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Simple Ways to Get Out of Unhealthy Habits (Drugteststrips)

Many people today are suffering from unhealthy habits such as smoking, alcohol or illegal substance abuse. Unhealthy habits often result in health related issues. They can also negatively impact professional, social and economic well-being of an individual. Being aware of the harmful effects of unhealthy habits, many people are continuing with them assuming that getting out of these habits is very difficult. Some even think that it is impossible. In this article, we have mentioned some simple tips to help them come out of the unhealthy habits.

Do you want to change your unhealthy habit?:
If your answer is 'yes', then you can easily come out of unhealthy habits! It's true! The desire to break your bad habits itself is the primary step to achieve it. There are many people who do not even think of stopping these habits in spite of being aware of their harmful effects. You are at least better than that kind of people. But, don't just limit it to imagination. Make a proper planning and employ right measures to make your wish come true.

Take a firm decision:
A strong decision to quit bad habits can bring a positive change in your life. It is very difficult to achieve success if you don't have commitment. So, make firm determination to get out of substance abuse. Take it as a challenge and define specific goals to achieve success in a step-wise process. Practice healthy habits in your daily routine to detach yourself from unhealthy habits.

Stay away from substance abusing friends:
You may encounter many obstacles in the process of quitting unhealthy habits. It will be very difficult for you to break these habits in the company of substance abusing friends. It is better to avoid them. Simply reject any invitations from them and be bold to make them know that you are not interested in those habits.


Spend more time with family:
Emotional support from your family can help you get rid of drug or alcohol abusing habits. Instead of going out with your drug abusing friends, go for a walk or an outing with your family members. Get involved in family-related responsibilities, functions or activities.

One of the common reasons for drug abuse in many individuals is stress. Abusing drugs in order to reduce stress aggravates the situation. Individual may suffer from compound effects of stress and substance abuse. Therefore, this unhealthy habit of managing stress should be replaced with healthy options. You can have a simple and open chat with your family members. Share your feelings on substance abuse and accept their suggestions to give up the habit.

See the positive side of life:
Look at the benefits of healthy lifestyle. Inculcate healthy habits like regular exercise. Include nutritional food in your diet. They are known to reduce the risk of serious health issues like heart attacks and cancer.

Breaking unhealthy habits like substance abuse is possible. In fact, you can successfully get rid of unhealthy habits with the help of the above mentioned tips. So, be prepared to enjoy your healthy life by quitting unhealthy habits.

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The Power of Conversational Hypnosis Price Worthy?

You may be quite anxious to get started on your hypnosis journey, but you need to ask yourself these two important questions:

"What hypnosis course is the best and what is its cost?"

For the first question, it can be debated but a majority of experts and serious students highly rate the Power of Conversational Hypnosis by Igor Ledochowski. As a matter of fact, there are hardly any good courses on the market and it is because of the truth that most so called experts really don't teach people how to properly apply their techniques to actual life situations.

Igor Ledochowski does show you how to apply his approaches to everyday conversations. This is particularly important because there is no point of learning covert hypnosis if you don't understand how to put it on the real world to real people. Not only will it be embarrassing but you will not be taken seriously by that person.

Igor has a large amount of experience in the corporate world and he also owned a hypnotherapy clinic. He spent time as a highly rated lawyer and was also on several Fortunate 500 company boards where serious negotiations were common. After you learn that he actually knows covert hypnosis, his success is not a surprise.

Discover The Power of Conversational Hypnosis Price

Will the Course Surpass The Price?

Proclaiming that this course is very large is just not an exaggeration. It's not to claim that just because it has a lot of information indicates that this is a great course. However, you will find there's good reason for any section of information to be there.

The fourteen hours incorporated into this program features productive and relevant content with no filler stuff which is often included in various other courses. If you would like read the information instead, you will also receive a pdf file of the audio transcript together with the course. It just means that you'll be able to upload it onto a media player or eBook reader so you can read it on the way to work or elsewhere.

The best part of it occurs when you put what you have learned into practice and the exercises in every single part enables you to do that. This might be the easiest strategy for learning which is assisted with the included cheat sheets. You won't find another course about hypnosis as comprehensive as this one.

What's The Power of Conversational Hypnosis Price?

In terms of the course price, there really isn't any other course that can match it for value. I have just given you a really brief introduction to the Power of Conversational Hypnosis, but my short explanation isn't going to do it the justice it really deserves. But in order to have a better perspective of things:

Igor Ledochowski charges how much money for private training classes? $6,900The proper worth of the Power of Conversational Hypnosis is what? $7,200...How much must you spend on the Power of Conversational Hypnosis?

Many more people around the globe can receive Igor's knowledge at that distinct price, which means they are able to also apply covert hypnosis techniques to strengthen their lives.

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More Science on the Desktop

If you took Bacteriology 101, you were probably subjected to (maybe even tested on) the standard mythology about anaerobes lacking the enzyme catalase. The standard mythology goes like this: Almost all life forms (from bacteria to dandelions to humans) have a special enzyme called catalase that detoxifies hydrogen peroxide by breaking it down to water and molecular oxygen. The only exception: strict anaerobes (bacteria that cannot live in the presence of oxygen). They seem to lack catalase.

I've written on this subject before, so I won't bore you with a proper debunking of all aspects of the catalase myth here. (For that, see this post.) Right now, I just want to emphasize one point, which is that, contrary to myth, quite a few strict anaerobes do have catalase. I've listed 87 examples by name below. (Scroll down.)

I have to admit, even I was shocked to find there are 87 species of catalase-positive strict anaerobes among the eubacteria. It's about quadruple the number I would have expected.

If you're curious how I came up with a list of 87 catalase-positive anaerobes, here's how. First, I assembled a sizable (N=1373) list of bacteria, unduplicated at the species level. (So in other words, E. coli is listed only once, Staphylococcus aureus is listed only once, etc. No species is listed twice.) I then used the free/online CoGeBlast tool to run two Blast searches: one designed to identify aerobes, and another to identify catalase-positive organisms. In the end, I had all 1,373 organisms tagged as to whether each was aerobic, anaerobic, catalase-positive, or catalase-negative.

