Mettet 2 – eksperimentet

I retorikkens og logikkens verden har man det som kalles logiske feilslutninger. For eksempel det som kalles «argumentum ad auctoritatem», eller argument fra autoritet, som betyr at vi sier noe er sant fordi en autoritet har sagt det (og det kan man jo ikke si). På engelsk opererer man også med begrepet «the fallacy fallacy» som sier at man ikke kan forkaste noens argumentasjon eller andre påstander fordi de en plass i argumentasjonen eller tidligere har begått en logisk feilslutning. Det ville vært en logisk feilslutning i seg selv. Vi kan nemlig ta feil om noe og likevel ha rett om noe annet.

Nylig skrev Kjetil Rolness et innlegg i Dagbladet om kosthold og ernæring av alle ting kalt «Den store feite forskningsskandalen». Her skriver han om hvordan ernæringsvitenskapen har en svært broket historie, som kan ha ført til både formulering av kostholdsråd som ikke er helsemessig forsvarlige og også at personer som har sagt imot gjeldene råd har blitt latterliggjort. Innlegget til Rollnes var i stor grad inspirert av en sak skrevet av forfatter og journalist Ian Leslie i the Guardian.

Leslie sin sak er et must å lese om man er interessert i helse og ernæring. Leslie argumenterer også for at vi har blitt villedet når det gjelder kosthold, blant annet på grunn av dårlige og uærlige forskere, markedskrefter og ikke minst en utstrakt bruk at et vitenskapelig verktøy som er svært dårlig egnet for feltet, nemlig epidemiologi. Som Leslie skriver:

«Epidemiological research involves the collection of data on people’s behaviour and health, and a search for patterns. Originally developed to study infection, Keys and his successors adapted it to the study of chronic diseases, which, unlike most infections, take decades to develop, and are entangled with hundreds of dietary and lifestyle factors, effectively impossible to separate.»

BEST-SELLER-cover-imageDet er spennende at ernæringsfaget de siste årene har blitt preget av personer som ikke er ernæringsfaglig utdannet selv, og som påvirker gjennom å skrive om historien til faget. Gary Taubes hadde stor gjennomslagskraft med sin bok om ernæringshistorien og ernæringsfagfeltet, selv om han selv er utdannet innen fysikk. Nylig har Nina Teicholz hatt stor påvirkningskraft og skapt mange overskrifter etter hun gav ut boka «The Big Fat Surprise». I likhet med Tuabes sin Good Calories Bad Calories er The Big Fat Surprise et enormt stykke arbeid som avslører hva som ligger bak vår tro og kunnskap om kosthold og de er begge viktige bøker  å lese for ernæringsfaglige.

Når man ser på historien til kostholdsanbefalingene blir man nødvendigvis trukket mot historien om Ancel Keys, hans Six og Seven Countries studier og utallige videre studier i tillegg til hans korstog mot alle som sa hans teorier imot. Etter alt man har lest om Ancel Keyes opp gjennom årene er det vanskelig å trekke noen annen konklusjon enn at han må ha vært en drittsekk uten sidestykke, selv om han kanskje for det meste hadde gode intensjoner. Hans vitenskapelige fremtoning er garantert ikke et eksempel til etterfølgelse, men det er likevel hans fremtoning som i stor grad er grunnen til at vi er der vi er i dag med tanke på hva vi tror (legg merke til ordet «tror» her) er sunt. Mye av diskusjonen i etterkant av Rolness sitt innlegg handler om data fra Keys studier.

mg_9698
Erik Arnesen

En som ikke overraskende reagerte på Rolness sitt innlegg i Dagbladet, var Erik Arnesen. Arnesen er helsefaglig rådgiver i Landsforeningen for hjerte- og lungesyke (LHL) og leder mettet fett gruppen i Nasjonalt råd for ernæring. Arnesen skriver om Rolness på sin blogg:

«I tillegg serverer han saftige utsagn som at vi har et ‘diettpoliti som har gjort et ukontrollert eksperiment på hele befolkningen over flere tiår’ og at flere tusen dødsfall skyldes ‘statlige sunnhetsråd'».

Arnesen ser ut til å være mest opptatt av å motbevise Rolness sine påstander om at man har fokusert for lite på sukker og for mye på fett. Hadde bare Rollnes brukt ordet sukker i utvidet forstand og ment sukker, stivelsesrike og raffinerte matvarer så hadde han hatt mer rett. Man må huske at om sukker dømmes for å ha forårsaket vår uhelse, så dømmes også i stor grad stivelsesrike matvarer. Men selv om Rolnese ikke har fått alle fakta helt på bordet angående Keys og fokus på sukker og fett, så skriver han som vist at det har vært gjort et «…ukontrollert eksperiment på hele befolkningen over flere tiår.»

