosure poses such a serious psychological threat of detriment to the patient as to be medically contraindicated. Social policy does not accept the paternalistic view that the physician may remain silent because divulgence might prompt the patient to forego needed therapy. Rational, informed patients should not be expected to act uniformly, even under similar circumstances, in agreeing to or refusing treatment'.And this is more or less the landscape we've operated in ever since, with adequate and appropriate methods for obtaining informed consent remaining a perennially grey area, especially as clinical trials globalize and involve research subjects with vastly different cultural, linguistic and educational norms.Bibliography1. Marshall, Geoffrey, et al. "Streptomycin treatment of pulmonary tuberculosis: a Medical Research Council investigation." BMJ 2.4582 (1948): 769-782.2. Salgo v. Leland Stanford Jr. University Board of Trustees, 317 P.2d 170, 181 (1957).3. Natanson v. Kline, 350 P.2d 1093, 186 Kan. 393, 186 Kansas 393 (1960).4. Canterbury v. Spence, 464 F.2d 772 (D.C. Cir. 1972).5. Faden, Ruth R., Tom L. Beauchamp, and Nancy M. King. "A history and theory of informed consent." (1986). Oxford University Press.6. Marston, Robert Q. "Medical science, the clinical trial and society." Hastings Center Report 3.2 (1973): 1-4.7. The New York Post, Allen M. Hornblum, Dec 28, 2013. NYC's forgotten cancer scandal8. MATTER OF HYMAN v. Jewish Hosp., 15 N.Y.2d 317, 206 N.E.2d 338, 258 N.Y.S.2d 397 (1965).9. Katz, Jay, Alexander Morgan Capron, and Eleanor Swift Glass. Experimentation with human beings: The authority of the investigator, subject, professions, and state in the human experimentation process. Russell Sage Foundation, 1972.10. Langer, Elinor. "Human Experimentation: New York Verdict Affirms Patient's Rights." Science 151.3711 (1966): 663-666.11. Goldby, Stephen. "Experiments at the Willowbrook state school." The Lancet 297.7702 (1971): 749.12. Krugman, Saul, Joan P. Giles, and Jack Hammond. "Infectious hepatitis: Evidence for two distinctive clinical, epidemiological, and immunological types of infection." Jama 200.5 (1967): 365-373.13. Is Serum Hepatitis Only A Special Type of Infectious Hepatitis? JAMA. 1967;200(5):406-407. doi:10.1001/jama.1967.03120180094017.14. Annas, George J., Leonard H. Glantz, and Barbara F. Katz. Informed consent to human experimentation: The subject's dilemma. Ballinger Pub. Co., 1977.15. Goldman, Louis. "The Willowbrook Debate." World Med 7 (1971): 23-25.16. Ingelfinger, F. J. "Ethics of experiments on children." New England Journal of Medicine 288.15 (1973): 791-792.More details on the journey to, the process of, and grey areas in informed consent available in these answers:* Tirumalai Kamala's answer to Do you believe placebos are morally permissible? Why or why not?** Tirumalai Kamala's answer to Should we have an international forum to resolve clinical trial mishaps?*** Tirumalai Kamala's answer to Is it true that Bill Gates faced trial in India for illegally testing tribal children with vaccines?Thanks for the A2A, Kritika Gupta.