It's not as easy as you'd think to identify strict anaerobes. There is no single enzymatic marker that can be used to identify anaerobes reliably (across 1,373 species), as far as I know. I took the opposite approach, tagging as aerobic any organism that produces cytochrome c oxidase and/or NADH dehydrogenase. (These are enzymes involved in classic oxidative phosphorylation of the kind no strict anaerobe participates in.) In particular, I used the following set of amino acid sequences as markers of aerobic respiration (non-biogeeks, scroll down):

>sp|Q6MIR4|NUOB_BDEBA NADH-quinone oxidoreductase subunit B OS=Bdellovibrio bacteriovorus (strain ATCC 15356 / DSM 50701 / NCIB 9529 / HD100) GN=nuoB PE=3 SV=1
MHNEQVQGLVSHDGMTGTQAVDDMSRGFAFTSKLDAIVAWGRKNSLWPMPYGTACCGIEF MSVMGPKYDLARFGAEVARFSPRQADLLVVAGTITEKMAPVIVRIYQQMLEPKYVLSMGA CASSGGFYRAYHVLQGVDKVIPVDVYIPGCPPTPEAVMDGIMALQRMIATNQPRPWKDNW KSPYEQA
>sp|P0ABJ3|CYOC_ECOLI Cytochrome o ubiquinol oxidase subunit 3 OS=Escherichia coli (strain K12) GN=cyoC PE=1 SV=1
MATDTLTHATAHAHEHGHHDAGGTKIFGFWIYLMSDCILFSILFATYAVLVNGTAGGPTG KDIFELPFVLVETFLLLFSSITYGMAAIAMYKNNKSQVISWLALTWLFGAGFIGMEIYEF HHLIVNGMGPDRSGFLSAFFALVGTHGLHVTSGLIWMAVLMVQIARRGLTSTNRTRIMCL SLFWHFLDVVWICVFTVVYLMGAM 

>sp|Q9I425|CYOC_PSEAE Cytochrome o ubiquinol oxidase subunit 3 OS=Pseudomonas aeruginosa (strain ATCC 15692 / PAO1 / 1C / PRS 101 / LMG 12228) GN=cyoC PE=3 SV=1
MSTAVLNKHLADAHEVGHDHDHAHDSGGNTVFGFWLYLMTDCVLFASVFATYAVLVHHTA GGPSGKDIFELPYVLVETAILLVSSCTYGLAMLSAHKGAKGQAIAWLGVTFLLGAAFIGM EINEFHHLIAEGFGPSRSAFLSSFFTLVGMHGLHVSAGLLWMLVLMAQIWTRGLTAQNNT RMMCLSLFWHFLDIVWICVFTVVYLMGAL
>tr|Q7VDD9|Q7VDD9_PROMA Cytochrome c oxidase subunit III OS=Prochlorococcus marinus (strain SARG / CCMP1375 / SS120) GN=cyoC PE=3 SV=1
MTTISSVDKKAEELTSQTEEHPDLRLFGLVSFLVADGMTFAGFFAAYLTFKAVNPLLPDA IYELELPLPTLNTILLLVSSATFHRAGKALEAKESEKCQRWLLITAGLGIAFLVSQMFEY FTLPFGLTDNLYASTFYALTGFHGLHVTLGAIMILIVWWQARSPGGRITTENKFPLEAAE LYWHFVDGIWVILFIILYLL
>sp|Q8KS19|CCOP2_PSEST Cbb3-type cytochrome c oxidase subunit CcoP2 OS=Pseudomonas stutzeri GN=ccoP2 PE=1 SV=1
MTSFWSWYVTLLSLGTIAALVWLLLATRKGQRPDSTEETVGHSYDGIEEYDNPLPRWWFM LFVGTVIFALGYLVLYPGLGNWKGILPGYEGGWTQVKEWQREMDKANEQYGPLYAKYAAM PVEEVAKDPQALKMGGRLFASNCSVCHGSDAKGAYGFPNLTDDDWLWGGEPETIKTTILH GRQAVMPGWKDVIGEEGIRNVAGYVRSLSGRDTPEGISVDIEQGQKIFAANCVVCHGPEA KGVTAMGAPNLTDNVWLYGSSFAQIQQTLRYGRNGRMPAQEAILGNDKVHLLAAYVYSLS QQPEQ
>sp|P57542|CYOC_BUCAI Cytochrome o ubiquinol oxidase subunit 3 OS=Buchnera aphidicola subsp. Acyrthosiphon pisum (strain APS) GN=cyoC PE=3 SV=1
MIENKFNNTILNSNSSTHDKISETKKLFGLWIYLMSDCIMFAVLFAVYAIVSSNISINLI SNKIFNLSSILLETFLLLLSSLSCGFVVIAMNQKRIKMIYSFLTITFIFGLIFLLMEVHE FYELIIENFGPDKNAFFSIFFTLVATHGVHIFFGLILILSILYQIKKLGLTNSIRTRILC FSVFWHFLDIIWICVFTFVYLNGAI