Og tilsynelatende fordi Rolness ikke har alle fakta helt på plass og muligens gjør noen logiske feilslutninger i polemikkens gode navn, avfeier Arnesen dette utsagnet med:  «Å kalle kostrådene, og spesifikt kostrådene om fett, for et ‘ukontrollert eksperiment’ strider imidlertid mot både fornuft og data.» (det gis imidlertid ikke noen gode data for å støtte dette utsagnet og Arnesen forsøker seg med å si at evolusjonært sett har vi sannsynligvis ikke spist så mye mettet fett likevel).

Men om Rolness, og evt andre som hevder det samme, tar feil om andre ting, så betyr det ikke at han tar feil når han kaller det et eksperiment. Å si dette ville vært et eksempel på en feilslutning feilslutning (fallacy fallacy).

Det har blitt gjort et eksperiment, fordi det aldri har eksistert data som har gitt grunn til å tro at mettet fett stod bak livsstilssykdommene våre. Man har på bakgrunn av utvikling i livsstilssykdommer og utvikling av overvekt hatt et enormt fokus på fettreduksjon i offentlige kostråd og man har ikke ant konsekvensen av hva som skjer dersom befolkningen reduserer sitt totale fettinntak og erstatter det med stivelsesrike karbohydrater, eller hva som skjer om befolkningen erstatter animalsk fett rikt på mettet fett med planteoljer. Med et fullstendig manglende vitenskapelig grunnlag og ingen anelse om hva som kommer til å skje med oss om vi følger anbefalingene (for slik har mennesker aldri spist tidligere i noen samfunn) må vi kalle det et eksperiment.

Når Arnesen skriver at vi sannsynligvis ikke har spist så mye mettet fett evolusjonært sett, som ikke i seg selv er et argument for at mettet fett er usunt, så refererer han til en artikkel med Loren Cordain som hovedforfatter, mannen som står bak paleokostholdet og som sier om at det er en ting vi ikke burde spise, så er det kornprodukter, noe vi sannsynligvis har spist mye av i stedet for animalsk produkter siden myndighetene i det uendelige maser om hvor sunt korn er og hvor usunt animalsk fett er.

Ian Leslie, Gary Taubes, Nina Teicholz og andre som har vist at ernæringsfaget er skammelig uvitenskapelig og vist at de siste ca. 50 årene ikke kan kalles noe særlig annet et eksperimentelle, hva angår kostholdsanbefalingers påvirkning på helse, støttes av store mengder data.

For å ta et par korte eksempler (det finnes mye mer). I 1966 til 1973 ble The Sydney Diet Heart Study gjennomført. Studien har blitt brukt som grunnlag for å si og anbefale at vi må bytte ut mettet fett med flerumettet fett.

I studien var en intervensjonsgruppe som økte inntaket av flerumettet fett (først og fremst omega 6) og reduserte sitt inntak av mettet fett. I tillegg hadde man en kontrollgruppe som ikke fikk noen spesielle råd. En ny gjennomgang av data fra denne studien publisert i BMJ i 2013 (1) viste at intervensjonsgruppen hadde 70% økt kardiovaskulær dødelighet sammenlignet med kontrollgruppen. Tilsynelatende ikke en smart kostholdsendring.

Ramsden-LMBB
Christoffer Ramsden

Her om dagen kom en ny artikkel ut, skrevet av Christoffer Ramsden og kolleger. Det var Ramsden som stod bak artikkelen om Sydney Diet Heart Study også. Denne gangen hadde han sett på tidligere upubliserte (woops!) data fra Minnesota Coronary Experiment (1968-73) (2). Studien hadde en gruppe som byttet ut mettet fett med plantefett og margarin og en gruppe som spiste mer mettet fett.

Dataene viste at de som spiste mindre mettet og mer umettet plantefett reduserte kolesterolnivået mye og jo mer de reduserte kolesterolnivået jo mer økte risikoen deres for å dø. Man så ingen fordeler av denne kostholdsendringen med tanke på hjerte- og karsykdom. For å virkelig spikre igjen kista til rådet om å bytte mettet fett med margarin og planteoljer, inkluderte Ramsden og kolleger 5 andre studier (til sammen over 10 000 deltakere) og gjorde en metaanalyse som viste at man verken forebygger hjerte- og karsykdom eller total dødelighet ved å bytte mettet med umettet.

Deres konklusjon lød som følger:

«Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.»

Gary Taubes intervjuet Ivan Franz, som stod bak Minnesotastudien. Dette var en enorm og godt gjennomført studie, men den ble aldri spesielt populær fordi resultatene fra den ikke støttet den gjeldende hypotesen. Franz, som da jobbet sammen med Ancel Keys, ventet faktisk 16år med å publisere sine data til etter han hadde pensjonert seg og da i lite populære og innflytelsesrike journaler. Som forklaring på dette sa Franz ganske enkelt: «We were just disappointed in the way it came out.»