90% Serotonin (5-hydroxytryptamine, 5-HT) refers to where it's made. ~90% of the body's 5-HT is apparently made by the gastrointestinal Enterochromaffin cell, ~5% each by the myenteric (gut-associated) neurons and the brain (1, 2). However, the bulk of enterochromaffin-derived 5-HT isn’t kept locally but rather deposited into the blood circulation inside densely packed Platelet granules and how it's delivered to distant sites is still a mystery as is whether it indeed acts as an endocrine hormone (3).Selective serotonin reuptake inhibitor (SSRI) & Weight Gain: Not Universal, Depends On The DrugAccording to a systematic literature review, SSRI's influence on weight depends on the specific SSRI (see table below from 4).Weight gain: Paroxetine, Citalopram, Clomipramine, Duloxetine, EscitalopramMinimal effect: Fluvoxamine, Fluvoxamine CR (Controlled Release), Sertraline, FluoxetineGiven 5-HT's abundant production in the GI tract and such striking differences in how different SSRIs influence weight, it would indeed seem obvious to assessGut microbiota's role in Major depressive disorder (MDD).How, being among the most commonly prescribed Antidepressant, Selective serotonin reuptake inhibitor (SSRI) might affect gut microbiota.Of three possible ways to assess how SSRIs could affect gut microbiota, i.e., study their effect on human or animal model gut microbiota or their direct effect on microbes, only the last is best studied to date.Human Gut Microbiota Are Different Between Major depressive disorder (MDD) Patients & Healthy Controls (4 studies as of 2016). Relevance? Not Clear.As of 2016, a handful of studies compared gut microbiota composition differences between MDD patients and healthy controls. However, none adequately addressed how SSRIs affect gut microbiota composition.At least 4 different studies found fecal microbiota of MDD patients and healthy controls to be different (5, 6, 7, 8). However, with respect to what’s different there's little consensus between these studies so not yet clear what these data imply. As for how SSRI might affect gut microbiota, only one of these studies (6) addressed that tangentially without coming to a clear conclusion so even less is known about it.Two of these studies even transferred fecal microbiota samples from MDD patients and healthy controls into experimental mice (7) or rats (8) to see if animals that receive MDD fecal microbiota recapitulate depression features, as assessed in experimental animals. Apparently they recapitulated some features such as alterations in FST (forced swim test, Behavioural despair test), and Anhedonia and other anxiety-like behaviors, implying gut microbiota may have a causative role in depression.A few individuals with clinically diagnosed depression including those on antidepressants were part of two linked, much larger gut microbiota studies (9, 10) attempting to build a picture of the core human gut microbiota. While one of these studies found antidepressants to be among the 13 drugs associated with gut microbiota variation, unfortunately the antidepressant in question wasn't SSRI but rather the SNRI (Serotonin–norepinephrine reuptake inhibitor), Venlafaxine (10). In any case, those on Venlafaxine (23 women and 6 men) were a tiny proportion of the total study population of 1106, making the linkage statistically weak so this is very much preliminary data.Direct SSRI effect on microbes: Direct & Synergistic Antimicrobial Effects On Microbial Cultures In VitroA number of studies reported direct antimicrobial effect of psychotropic drugs like SSRI (11, 12, 13). Majority of such studies found Sertraline to be active against bacteria, fungi and even an eukaryotic parasite, a quite surprising effect since human epidemiological data suggest Sertraline minimally affects weight.Bacteria: The SSRI Paroxetine was active against Staphylococcus aureus (14) and Sertraline against Escherichia coli (15).Fungi: The SSRI Fluoxetine and Sertraline were more active compared to Paroxetine, Reboxetine and Seroxate against the fungus Aspergillus (16), and Sertraline against Candida (fungus) (17), Saccharomyces cerevisiae (yeast) (18), Cryptococcus (19, 20) and Coccidioides (21)Eukaryotic parasites: The SSRI Sertraline against the parasite Leishmania donovani (22).While early speculation suggested such activity is non-specific (23), subsequent studies showed that SSRIs can also synergize with traditional antibiotics (24) and antifungals (25, 26).SSRI may inhibit or kill microbes through their effect on the microbial Efflux (microbiology) pump, i.e., generalizable energy-dependent mechanisms that vastly different microbes use to pump out substances that are toxic for them. Efflux pump mechanisms being greatly conserved between