>sp|O24958|CCOP_HELPY Cbb3-type cytochrome c oxidase subunit CcoP OS=Helicobacter pylori (strain ATCC 700392 / 26695) GN=ccoP PE=3 SV=1
MDFLNDHINVFGLIAALVILVLTIYESSSLIKEMRDSKSQGELVENGHLIDGIGEFANNV PVGWIASFMCTIVWAFWYFFFGYPLNSFSQIGQYNEEVKAHNQKFEAKWKHLGQKELVDM GQGIFLVHCSQCHGITAEGLHGSAQNLVRWGKEEGIMDTIKHGSKGMDYLAGEMPAMELD EKDAKAIASYVMAELSSVKKTKNPQLIDKGKELFESMGCTGCHGNDGKGLQENQVFAADL TAYGTENFLRNILTHGKKGNIGHMPSFKYKNFSDLQVKALLNLSNR
>sp|P0ABI8|CYOB_ECOLI Ubiquinol oxidase subunit 1 OS=Escherichia coli (strain K12) GN=cyoB PE=1 SV=1
MFGKLSLDAVPFHEPIVMVTIAGIILGGLALVGLITYFGKWTYLWKEWLTSVDHKRLGIM YIIVAIVMLLRGFADAIMMRSQQALASAGEAGFLPPHHYDQIFTAHGVIMIFFVAMPFVI GLMNLVVPLQIGARDVAFPFLNNLSFWFTVVGVILVNVSLGVGEFAQTGWLAYPPLSGIE YSPGVGVDYWIWSLQLSGIGTTLTGINFFVTILKMRAPGMTMFKMPVFTWASLCANVLII ASFPILTVTVALLTLDRYLGTHFFTNDMGGNMMMYINLIWAWGHPEVYILILPVFGVFSE IAATFSRKRLFGYTSLVWATVCITVLSFIVWLHHFFTMGAGANVNAFFGITTMIIAIPTG VKIFNWLFTMYQGRIVFHSAMLWTIGFIVTFSVGGMTGVLLAVPGADFVLHNSLFLIAHF HNVIIGGVVFGCFAGMTYWWPKAFGFKLNETWGKRAFWFWIIGFFVAFMPLYALGFMGMT RRLSQQIDPQFHTMLMIAASGAVLIALGILCLVIQMYVSIRDRDQNRDLTGDPWGGRTLE WATSSPPPFYNFAVVPHVHERDAFWEMKEKGEAYKKPDHYEEIHMPKNSGAGIVIAAFST IFGFAMIWHIWWLAIVGFAGMIITWIVKSFDEDVDYYVPVAEIEKLENQHFDEITKAGLK NGN
>sp|P0ABK2|CYDB_ECOLI Cytochrome d ubiquinol oxidase subunit 2 OS=Escherichia coli (strain K12) GN=cydB PE=1 SV=1
MIDYEVLRFIWWLLVGVLLIGFAVTDGFDMGVGMLTRFLGRNDTERRIMINSIAPHWDGN QVWLITAGGALFAAWPMVYAAAFSGFYVAMILVLASLFFRPVGFDYRSKIEETRWRNMWD WGIFIGSFVPPLVIGVAFGNLLQGVPFNVDEYLRLYYTGNFFQLLNPFGLLAGVVSVGMI ITQGATYLQMRTVGELHLRTRATAQVAALVTLVCFALAGVWVMYGIDGYVVKSTMDHYAA SNPLNKEVVREAGAWLVNFNNTPILWAIPALGVVLPLLTILTARMDKAAWAFVFSSLTLA CIILTAGIAMFPFVMPSSTMMNASLTMWDATSSQLTLNVMTWVAVVLVPIILLYTAWCYW KMFGRITKEDIERNTHSLY
>sp|Q6MIR4|NUOB_BDEBA NADH-quinone oxidoreductase subunit B OS=Bdellovibrio bacteriovorus (strain ATCC 15356 / DSM 50701 / NCIB 9529 / HD100) GN=nuoB PE=3 SV=1
MHNEQVQGLVSHDGMTGTQAVDDMSRGFAFTSKLDAIVAWGRKNSLWPMPYGTACCGIEF MSVMGPKYDLARFGAEVARFSPRQADLLVVAGTITEKMAPVIVRIYQQMLEPKYVLSMGA CASSGGFYRAYHVLQGVDKVIPVDVYIPGCPPTPEAVMDGIMALQRMIATNQPRPWKDNW KSPYEQA
>sp|Q89AU5|NUOB_BUCBP NADH-quinone oxidoreductase subunit B OS=Buchnera aphidicola subsp. Baizongia pistaciae (strain Bp) GN=nuoB PE=3 SV=1
MKYTLTRVNISDDDQNYPREKKIQVSDPTKKYIQKNVFMGTLSKVLHNLVNWGRKNSLWP YNFGLSCCYVEMVTSFTSVHDISRFGSEVLRASPRQADFMVIAGTPFIKMVPIIQRLYDQ MLEPKWVISMGSCANSGGMYDIYSVVQGVDKFLPVDVYIPGCPPRPEAYIHGLMLLQKSI SKERRPLSWIIGEQGIYKANFNSEKKNLRKMRNLVKYSQDKN
>sp|Q82DY0|NUOB1_STRAW NADH-quinone oxidoreductase subunit B 1 OS=Streptomyces avermitilis (strain ATCC 31267 / DSM 46492 / JCM 5070 / NCIMB 12804 / NRRL 8165 / MA-4680) GN=nuoB1 PE=3 SV=1
MGLEEKLPSGFLLTTVEQAAGWVRKASVFPATFGLACCAIEMMTTGAGRYDLARFGMEVF RGSPRQADLMIVAGRVSQKMAPVLRQVYDQMPNPKWVISMGVCASSGGMFNNYAIVQGVD HIVPVDIYLPGCPPRPEMLIDAILKLHQKIQSSKLGVNAEEAAREAEEAALKALPTIEMK GLLR