Vitenskapelige data støtter med andre ord ikke anbefalingene vi blir gitt, og mye tyder på at noen av anbefalingene gjør mer vondt enn godt. Å gi denne anbefalingen om å bytte mettet med umettet, har vært et eksperiment tidligere og det er et eksperiment nå. Heldigvis kan mange av oss velge om vi vil være med på eksperimentet og jeg er garantert ikke med på det. Jeg nyter mitt kosthold rikt på mettet fett fra planter og dyr og holder meg langt unna margariner og planteoljer rike på omega 6.

PS. Få også med deg Turid Sylte sitt innlegg i Verdens Gang kalt «Bacon er sunnere enn sukker» her.

  1. Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ (Clinical research ed). 2013;346:e8707.
  2. Ramsden CE, Zamora D, Majchrzak-Hong S, Faurot KR, Broste SK, Frantz RP, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ (Clinical research ed). 2016;353:i1246.

 

Litt av hvert fra februar

En ny måned er over og det må vel konkluderes med at ting går fremover med tanke på kunnskap om kosthold, trening og helse.

Arbeidet jeg gjør med å skrive på blogger er en hobby for meg. Jeg har enn så lenge unngått å ha noen form for reklame på sidene mine og ønsker å fortsette med å være helt uavhengig og skrive det jeg ønsker å skrive. Det betyr at om jeg skriver positivt om noe, så er det ikke fordi jeg får betalt for det, men fordi jeg mener det fortjener positiv omtale. Det er kommet en ny knapp på høyre side av denne bloggen (doner-knappen). Den er en mulighet for lesere til å gi et lite beløp og dermed indirekte spandere en kaffe på meg (jeg er veldig glad i kaffe) om man skulle ønske.

Her i Norge har man i februar kranglet om brunosten, en krangel som har vært preget av følelser fremfor fakta og som jeg derfor ikke har funnet verken interessant eller konstruktiv.

1. mars arrangerte Kostreform for bedre helse sin nystartede Vestfoldavdeling Kostholdskonferansen 2014. Jeg var der og holdt foredrag om hva mennesket egentlig er laget for å spise. Sofie Hexeberg snakket om hvordan man kan bli frisk med lavkarbo, mens Erik Hexeberg stilte spørsmål ved om vi kan stole på Helsedirektoratets råd om ernæring og helse. Tore Jardar S. Wirgenes, som driver den økologiske gården Virgernes gård (like gårdens side på facebook her) pratet om det viktige arbeidet han og andre økologiske bønder gjør. Bor du i Larviksområdet er denne gården verdt å benytte seg av. Filmer av foredragene vil etter hvert bli lagt ut på konferansens nettside.

Et fantastisk bilde for de anatomiinteresserte
New York Times skrev denne måneden at nye data tyder på at amerikanerne til en viss grad lykkes med å stagge utviklingen av overvekt hos barn. Samtidig rapporteres det om at utviklingen av overvekt og fedme generelt i USA ikke ser ut til å endre seg nevneverdig.

En ny studie tyder ikke overraskende på at det å drikke alkohol rett etter en treningsøkt kan gi dårligere restitusjon og treningsutbytte.

For ikke lenge siden var fettlever noe alkoholikere fikk. Nå er det helt vanlig å få uavhengig av alkoholinntak og til og med ned i ung alder. Årsaken ligger i kostholdet og spesielt karbohydratene. Fettlever kan regnes som et annet symptom på vår dårlige livsstil og kunne nesten vært regnet som en del av det metabolske syndrom. Heldigvis er det mulig å gjøre noe med det og stadig mer forskning viser at karbohydratrestriksjon bør spille en grunnleggende rolle når man skal fikse en lever ødelagt av moderne livsstil. 

Et ketogent kosthold med lite karbohydrater gjør at sultfølelsen går ned. En ny studie undersøkte om dette hadde sammenheng med at de delene av hjernen som påvirker sult endrer energikilde. I studien målte man opptak av sukker i disse områdene i hjernen på et kosthold med lite karbohydrater og et med mer karbohydrater. Studien viste et likt opptak av sukker på de ulike kostholdene noe som tyder på at den sulthemmende effekten av ketogen kost ikke kommer av at hjernen endrer drivstoff.