microbes as disparate as bacteria, fungi and eukaryotic parasites suggests it may be quite difficult for them to successfully mutate molecules that SSRIs target.On the one hand SSRIs being able to inhibit and/or kill microbes in culture indirectly suggests they could affect human gut microbiota. On the other hand bulk of such data is for Sertraline which epidemiological studies suggest has minimal effect on weight. In other words, we're still firmly at square one as to whether and how SSRIs could affect human gut microbiota.Bibliography1. Gershon, Michael D., Anna B. Drakontides, and Leonard L. Ross. "Serotonin: synthesis and release from the myenteric plexus of the mouse intestine." Science 149.3680 (1965): 197-199.2. Gershon, Michael D., and Jan Tack. "The serotonin signaling system: from basic understanding to drug development for functional GI disorders." Gastroenterology 132.1 (2007): 397-414. https://www.researchgate.net/profile/Michael_Gershon/publication/6560987_The_serotonin_signaling_system_from_basic_understanding_to_drug_development_for_functional_GI_disorders/links/00b7d5345fee28c304000000.pdf3. Gershon, Michael D. "5-Hydroxytryptamine (serotonin) in the gastrointestinal tract." Current opinion in endocrinology, diabetes, and obesity 20.1 (2013): 14. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708472/pdf/nihms477208.pdf4. Dent, Robert, et al. "Changes in body weight and psychotropic drugs: a systematic synthesis of the literature." PLoS One 7.6 (2012): e36889. http://journals.plos.org/plosone/article/asset?id=10.1371%2Fjournal.pone.0036889.PDF5. Naseribafrouei, A., et al. "Correlation between the human fecal microbiota and depression." Neurogastroenterology & Motility 26.8 (2014): 1155-1162. http://onlinelibrary.wiley.com/doi/10.1111/nmo.12378/epdf6. Jiang, Haiyin, et al. "Altered fecal microbiota composition in patients with major depressive disorder." Brain, behavior, and immunity 48 (2015): 186-194. Elsevier: Article Locator7. Zheng, P., et al. "Gut microbiome remodeling induces depressive-like behaviors through a pathway mediated by the host’s metabolism." Molecular psychiatry 21.6 (2016): 786-796.8. Kelly, John R., et al. "Transferring the blues: Depression-associated gut microbiota induces neurobehavioural changes in the rat." Journal of Psychiatric Research 82 (2016): 109-118.9. Zhernakova, Alexandra, et al. "Population-based metagenomics analysis reveals markers for gut microbiome composition and diversity." Science 352.6285 (2016): 565-569.10. Falony, Gwen, et al. "Population-level analysis of gut microbiome variation." Science 352.6285 (2016): 560-564.11. Munoz-Bellido, J. L., S. Munoz-Criado, and J. A. Garcıa-Rodrıguez. "Antimicrobial activity of psychotropic drugs: selective serotonin reuptake inhibitors." International journal of antimicrobial agents 14.3 (2000): 177-180).12. Samanta, Amalesh, et al. "Evaluation of in vivo and in vitro antimicrobial activities of a selective Serotonin reuptake inhibitor Sertraline Hydrochloride." Anti-Infective Agents 10.2 (2012): 95-104. https://www.researchgate.net/profile/Chandrima_Sinha/publication/226645038_Evaluation_of_In_Vivo_and_In_Vitro_Antimicrobial_Activities_of_a_Selective_Serotonin_Reuptake_Inhibitor_Sertraline_Hydrochloride/links/549868ef0cf2519f5a1de2f0.pdf13. Kalaycı, Sadık, Selami Demirci, and Fikrettin Sahin. "Antimicrobial Properties of Various Psychotropic Drugs Against Broad Range Microorganisms." Current Psychopharmacology 3.3 (2014): 195-202. https://www.researchgate.net/profile/Sadik_Kalayci/publication/277904113_Antimicrobial_Properties_of_Various_Psychotropic_Drugs_Against_Broad_Range_Microorganisms/links/5592effb08ae5af2b0eb64fb.pdf14. Kaatz, Glenn W., et al. "Phenylpiperidine selective serotonin reuptake inhibitors interfere with multidrug efflux pump activity in Staphylococcus aureus." International journal of antimicrobial agents 22.3 (2003): 254-261. https://www.researchgate.net/profile/Glenn_Kaatz/publication/9887482_Phenylpiperidine_selective_serotonin_reuptake_inhibitors_interfere_with_multidrug_efflux_pump_activity_in_Staphylococcus_aureus/links/0912f511239e17be72000000.pdf15. Bohnert, Jürgen A., et al. "Efflux inhibition by selective serotonin reuptake inhibitors in Escherichia coli." Journal of antimicrobial chemotherapy 66.9 (2011): 2057-2060. Efflux inhibition by selective serotonin reuptake inhibitors in Escherichia coli16. Lass-Flörl, C., et al. "Antifungal properties of selective serotonin reuptake inhibitors against Aspergillus species in vitro." Journal of Antimicrobial Chemotherapy 48.6 (2001): 775-779. Antifungal properties of selective serotonin reuptake inhibitors against Aspergillus species in vitro17. 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