Astonishingly, certain bacteria that "everyone knows" are anaerobic turned up as aerobic when checked with the above Blast-query. (For example: Bacteroides fragilis, Desulfovibrio gigas, Moorella thermoacetica, and others.) It seems quite a number of so-called anaerobes have non-copper (heme only) cytochrome oxidases. (See this paper for further discussion.)

In any event, my Blast search turned up 1,089 positives (putative aerobes, some facultatively anaerobic) out of 1,373 bacterial species. I tagged the non-positives as anaerobes.

Of the 284 putative anaerobes, 87 scored positive in a Blast protein search (t-blast-n) for catalase. I used the following catalase sequences in my query: 


>sp|B0C4G1|KATG_ACAM1 Catalase-peroxidase OS=Acaryochloris marina (strain MBIC 11017) GN=katG PE=3 SV=1
MSSASKCPFSGGALKFTAGSGTANRDWWPNQLNLQILRQHSPKSNPMDKAFNYAEAFKSL DLADVKQDIFDLMKSSQDWWPADYGHYGPLFIRMAWHSAGTYRIGDGRGGAGTGNQRFAP INSWPDNANLDKARMLLWPIKQKYGAKISWADLMILAGNCALESMGFKTFGFAGGREDIW EPEEDIYWGAETEWLGDQRYTGDRDLEATLGAVQMGLIYVNPEGPNGHPDPVASGRDIRE TFGRMAMNDEETVALTAGGHTFGKCHGAGDDAHVGPEPEGARIEDQCLGWKSSFGTGKGV HAITSGIEGAWTTNPTQWDNNYFENLFGYEWELTKSPAGANQWVPQGGAGANTVPDAHDP SRRHAPIMTTADMAMRMDPIYSPISRRFLDNPDQFADAFARAWFKLTHRDMGPRSRYLGP EVPEEELIWQDPVPAVNHELINEQDIATLKSQILATNLTVSQLVSTAWASAVTYRNSDKR GGANGARIRLAPQRDWEVNQPAQLATVLQTLEAVQTTFNHSQIGGKRVSLADLIVLGGCA GVEQAAKNAGWYDVKVPFKPGRTDATQAQTDVTSFAVLEPRADGFRNYLKGHYPVSAEEL LVDKAQLLTLTAPEMTVLVGGLRVLNANVGQAQHGVFTHRPESLTNDFFLNLLDMSVTWA ATSEAEEVFEGRDRKTGALKWTGTRVDLIFGSNSQLRALAEVYGCEDSQQRFVQDFVAAW DKVMNLDRFDLA
>tr|D9RGS2|D9RGS2_STAAJ Catalase OS=Staphylococcus aureus (strain JKD6159) GN=katE PE=3 SV=1
MSQQDKKLTGVFGHPVSDRENSMTAGPRGPLLMQDIYFLEQMSQFDREVIPERRMHAKGS GAFGTFTVTKDITKYTNAKIFSEIGKQTEMFARFSTVAGERGAADAERDIRGFALKFYTE EGNWDLVGNNTPVFFFRDPKLFVSLNRAVKRDPRTNMRDAQNNWDFWTGLPEALHQVTIL MSDRGIPKDLRHMHGFGSHTYSMYNDSGERVWVKFHFRTQQGIENLTDEEAAEIIASDRD SSQRDLFEAIEKGDYPKWTMYIQVMTEEQAKSHKDNPFDLTKVWYHDEYPLIEVGEFELN RNPDNYFMDVEQAAFAPTNIIPGLDFSPDKMLQGRLFSYGDAQRYRLGVNHWQIPVNQPK GVGIENICPFSRDGQMRVVDNNQGGGTHYYPNNHGKFDSQPEYKKPPFPTDGYGYEYNQR QDDDNYFEQPGKLFRLQSEDAKERIFTNTANAMEGVTDDVKRRHIRHCYKADPEYGKGVA KALGIDINSIDLETENDETYENFEK
>sp|P60355|MCAT_LACPN Manganese catalase OS=Lactobacillus plantarum PE=1 SV=1
MFKHTRKLQYNAKPDRSDPIMARRLQESLGGQWGETTGMMSYLSQGWASTGAEKYKDLLL DTGTEEMAHVEMISTMIGYLLEDAPFGPEDLKRDPSLATTMAGMDPEHSLVHGLNASLNN PNGAAWNAGYVTSSGNLVADMRFNVVRESEARLQVSRLYSMTEDEGVRDMLKFLLARETQ HQLQFMKAQEELEEKYGIIVPGDMKEIEHSEFSHVLMNFSDGDGSKAFEGQVAKDGEKFT YQENPEAMGGIPHIKPGDPRLHNHQG
>sp|P42321|CATA_PROMI Catalase OS=Proteus mirabilis GN=katA PE=1 SV=1
MEKKKLTTAAGAPVVDNNNVITAGPRGPMLLQDVWFLEKLAHFDREVIPERRMHAKGSGA FGTFTVTHDITKYTRAKIFSEVGKKTEMFARFSTVAGERGAADAERDIRGFALKFYTEEG NWDMVGNNTPVFYLRDPLKFPDLNHIVKRDPRTNMRNMAYKWDFFSHLPESLHQLTIDMS DRGLPLSYRFVHGFGSHTYSFINKDNERFWVKFHFRCQQGIKNLMDDEAEALVGKDRESS QRDLFEAIERGDYPRWKLQIQIMPEKEASTVPYNPFDLTKVWPHADYPLMDVGYFELNRN PDNYFSDVEQAAFSPANIVPGISFSPDKMLQGRLFSYGDAHRYRLGVNHHQIPVNAPKCP FHNYHRDGAMRVDGNSGNGITYEPNSGGVFQEQPDFKEPPLSIEGAADHWNHREDEDYFS QPRALYELLSDDEHQRMFARIAGELSQASKETQQRQIDLFTKVHPEYGAGVEKAIKVLEG KDAK