I 2008 var over 200 millioner men og nesten 300 millioner kvinner over 20 år fete (BMI > 30), og 65% av verdens befolkning bor i land hvor overvekt tar livet av flere mennesker enn undervekt. Til tross for at forekomsten av overvekt øker og karbohydratrestriksjon er et ypperlig verktøy for å takle overvekten, er fortsatt mange skeptiske til denne strategien – en skepsis som med all sannsynlighet gjør det vanskeligere å takle utviklingen i overvekt. Den italienske forskeren Antonio Paoli har skrevet en god artikkel om hvordan og hvorfor ketogent kosthold kan brukes i overvektsbehandling. Artikkelen ligger ute for alle å lese her.

Chris Kresser gir deg her flere gode grunner til at du bør tenke deg om flere ganger før du forsøker et vegetarisk kosthold og i hvert fall et vegansk kosthold. Personlig ville jeg også kunne vært vegeterianer om bacon vokste på trær.

Brasil har kommet med forslag til nye kostholdsråd som ser ut til å være verdt etterfølgelse. De fokuserer på det viktigste. Les mer her.

Gary Taubes skrev en kort kronikk i New York Times om hvorfor ernæring er så forvirrende. Absolutt verdt en les her.

En ny studie viser at steinalderkost er mer slankende enn offisielle kostråd. The Guardian skriver i samme ånd om at vi bør se til tradisjonelle kosthold for å lære hva næringsrikt kosthold er.

Har du lyst til å lage din egen leverpostei? Her har du én metode med bilder.

Scientific American skriver om hvordan glutenintoleranse ikke nødvendigvis handler om gluten i det hele tatt og at mange symptomer ser ut til å komme fra andre proteiner i korn og uten at det er synlig skade eller inflammasjon i tarmene. Selv om gluten kanskje er de verste proteinene i fra korn, er det mange andre potensielle syndere og glutenfritt kosthold kan være langt verre en kornfritt kosthold.

Og for de med ekstra interesse i fysiologi skriver Peter Attia kort og konkret om kreft og karbohydrater her.
Vel, det var kort om noe av alt det interessante som har sjedd i februar. March, here I come!

NuSi

Det er mulig det høres rart ut, men vi har egentlig ganske få gode data (informasjon fra vitenskapelige studier kalles gjerne data) om hvordan kostholdet påvirker helsen. Dette gjelder først og fremst detaljkunnskap. For vi kan slå oss til ro med at et sunt kosthold er et paleo-inspirert kosthold med lite moderne og høyt bearbeidede matvarer. Det er utrolig lite sannsynlig at denne kunnskapen vil endres betraktelig og det blir stadig mindre sannsynlig at det vil komme kunnskap som sier at denne strategien er dårlig. Man kan jo spørre seg hva som da er vitsen med å fortsette å forske på kosthold og helse? Kan vi ikke bare slå oss til ro med det vi nå vet, slenge et kjøttstykke på grillen og slappe av?

Vel, for de som ikke er spesielt kunnskapshungrige vil jeg kanskje anbefale nettopp dette; slenge litt kjøtt på grillen og slappe av, det er i hvert fall sunt. Men for de av oss som ønsker å forstå verden så godt som mulig, og jeg regner med at du som leser dette tilhører denne gruppen, ellers ville du ikke sittet her og lest, så er det fantastiske mengder med uoppdaget kunnskap om sammenhengene mellom helse og kosthold som bare venter på å oppdages.

Men vi må være særdeles bevisst hvordan vår nye kunnskap blir til. Vi har som sagt ikke så mye virkelig gode data. Den lave kvaliteten på den informasjonen vi allerede har, har bidratt til misforståelser, problemer og uhelse, og en av grunnene er at man har overvurdert kvaliteten til de eksisterende vitenskapelige dataene. Reduksjon i karbohydratinntak vil for eksempel gjøre oss slankere og burde være standard råd hos dem med type 2 diabetes, men dette er ikke standard råd ved verken overvekt eller diabetes. Spørsmålet er hvorfor?

En av grunnene er at i en overraskede stor del av ernæringsforskningen vet man ikke egenlig hva forsøkspersonene har spist. Ofte får de som er inkluderte i vitenskapelig studier bøker, brosjyrer eller informasjon om hva de skal gjøre for så å bli overlatt til seg selv. For å vite hva forsøkspersonene har spist bruker man gjerne spørreskjemaer eller matregistrering.

Jeg har selv gjort en studie der forsøkspersonene skulle spise lite karbohydrater. I løpet av forsøket skulle de ved to anledninger notere ned alt de spiste og drakk i fire dager. Dette ble samlet inn og brukt i analyser. Men sannheten er at vi egenlig ikke har anelse om hva de spiste. Vi så det tross alt ikke og vi er prisgitt forsøkspersonenes subjektive tilbakemelinger med alle feilkilder det inkludrer. Dette er den aller vanligste metoden for registrering av matinntak i kostholdsstudier og den gir svært usikre data både når det gjelder kvalitet og kvantitet på kostholdet.

Et alternativ er å innlegge forsøkspersoner på sykehus eller klinikker der de blir overvåket døgnet rundt og får all mat ferdig målt opp, tilrettelagt og servert av studiearrangørene. Men dette er dyrt og gjør både at slike studier har få deltakere og at de varer alt for kort for at man kan si noe om langtidseffekter. Det er også ofte en unaturlig setting som gjør at resultatene ikke nødvendigvis kan overføres til hverdagssituasjoner.

Mye av forskningen som ligger til grunn for overvektsbehandling har også blitt gjort på tynne personer, ved at man f.eks. har gjort overspisingsstudier (som er basert på hypotesen om at det eneste som betyr noe er mengden kalorier) eller studier der man endrer kostholdssammensetningen og måler endringer i vekt eller fettmasse. Men det er svært sannsynlig at tynne mennesker er nettopp de som er immune mot det som skaper overvekt hos andre og å bruke data fra slike studier er ikke bare meningsløst, det kan også gjøre at vi tar fullstendig feil. Spørsmålet er hva som gjør overvektige personer overvektige, ikke hva vi kan gjøre for å gjøre tynne overvektige.

Dette er bare noen av grunnene til at mye av kunnskapen vi har om blant annet kosthold og vekt er dårlig og usikker. Og svakheter ved de vitenskapelige dataene er en av hovedgrunnene til at Peter Attia og Gary Taubes startet Nutrition Science Initiative eller NuSI.

NuSi er en frivillig organisasjon med mål om å reduserer den økonomiske og sosiale byrden av fedme og fedmerelaterte sykdommer, gjennom å øke kvaliteten på vitenskapen innen forskning på ernæring og fedme.
Dette er et utrolig spennende initiativ og jeg tror det virkelig kan ha noe å si etter hvert. Nylig var Attia og pratet på TedMed (Ted.com er stedet å være for alle som ønsker å lære mer, nesten uansett felt) og det blir spennende å se foredraget når det kommer. For de av dere som er ekstra interessert i ernæringsvitenskap anbefaler jeg å se gjennom sidene til NuSI. Så håper jeg at det blir gjort mye god forskning fremover som kan gi oss enda mer og ikke minst bedre kunnskap om sammenhengene mellom helse og kosthold.

Her en kort film fra Attia som forklarer nærmere: 

A spark of reason

I’ve been reading through many (not all) of the comments on Guyenet’s rebuttal of the carbohydrate hypothesis. Although it can be rather tedious, especially because of the apparent mental hospital escapee ItsTheWoo2 (who does have a few good points but a complete lack of putting those point out there in a sane way), but Stephan finally got to his senses and blocked the comments from her (him?).

After reading both the blog post and the comments I find that I am rather unsure of what we are discussing. It seems we are dealing with to poorly defined theories and that much of the seemingly contradictory nature of those theories stem from a lack of clear definition.

The only comment I felt was really worth noting was that of Dave “Spark of reason” Dixon who had this to say:

@Stephan,
Just to clarify (and apologies if already discussed, I haven’t gone through all of the comments): what precisely is the «carbohydrate hypothesis» under discussion? Is it that carbohydrate is *necessary* for obesity, or *sufficient*? My reading of Taubes is the former, that you need carbohydrate to drive fat storage, but not that just eating carbohydrates will make you fat.
I don’t find anything in what you presented which is inconsistent with that view, e.g. examples of lean cultures with traditionally high-carbohydrate diets may simply indicate that other factors are needed to drive obesity, and particularly metabolic syndrome. Are there any examples of obesity occurring in the absence of dietary carbohydrate?

Isn’t this actually an important point? Does the carbohydrate hypothesis being discussed say that carbohydrates are necessary or sufficient for causing obesity? If, as Dave interprets GCBC, the theory says carbohydrates are necessary, then what exactly are people arguing about?

I don’ get it!

Macronutrients and food reward

If you see one bright red swan, you are not likely to give up a theory that says that all swans are white; you will instead go looking for the person who painted it. 

Imre Lakatos 

Much is being said on this subject. Bet many are getting pretty fed up by now. But I still think this is an interesting discussion and so I will take this opportunity to add some thoughts. After all, the goal here is to find the truth; to find out how the world works. In that respect, I would also like to say that I do not agree with any one side in this discussion. Scientifically speaking, agreeing is not very scientific. That would mean confusing matters of opinion with matters of fact. Things are just what they are.

Chris Kresser is of course right in that there is no single cause of obesity. In animal studies obesity can be induced in a number of ways, just as in humans. The fat tissue is a large part of our body and it has a wide range of receptors and interesting signaling, so it should not come as a surprise that there are many ways to become fat.