>sp|Q9Z598|CATA_STRCO Catalase OS=Streptomyces coelicolor (strain ATCC BAA-471 / A3(2) / M145) GN=katA PE=3 SV=1
MSQRVLTTESGAPVADNQNSASAGIGGPLLIQDQHLIEKLARFNRERIPERVVHARGSGA YGHFEVTDDVSGFTHADFLNTVGKRTEVFLRFSTVADSLGGADAVRDPRGFALKFYTEEG NYDLVGNNTPVFFIKDPIKFPDFIHSQKRDPFTGRQEPDNVFDFWAHSPEATHQITWLMG DRGIPASYRHMDGFGSHTYQWTNARGESFFVKYHFKTDQGIRCLTADEAAKLAGEDPTSH QTDLVQAIERGVYPSWTLHVQLMPVAEAANYRFNPFDVTKVWPHADYPLKRVGRLVLDRN PDNVFAEVEQAAFSPNNFVPGIGPSPDKMLQGRLFAYADAHRYRLGVNHTQLAVNAPKAV PGGAANYGRDGLMAANPQGRYAKNYEPNSYDGPAETGTPLAAPLAVSGHTGTHEAPLHTK DDHFVQAGALYRLMSEDEKQRLVANLAGGLSQVSRNDVVEKNLAHFHAADPEYGKRVEEA VRALRED
>Haloarcula marismortui strain ATCC 43049(v1, unmasked), Name: YP_136584.1, katG1, rrnAC2018, Type: CDS, Feature Location: (Chr: I, complement(1808213..1810405)) Genomic Location: 1808213-1810405
MLKTVLMPSPSKCSLMAKRDQDWSPNQLRLDILDQNARDADPRGTGFDYAEEFQELDLDAVKADLEELMTSSQDWWPADYGHYGPLFIRMAWHSAGTYRTTDGRGGASGGRQRFAPLNSWPDNANLDKARRLLWPIKKKYGRKLSWADLIVLAGNHAIESMGLKTFGWAGGREDAFEPDEAVDWGPEDEMEAHQSERRTDDGELKEPLGAAVMGLIYVDPEGPNGNPDPLASAENIRESFGRMAMNDEETAALIAGGHTFGKVHGADDPEENLGDVPEDAPIEQMGLGWENDYGSGKAGDTITSGIEGPWTQAPIEWDNGYIDNLLDYEWEPEKGPGGAWQWTPTDEALANTVPDAHDPSEKQTPMMLTTDIALKRDPDYREVMERFQENPMEFGINFARAWYKLIHRDMGPPERFLGPDAPDEEMIWQDPVPDVDHDLIGDEEVAELKTDILETDLTVSQLVKTAWASASTYRDSDKRGGANGARIRLEPQKNWEVNEPAQLETVLATLEEIQAEFNSARTDDTRVSLADLIVLGGNAAVEQAAADAGYDVTVPFEPGRTDATPEQTDVDSFEALKPRADGFRNYARDDVDVPAEELLVDRADLLDLTPEEMTVLVGGLRSLGATYQDSDLGVFTDEPGTLTNDFFEVVLGMDTEWEPVSESKDVFEGYDRETGEQTWAASRVDLIFGSHSRLRAIAEVYGADGAEAELVDDFVDAWHKVMRLDRFDLE
>sp|B2TJE9|KATG_CLOBB Catalase-peroxidase OS=Clostridium botulinum (strain Eklund 17B / Type B) GN=katG PE=3 SV=1
MTENKCPVTGKMGKATAGSGTTNKDWWPNQLNLNILHQNSQLSNPMSKDFNYAEEFKKLD FQALKVDLYMLMTDSQIWWPADYGNYGPLFIRMAWHSAGTYRVGDGRGGGSLGLQRFAPL NSWPDNINLDKARRLLWPIKKKYGNKISWADLLILTGNCALESMGLKTLGFGGGRVDVWE PQEDIYWGSEKEWLGDEREKGDKELENPLAAVQMGLIYVNPEGPNGNPDPLGSAHDVRET FARMAMNDEETVALIAGGHTFGKCHGAASPSYVGPAPEAAPIEEQGLGWKNTYGSGNGDD TIGSGLEGAWKANPTKWTMGYLKTLFKYDWELVKSPAGAYQWLAKNVDEEDMVIDAEDST KKHRPMMTTADLGLRYDPIYEPIARNYLKNPEKFAHDFASAWFKLTHRDMGPISRYLGPE VPKESFIWQDPIPLVKHKLITKKDITHIKKKILDSGLSISDLVATAWASASTFRGSDKRG GANGGRIRLEPQKNWEVNEPKKLNNVLNTLKQIKENFNSSHSKDKKVSLADIIILGGCVG IEQAAKRAGYNINVPFIPGRTDAIQEQTDVKSFAVLEPKEDGFRNYLKTKYVVKPEDMLI DRAQLLTLTAPEMTVLIGGMRVLNCNYNKSKDGVFTNRPECLTNDFFVNLLDMNTVWKPK SEDKDRFEGFDRETGELKWTATRVDLIFGSNSQLRAIAEVYACDDNKEKFIQDFIFAWNK IMNADRFEIK
>sp|Q59635|CATB_PSEAE Catalase OS=Pseudomonas aeruginosa (strain ATCC 15692 / PAO1 / 1C / PRS 101 / LMG 12228) GN=katB PE=3 SV=1
MNPSLNAFRPGRLLVAASLTASLLSLSVQAATLTRDNGAPVGDNQNSQTAGPNGSVLLQD VQLLQKLQRFDRERIPERVVHARGTGAHGEFVASADISDLSMAKVFRKGEKTPVFVRFSA VVHGNHSPETLRDPRGFATKFYTADGNWDLVGNNFPTFFIRDAIKFPDMVHAFKPDPRSN LDDDSRRFDFFSHVPEATRTLTLLYSNEGTPASYREMDGNSVHAYKLVNARGEVHYVKFH WKSLQGQKNLDPKQVAEVQGRDYSHMTNDLVSAIRKGDFPKWDLYIQVLKPEDLAKFDFD PLDATKIWPGIPERKIGQMVLNRNVDNFFQETEQVAMAPSNLVPGIEPSEDRLLQGRLFA YADTQMYRVGANGLGLPVNRPRSEVNTVNQDGALNAGHSTSGVNYQPSRLDPREEQASAR YVRTPLSGTTQQAKIQREQNFKQTGELFRSYGKKDQADLIASLGGALAITDDESKYIMLS YFYKADSDYGTGLAKVAGADLQRVRQLAAKLQD