If we are to look for a general cause, we could say that western, post agriculture lifestyle is to blame for obesity and our lifestyle diseases. But that does not mean you cannot get fat eating paleolithic foods, although if you did, you should blame your parents for the lousy chromosomes.

Neither carbohydrates nor food reward is able to explain all the observations. They both explain a part of the observations and so are both likely influential factors. Just how big a role each plays is an extremely difficult question to answer. Thus the current discussion.

The key question is: Why is not hunger down-regulated in humans becoming fat?

The Guru Walla
From what I can see, the Cameroonian Guru Walla is a bland food, overeating, fat gaining rite.

In the Guru Walla ritual, young Cameroonian men consume a diet made of red sorghum and cow milk (makes up over 95% of calories). The young men isolate themselves in different houses with a female attendant devoted exclusively to the preparation of Guru Walla meals. The diet and exclusion is supposed to lead to a certain level of purity. The men eat every 3 hour for 60 days, during which time body-weight can increase by an average of 17kg. Only 64-75% of the weight gain is fat [1].

Traditional food amongst these Cameroonians is about 75% CHO, 10% fat and 15% protein. During the Guru Walla it is 70% CHO, 15% fat and 15% protein.

The Guru Walla food is obviously fattening; at least if force fed and combined with minimal physical activity. The question we need to ask is: Would the Cameroonians be overweight if all they consumed was the Guru Walla diet?

It seems that the Cameroonians do not get fat because of the food itself. Rather they become fat because they force feed themselves. The newly gained weight is also lost after the ritual.

The reason I called the Guru Walla food bland, is that it most likely is very bland after the first few days. Try eating any one food exclusively for 2 months, and eat it even though you are not hungry (vomiting is also a part of the Guru Walla). The dopamine reward response should be minimal. Remember the Twinkie Professor who ate nothing but Twinkies, Oreos, donuts and similar crap but who lost 27 pounds in a 10 week experiment. He did consciously under eat, but my point is that we need to ask ourselves how lack of variation affects reward.

Food reward
While food reward might help explain why we overeat at a biochemical level, there is little evidence to indicate that a fat loss diet needs to be unrewarding, if by unrewarding we mean less palatable. We also need to know if it is possible to unconsciously overeat (become fat) on rewarding foods if we have a working metabolism and the rewarding foods do not mess with our metabolism. If not, whatever caused the metabolism to go out of whack is the real problem.

Stephan’s bland food through a straw experiment does not necessarily support a theory claiming that the study participants lost weight because of an inherently unrewarding quality of that particular diet. The finding could easily also support the theory that eating only one food, no matter how rewarding it may be when consumed intermittently, will make people lose weight because the rewarding quality of that food declines with increasing intake.

So we need to know if people could lose similar amounts of weight eating other foods exclusively.

Leptin
I am still having trouble seeing what’s the big fuzz about leptin. It is a signaling molecule. It signals energy surplus and the lack of leptin signals lack of energy. Leptin also increase fat oxidation. The leptin deficient animal models, that are obese, act and behave as they were starving and administering leptin normalize their behavior and induce weight loss. Either the body just needed to be told that it had stored energy to use, or we just needed to increase fat oxidation. If you increase fat oxidation by other means such as GH, ob/ob mice lose weight just as with leptin.

If for example high insulin levels cause leptin resistance, focusing on leptin does not add anything to obesity treatment. High insulin levels can also be caused (or at least be exacerbated) by factors other than carbohydrates. For example factors that messes with liver function.

“In particular, protein-rich foods such as beef can increase insulin secretion as much as certain starch foods such as pasta, or more.” 

The quote takes the results from trials out of context. It is an unfair statement, just like “proteins are inherently satiating” statement. A few days of beef eating will likely lead to lower insulin than a few days of pasta. I’ve written some about satiating proteins here.

In overweight people, as in overweight animal models, the key issue seems to be a reduced fat oxidation. Reduced fat oxidation with a high energy intake cause fat deposition in most all tissues and also insulin resistance.

Anything that increase fat oxidation in overweight animal or humans, cause weight loss and reduced food intake.

Lessons from insulin resistance
Stephan claims that overweight people have high serum free fatty acids. This is not completely true, at least if we are to listen to Keith Frayn at [2]. The claim may be true in general, but there are lots of overweight people with normal FFA levels. This however does not change Stephan’s argument. Generally the fat tissues of the overweight give out more FFA indicating adipose tissue insulin resistance.

Here is how we imagine insulin resistance to occur (roughly):

The pancreas has a direct route to the liver. The reason for this direct route is that the liver controls blood sugar level through its production of glucose. When blood sugar rises, the pancreas notice and secretes insulin. When the liver receives this insulin, glucose production is reduced. As the cells in the body are utilizing glucose for fuel, blood glucose level drop.

Somehow the liver becomes insulin resistant and keeps sending out glucose despite the insulin being sent from the pancreas. The reason seems to be inflammation and/or buildup of fat (NAFL). In this insulin resistant state, the muscles also fill up with fat. Once glycogen stores are full they become insulin resistant to avoid sugar poisoning, but keep taking up fatty acids. Because of the high carb diet and/or lack of physical activity the muscles do not burn fat and so it builds up. Also, there is some loss of muscle and liver mitochondria function and probably fatty acid transport into mitochondria.

The fat tissue takes up both glucose and fatty acids and expands if it takes up more than it gives out. The expansion of fat tissue eventually cause fat cells to send out stress signals (probably caused by endoplasmatic reticulum stress) and macrophages invade the tissue, gathering around dying fat cells. In this state, the fat tissue secretes a lot of fatty acids that wreak havoc around the body. But if free fatty acids are not burned they need to be re-esterefied. A high FFA level does not mean that we are not gaining weight or that we are losing weight (that more fat is leaving than entering the fat tissue). FFA are measured fasting and although the level might be higher in overweight and insulin resistant in that fasted state, this does not mean that over time more fat is leaving the fat tissue than are entering.

Stephan Guyenet takes the high FFA-level often observed in the overweight to mean that the fat tissue is insulin resistant and that they could not be gaining weight. This might be a wrong assumption. They have definitely been gaining weight and most overweight people are either weight stable or gaining weight. Is it impossible to gain weight while still having high FFA level?

Lean people also get insulin resistant. As do animals and humans with lipodystrophies. Many massively overweight do not become insulin resistant, and it seems that what causes the overflow of free fatty acids from adipose tissue is that it reaches its limit – a limit of course determined by both genetics and lifestyle.

In the insulin resistant state (metabolic syndrome), free fatty acids are usually high and fat builds up everywhere. Anything that increases fat oxidation helps. Pharmacological inhibition of the oxidation of fatty acids in the liver stimulates food intake in both humans and rats and stimulation of hepatic fatty acid oxidation reduces food intake, weight gain and adiposity in rats with diet-induced obesity [3].

FFA’s come from food, the liver or fat tissue. Carbohydrates are largely responsible for the amount secreted by the liver. At a cellular level, insulin resistance/metabolic syndrome seem to come from a high total energy intake. There is a surplus of both glucose (glycogen) and fat and the body can’t handle it all. Reducing the dietary fat load helps (at least if hypocaloric), but reducing dietary carbohydrate is the most efficient treatment to date. The question, though, is still why these people overeat.

Insulin

“…for insulin to cause fat gain, it must either increase energy intake, decrease energy expenditure, or both.” 

“If calories and protein are kept the same, high-carbohydrate meals cause equal or greater satiety than high-fat meals, and equal or less subsequent food intake, despite a much larger insulin response)” 

Stephan Guyenet

Insulin will reduce hunger as long as there is energy coming from ingested food. Once that flow of energy stops or is reduced, a high insulin level cause hunger. In order for insulin to cause overweight, the level only needs to be high enough for allowing fat oxidation to be less than fat storage in that particular individual over time.

Injecting both glucose and insulin reduce hunger. Injecting insulin alone increase hunger. Long term satiety is better with low carbohydrate diets than high. We need to remember that we adapt to burning different fuels. If we normally eat high carb and suddenly eat high fat we are likely to be poor fat burners and thus more likely to get hungry. This might also explain higher leptin levels after high fat meals in acute feeding studies.

“If blood glucose decreases enough, it activates a system called the «counter-regulatory response», designed to maintain blood glucose at all costs to protect the brain from the effects of hypoglycemia. Part of this response is hunger and increased food intake. However, this system is not activated except in severe hypoglycemia, which is rare except in diabetics, thus it is not relevant to common obesity.” 

This quote seriously needs references. It seems very unlikely.

These are just some thoughts. Nothing more.

References

1. Pasquet P, Brigant L, Froment A, Koppert GA, Bard D, de G, I, Apfelbaum M: Massive overfeeding and energy balance in men: the Guru Walla model. Am J Clin Nutr 1992, 56: 483-490.

2. Taubes G: Insulin resistance. Prosperity’s plague. Science 2009, 325: 256-260.

3. Ji H, Friedman MI: Reduced capacity for fatty acid oxidation in rats with inherited susceptibility to diet-induced obesity. Metabolism 2007, 56: 1124-1130.

What is the best exercise for fat loss?

You’d think this question was easy to answer after studying exercise and health for many years. You’d think I would know. I would think I would know, but when asking myself the question recently, it struck me that I didn’t. I can make a calculated guess, but I should know.