The first of these is a cyanobacterial katG (large subunit) type of catalase, perhaps representative of primitive protobacterial catalase. The second sequence in the above list is classic Staphylococcus catalase (katE). The third is a manganese-containing catalase from Lactobacillus. (This brought the most hits, by the way.) The others are, in turn, katA catalase from Proteus and Streptomyces, two organisms that are far apart in genomic G+C content (and rather distant phylogenetically); an Archaeal catalase (even though none of the 1,373 species in my organism list was Archaeal in origin; but you never know whether a given bacterium may have obtained its catalase through horizontal gene transfer); then a known-valid anaerobic catalase from Clostridium botulinum, and finally a Pseudomonas katB catalase. The idea was to cover as much ground, phylogenetically and enzymatically, as possible, with big and small-subunit catalases, of the heme as well as the manganese variety, from aerobic and anaerobic bacteria of high and low genomic G+C content, as well as an archaeal catalase for good measure.

Here, then, finally, is the list of 87 catalase-positive strict anaerobes:

Acetohalobium arabaticum strain DSM 5501
Alkaliphilus metalliredigens strain QYMF
Alkaliphilus oremlandii strain OhILAs
Anaerococcus prevotii strain ACS-065-V-Col13
Anaerococcus vaginalis strain ATCC 51170
Anaerofustis stercorihominis strain DSM 17244
Anaerostipes caccae strain DSM 14662
Anaerostipes sp. strain 3_2_56FAA
Anaerotruncus colihominis strain DSM 17241
Bacteroides capillosus strain ATCC 29799
Bacteroides pectinophilus strain ATCC 43243
Brachyspira hyodysenteriae strain ATCC 49526; WA1
Brachyspira intermedia strain PWS/A
Brachyspira pilosicoli strain 95/1000
Candidatus Arthromitus sp. SFB-mouse-Japan
Carnobacterium sp. strain 17-4
Clostridium acetobutylicum strain ATCC 824
Clostridium asparagiforme strain DSM 15981
Clostridium bartlettii strain DSM 16795
Clostridium bolteae strain ATCC BAA-613
Clostridium botulinum A2 strain Kyoto
Clostridium butyricum strain 5521
Clostridium cellulovorans strain 743B
Clostridium cf. saccharolyticum strain K10
Clostridium citroniae strain WAL-17108
Clostridium clostridioforme strain 2_1_49FAA
Clostridium difficile QCD-37x79
Clostridium hathewayi strain WAL-18680
Clostridium hylemonae strain DSM 15053
Clostridium kluyveri strain DSM 555
Clostridium lentocellum strain DSM 5427
Clostridium leptum strain DSM 753
Clostridium ljungdahlii strain ATCC 49587
Clostridium novyi strain NT
Clostridium ramosum strain DSM 1402
Clostridium saccharolyticum strain WM1
Clostridium scindens strain ATCC 35704
Clostridium spiroforme strain DSM 1552
Clostridium sporogenes strain ATCC 15579
Clostridium tetani strain Massachusetts substrain E88
Coprobacillus sp. strain 3_3_56FAA
Coprococcus comes strain ATCC 27758
Coprococcus sp. strain ART55/1
Dethiobacter alkaliphilus strain AHT 1
Dorea formicigenerans strain 4_6_53AFAA
Dorea longicatena strain DSM 13814
Erysipelotrichaceae bacterium strain 21_3
Eubacterium dolichum strain DSM 3991
Eubacterium eligens strain ATCC 27750
Eubacterium siraeum strain 70/3
Eubacterium ventriosum strain ATCC 27560
Flavonifractor plautii strain ATCC 29863
Halothermothrix orenii strain DSM 9562; H 168
Holdemania filiformis strain DSM 12042
Lachnospiraceae bacterium strain 1_1_57FAA
Lactobacillus curvatus strain CRL 705
Lactobacillus sakei subsp. sakei strain 23K
Mahella australiensis strain 50-1 BON
Natranaerobius thermophilus strain JW/NM-WN-LF
Oscillibacter valericigenes strain Sjm18-20
Parabacteroides distasonis strain ATCC 8503
Parabacteroides johnsonii strain DSM 18315
Parabacteroides sp. strain D13
Pediococcus acidilactici strain DSM 20284
Pediococcus pentosaceus strain ATCC 25745
Pelotomaculum thermopropionicum strain SI
Pseudoflavonifractor capillosus strain ATCC 29799
Pseudoramibacter alactolyticus strain ATCC 23263
Roseburia hominis strain A2-183
Roseburia intestinalis strain M50/1
Ruminococcaceae bacterium strain D16
Ruminococcus bromii strain L2-63
Ruminococcus obeum strain A2-162
Ruminococcus sp. strain 18P13
Ruminococcus torques strain L2-14
Sphaerochaeta pleomorpha strain Grapes
Spirochaeta coccoides strain DSM 17374
Spirochaeta sp. strain Buddy
Subdoligranulum sp. strain 4_3_54A2FAA
Tepidanaerobacter sp. strain Re1
Thermoanaerobacter brockii subsp. finnii strain Ako-1
Thermoanaerobacter ethanolicus strain CCSD1
Thermoanaerobacter pseudethanolicus strain 39E; ATCC 33223
Thermoanaerobacter sp. strain X514
Thermosediminibacter oceani strain DSM 16646
Treponema brennaborense strain DSM 12168
Turicibacter sanguinis strain PC909


Note that these are all bacteria; no archaeons are included. (And yes, there are catalase-positive anaerobes among the Archaea.) The reason you don't see Bacteroides fragilis (which is catalase-positive) on the list is that, as explained before, B. fragilis ended up being classified an aerobe by my cytochrome-oxidase-based initial search. Even though "everybody knows" B. fragilis is anaerobic.

Incidentally, Blast searches were done with an E-value cutoff of 1e-5, to reduce the chance of false positives. (E-value is a measure of how likely it is that a given Blast match could have occurred due to chance. A threshold value of 1e-5 means the only matches that will be accepted are those that have less than a 1-in-100,000 chance of occurring by chance.)

If you learn of any other catalase-positive anaerobes that should be on this list, do be sure to let me know!
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Hypnosis and Its Role in Society

By hypnosis the hypnotist produces a hypnotic state in an individual and uses this mental state to manipulate and control the person. A person in a hypnotic state reacts in the following ways:

He is intensely concentrated on one object or on things going on in one specific direction, for example the talk of the hypnotist.He senses and remembers very easily what is going on in that particular direction.He does not sense other objects or happenings around him, unless these other things are particularly violent.He believes anything told without assessing it logically, and can be brought to sense things that are not real.He tends to perform any order without objections, unless these orders are strongly opposed to the persons most basic moral.He is physically relaxed

A hypnotist can bring a person into a hypnotic state by many methods. By most methods the hypnotist will use the following general approach:

He makes the surroundings comfortable with no disturbing elements.He brings the person's attention towards himself and relax him further by a calm speech, and possibly with some soft music or other artistic tools.He shows an object that sticks distinctly out from the surroundings. The classical example is a watch in a chain, but sometimes the hypnotist only uses his hand. The hypnotist commands the person to concentrate upon the object.He lets the object make some simple action that is repeated for a while, for example lets the watch swing back and forth. The hypnotist can also speak calmly and comment the action of the object.Then he stops the action and directs the attention of the person solely towards his voice.At this point, but sometimes also before, he suggests to the person that he feels relaxed, warm or have other good feelings.

By now the patient should be in a hypnotic state. A good hypnotist will however not use this procedure mechanically. He will assess the patient's mental state, and prolong or repeat parts of the procedure until the hypnosis is effective.

While the patient is under hypnosis the hypnotist can direct the attention of the patient in directions suitable for his purposes and work on the patient by suggestions, stimulations, commands and passing of information. When the hypnotist has finished his work, the hypnosis is stopped by a distinct signal. The person will often be instructed to wake up again when he sees or hears the signal.

A professional hypnotist, which typically has a healthcare education before being trained in hypnosis, can use the hypnotic state for many purposes. He can motivate a person for lifestyle changes like cessation of substance abuse. He can motivate for results within sport or business, and he can ease learning of information.

Hypnosis is commonly used to take away pain and to bring relaxation. This can be the main purpose, or the more comfortable state of the patient can be utilized to perform other types of psychological or physical treatment.

Hypnosis is used as a psychiatric diagnostic tool. A suspected victim of a crime, for example child sexual abuse, is sometimes hypnotized to bring forth evidence. This method can easily produce false evidence, though, caused by suggestions during hypnosis. For these purposes the victim and the suspected person are often interrogated in a way that gives an hypnotic effect, even though it is not called hypnosis. Hypnotic techniques for diagnosis and investigation are sometimes, and probably more often that publicly known, supported by administering of drugs that suppress critical thinking and resistance.

The success of political mass movements is often due to deliberate use of hypnotic techniques towards grand audiences, even though these techniques are seldom called hypnosis. These techniques have often been developed during a long tradition within the political or religious organizations, or cooperating ones.

The leaders are deliberately trained in the use of these techniques, often in secrecy for the common members. Traditionally the techniques are used in the education of common followers at courses, schools, meetings and arrangements. But at some point in time the leaders decide to use the techniques in a grand scale in order to turn their organization into a mass movement.

Knut Holt Photo Knut Holt is an Internet marketer and business consultant with a focus on the health field. Please see his web-site to find more health information. There are also presentations of products to improve health, fitness products and also of hobby items. http://www.abicana.com/
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Exercise and Weight Reduction Fail to Save Lives in Diabetes Study

I hate having to tell people about pointless studies like the one just published in The New England Journal of Medicine by the nameless "Look AHEAD Research Group," but unfortunately, it's the kind of study that will have a lot of people saying "See this? Dieting and exercise won't make you live longer." (With the unspoken message: "So live it up. Have another Big Mac, light another Camel. When your time is up, your time is up.") In other words, people may leap to the wrong conclusion. So let's look at what was actually found.

The study followed two groups of obese type 2 diabetics (2,570 in the control group and 2,575 in the study group) for a median period of 9.6 years. The study group was subject to an "intensive intervention" of diet and exercise consisting of weekly group and individual counseling sessions for the first six months, sessions that occurred "with decreasing frequency over the course of the trial." Not surprisingly, subjects lost a modest amount of weight (just under ten kilos) in Year One, then gained much of the weight back, then lost some of the gainback toward the end of the study. But the control group also lost weight over the study period. By the end of the period, in fact, the control and study groups differed only 2.5% in weight. (The study group ended up at minus 6%; the control group, minus 3.5%.) Both started out with a body mass index of 36 (plus or minus 5.8 for the control group and 6.0 for the study group) and an average weight of 101 kg.

The major finding of the study was that the death rate among the two groups was not statistically different after 9.6 years. In the control group, 202 people died (57 from cardiovascular causes) while in the study group 174 died (52 cardio). In the words of the authors: "In conclusion, our study showed that an intensive lifestyle intervention did not reduce the risk of cardiovascular morbidity or mortality."

I have only two comments. One is that the study was not sized properly. The researchers admit they were banking on seeing an 18% difference between the two groups; and so they'd sized the study with that in mind. It seems clear to me that had they been more conservative and aimed for a higher enrollment target, the study's authors might very well have found statistically significant results. As it is, more people died in the control group. But the difference wasn't statistically significant.

A second way the study could have been improved would, of course, have been to get serious about weight loss. How can you call weekly meetings (for six months, in a study lasting ten years) an "intensive intervention"? How can you call 6% weight loss serious weight loss? When someone with a BMI of 36 who weighs 220 pounds loses 20, then gains some of it back, finishing the study at well over 200 pounds, that's not serious weight reduction, my friend. Not even close.

In "Cardiovascular Effects of Intensive Lifestyle Intervention in Type 2 Diabetes," New England Journal of Medicine, 24 June 2013, what we have are two groups of obese diabetics, each of which lost an unremarkable amount of weight and each of which suffered casualties at (surprise!) just about the same rate, over a ten-year period. That's not science, in my book. That's a waste of NIH grant money. But that's what passes for science in modern America.

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Do beliefs contain useful information?



The "Do bets reveal beliefs?" discussion continues. This is very interesting to me, since in finance experiments, you often depend on bets accurately revealing beliefs.

But lost in the mayhem of the debate is a second question: Do beliefs contain useful information in the first place?

In an econ experiment, of course they do, because researchers want to understand how humans process information. But how about in the real world? Take my bet with Brad DeLong. Suppose that bet did reveal my true belief, i.e. that inflation is going to spike. Suppose I really really really believed that, very strongly. So what? The belief of Noah Smith, no matter how strong, tells you incredibly little about the future path of inflation that the market for TIPS didn't already tell you.

Now, maybe there are exceptions to this. Suppose you have a well-respected, widely trusted expert in monetary economics, such as Steve Williamson. Last March, Steve Williamson confidently predicted a near-term spike in inflation, despite low TIPS breakevens, claiming that his understanding of monetary economics gave him private information that the market did not possess. If you believed that expert prediction, and increased your inflation hedging accordingly, then you lost money. Perhaps you are mad at Steve for losing you money, and you sulkily suspect that maybe Steve didn't really believe his own prediction. You wish that Steve had been forced to somehow reveal that he really, truly believed that inflation would spike, and was not pulling your leg.

But even in the case of experts, I think you need to be very, very confident in the expert's record before you give special weight to that expert's opinion. For example, Michael Boskin is legendary for getting every major macroeconomic prediction wrong since the beginning of time (update: Scott Sumner dutifully informs us that some of Boskin's so-called "predictions" were actually just implausible and unverifiable explanations for things, not true predictions). Paul Krugman is somewhat ahead of the average of pundits, though it's a small sample. Robert Shiller has an impeccable record of bubble prediction, but that sample is even smaller.

So the only time beliefs reveal useful information about financial outcomes, such as inflation, is if you trust a very special expert. If that expert is pulling your leg, then you have a problem. But I contend that this situation is very very very rare, because reliably market-beating experts are very very very rare.

So we see that the situations in which (economics) bets can most easily be made - concrete, financially important outcomes - are not only the situations in which bets are least likely to reveal beliefs (because either hedging or making the same bet with better odds is always possible using public markets), but also the situations in which individual beliefs are the least likely to contain useful new information.

But I suspect that the bet advocates (Alex Tabarrok and Bryan Caplan) want to extract a different kind of information from bets. I suspect -  and if I'm wrong, please correct me - that they are concerned with the ulterior motives of people who advance economic theories. For example, perhaps they suspect that Keynesians don't really believe in Keynesian business cycle models, but want increased government spending for the sake of redistribution. Or perhaps they believe that inflation hawks don't really believe their dire warnings of inflation, but want higher real interest rates for the sake of redistribution.

In this case, forcing an economist to reveal his or her true beliefs might be very useful. If it was revealed that an economist didn't really believe in the quantitative predictions of a theory that (s)he had spent a great deal of time and effort promoting, then that might be a signal that the economist had promoted the theory because of some ulterior motive.

And knowing the ulterior motives of would-be experts can be very useful information in situations in which public financial markets can't give you an answer. For example, suppose Economist A says "The Fed should lower interest rates to boost the economy! I know this because of my New Keynesian model." And Economist B says "Lower interest rates will just lead to inflation without boosting the economy! I know this because of my RBC model." And suppose that the New Keynesian model also just happens to predict lower inflation over the next 6 months, while the RBC model also just happens to predict higher inflation. In that case, forcing Economists A and B to make a bet on upcoming inflation might - or so Tabarrok and Caplan seem to hope - be able to reveal whether one or both of these economists actually has little confidence in his own theory. That in turn would reveal that that economist very possibly had some ulterior motive in advocating for that theory in the first place, which in turn would tell you not to trust that economist on policy matters in which the ulterior motive might apply.

This is what I think Alex Tabarrok is hoping when he says that a bet is a "tax on bullshit". He wants not to extract useful information about financial markets, but to reveal the ulterior motives of disingenuous public intellectuals, and thus get a better idea of whom to trust in the Marketplace of Ideas.

This, I think, is an excellent goal. Some kinds of bullshit are useful and should not be taxed, but disingenuous theory-promotion by public intellectuals seems to produce a negative externality that should be taxed away. The question of whether public bets are the tool to accomplish this goal, however, seems to hings on a lot of the questions Tyler Cowen has raised, such as what a public intellectual really risks when making a bet.
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Four levels of science



More philosophy-of-science blogging!

If you haven't yet read "Tantalus on the Road to Asymptotia", Ed Leamer's recent essay, and if you're at all interested in statistics, empirical economics, or science in general, then you should go read it. The essay is primarily a reply to an extremely important 2010 discussion paper by Joshua Angrist and Jorn-Steffen Pischke, called "The Credibility Revolution in Empirical Economics". That paper in turn is mainly a response to a 1983 Leamer essay called "Let's Take the Con Out of Econometrics". Such are the time scales over which deep academic debates are conducted. Actually, you should read all three.

The more recent two essays are discussing the idea of "natural experiments", and to what degree these make empirical economic studies (econometrics) more reliable. This is a very deep question about science. Normally, statistics can only see correlation, not causation; for example, you see that every time roosters crow, the sun comes up shortly afterward, but this doesn't tell you which caused which. A "natural experiment" would be if, for example, some disease killed all the roosters in town. Seeing that even without roosters, the sun still came up, you could conclude that rooster crowing (or, at least, rooster crowing in this specific town) was not necessary to summon the sun.

This natural experiment is very similar to a lab experiment. In fact, how is it different? Well, you might say, a lab experiment is controlled, and a natural experiment is not; in a lab, you can make sure outside stuff isn't disturbing your setup, while in a natural experiment you can't. This, in fact, is Ed Leamer's critique of natural experiments.

But I'm not sure that's right. In a lab experiment, we only convince ourselves that we've excluded all the outside causes. But sometimes, stuff that we didn't think about is messing with our experiment - cosmic rays, or the composition of the air, etc. Sure, lab experiments tend to exclude a lot more causes than natural experiments, but this need not be the case. For example, in finance experiments, even if you use an incredibly simple asset-market setup, subjects' behavior may be distorted by their pre-existing beliefs about the real-world stock market.

As I see it, the biggest advantage of lab experiments is that you can do them many times. You just can't do that with natural experiments. First of all, that allows you to control for a lot more things, since any confounding influence would have to be constant over space and time. Second, you can generate as much data as you want, making small-sample problems (another problem noted by Leamer) irrelevant. And third, it allows you to vary the setup intentionally, exploring the scope of an effect or a theory, and gaining a more complete picture of how the thing works. In other words, in even a perfectly designed natural experiment, we don't get to choose the questions we ask the world. In the lab, we do.

Ed Leamer focuses on the effect of confounding influences in natural experiments. He suggests doing sensitivity analysis to find what assumptions and specifications you need for a result to hold. I think that's a good idea. Basically, it's a way of groping around for something that looks like a set of scope conditions - testing the hypothesis to failure, to get a slightly better idea of when your theory works and when it doesn't. (Of course, if the natural experiment were a lab experiment, you could do this infinitely better, but if wishes were horses...)

As I see it, there are basically four "levels" of science. Each level gives you more confidence in your understanding of the world (i.e., in your theories and models). The levels are:

Level 1: History
This is basically just establishing precedents. It helps you define the set of things that can happen. Imagine a world without writing, and you'll see how important history is.

Level 2: Non-causal statistics
This is basically hunting for correlations. It can help you generate some guesses and ideas about what might cause what. It can also throw cold water on existing theories, since if A causes B, then we should probably see some kind of correlation, however variable or out-of-order, between A and B.

Level 3: Natural experiments
This is when you have some sort of randomized variation, but no ability to control the environment. An ideal natural experiment lets you establish that a causal effect occurred, but it's very hard to tell whether the setting was ideal or confounded, and you get only a limited amount of data.

Level 4: Lab experiments
By allowing replication and control of the environment, lab experiments usually produce more convincing  conclusions about causal effects, generate as much data as you want, and allow you to explore the scope of the scope of the effects you find (i.e. when they do and don't happen).

If we could always understand the world through lab experiments, we would. When we can't put things in a lab - like the macroeconomy, or the Milky Way galaxy - then we should look for natural experiments. But if we can't find sources of random variation, then we should at least look for correlations. And if we don't have reliable quantitative data, the best we can do is just write down what we see.


Update: Noah receives a partial smackdown from...Noah's dad! The father is not satisfied with my one-dimensional classification of research methods, and wants to bring external validity into the picture:
Briefly, research methods vary on two important dimensions, one we can call internal validity (how sure are we that we know what caused our results?), and the other ecological validity (do our observations relate to the real world?). Only the experimental method can logically show cause-and-effect, so it is highest in internal validity, but the artificial situations created by controlling so many factors make it low in ecological validity (also, experiments can be flawed in many ways, such as poor methods, restriction in the range of observations, confounding factors we didn't think about, etc., which is why replication and attempts to falsify claims are intrinsically important to experimental science). Naturalistic observation is highest in ecological validity, lowest in internal validity. Other methods, such as correlation, ex post facto "experiments" (aka, "natural" experiments), and case studies are in-between on both dimensions.  
Even experiments can vary on these two dimensions, some tightly controlled and measured, some using more naturalistic real-world manipulations and more complex settings in which many factors can interact. The ideal situation is one in which experiments at both ends of this continuum show the same thing, thereby bolstering internal and ecological validity. I refer to this approach as "alignment" in a research area, which helps tie real-world phenomena to causes. This ties, for example, my highly controlled lab research on creative cognitive processes (like fixation or incubation) to more naturalistic research with design students, and to research with real designers with real jobs.
Well, there you have it. Note that I was originally trained as a physicist, and in physics, the Principle of Superposition assures you that any conclusion with internal validity will have external validity as well (i.e., the real-world motion of objects is just assumed to be caused by a straightforward combination of things that you can observe in labs). This is less so in other sciences, and much less so in social sciences like psychology and econ.
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