What sort of exercise would you recommend for an overweight person wanting to lose weight? Cardio, strength, plyometrics, combos? What about sets, repetitions, load, restitution and what about energy expenditure? Different exercise forms give different stimuli and affect different tissues, so it is likely that some forms of exercise are to be preferred to others. But which? 

In «the Biggest Loser,» overweight people are pushed through extreme exercise to lose weight
The Science

Let’s look at the basic science as an introduction.

If I was to give an overweight person exercise advice based on a superficial glance at the scientific literature, the advice would be, “Don’t exercise. It doesn’t work”. Exercise trials are usualy ineffective unless accompanied by a dietary intervention. 

A 1995 meta-analysis [1] concluded that:.

Aerobic exercise causes a modest loss in weight without dieting. Exercise provides some conservation of FFM [fat free mass] during weight loss by dieting, probably in part by maintaining glycogen and water.

When the John E. Fogarty International Center at the National Institutes of Health sponsored two conferences that dealt with obesity as a public health problem, there was controversy surrounding the question of cause and effect and they concluded: “The importance of exercise in weight control is less than might be believed, because increases in energy expenditure due to exercise also tend to increase food consumption, and it is not possible to predict whether the increased caloric output will be outweighed by the greater food intake.

A recently published study showed how overweight women put to exercise regularly, unconsciously compensated for the increased activity level by being less active when not exercising [2]. Based on my own experience with sports, I don’t find this odd at all.

Joseph E. Donnelly from the University of Kansas was the lead author of the American College of Sports Medicine position stand on “Appropriate Physical Activity Intervention Strategies for Weight Loss and Prevention of Weight” from 2009 [3].

On the question of whether physical activity will prevent weight gain they give it evidence category A. Evidence category A is in the words of NHLBI «Evidence is from endpoints of well-designed RCTs (or trials that depart only minimally from randomization) that provide a consistent pattern of findings in the population for which the recommendation is made. Category A therefore requires substantial numbers of studies involving substantial numbers of participants.« 

Trouble is, there are no studies that can point to exercise being the cause of weight not gained. It’s all based on the much observed inverse relationship between body weight and physical activity level. It is based on two factors co appearing i.e. leanness and exercise, but we do not have any data suggesting that the exercise is the cause of the leanness. Evidence category A anyone?

On the question of whether physical activity will prevent weight regain after weight loss they gave it an evidence category B. Evidence category B is defined thusly: “Evidence is from endpoints of intervention studies that include only a limited number of RCTs, post hoc or subgroup analysis of RCTs, or meta-analysis of RCTs. In general, Category B pertains when few randomized trials exist, they are small in size, and the trial results are somewhat inconsistent, or the trials were undertaken in a population that differs from the target population of the recommendation.

Donnely et al refer to the 2000 systematic review by Finnish researchers Mikael Fogelholm and Katriina T. Kukkonen-Harjula [4]. This review concluded that “…the role of prescribed physical activity in prevention of weight gain remains modest.” Much of the blame is placed with study participants who showed poor adherence to exercise programs.

Joseph E. Donnelly
But Donnelly and colleagues agrees that physical activity is a poor strategy for weight loss and writes: «Few studies with sedentary overweight or obese individuals using PA as the only intervention result in >3% decreases of baseline weight. Therefore, most individuals who require substantial weight loss may need additional interventions (i.e., energy restriction) to meet their weight loss needs.» 
As Gary Taubes pointed out in The scientist and the stairmaster: «Rare is the person who decides the time has come to lose weight and doesn’t also decide perhaps it’s time to eat fewer sweets, drink less beer, switch to diet soda, and maybe curtail the kind of carb-rich snacks—the potato chips and the candy bars—that might be singularly responsible for driving up their insulin and so their fat.«
Even the ultimate tome of complete gibberish, the report by the World Cancer Research Fund: “Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective” (http://www.dietandcancerreport.org/) gets at least something right and writes: “Eventually, food intake will increase to compensate for the exercise-induced energy loss, although the degree of compensation may vary greatly between individuals.

The report from WCRF gives us several references in support of their argument that physical activity reduces the risk of obesity, but a closer look at the references reveals that more of the references go against the conclusion than are in support and none of the studies can show anything but correlation.

A new analysis in JAMA that notes an association between physical activity and weight gain start off with saying: “Data supporting physical activity guidelines to prevent long-term weight gain are sparse, particularly during the period when the highest risk of weight gain occurs.

Another quite recent prospective cohort study involving 34 079 healthy US women (Women’s Health Study) found that among women consuming a usual diet, physical activity was associated with less weight gain only among women whose BMI was lower than 25, suggesting that if you’re already fat physical activity does not help. The study authors wrote: “…once overweight, it may be too late because physical activity—at least, at levels carried out by study participants—was not associated with less weight gain.”[5]

It is not hard to paint a bleak picture of the role of exercise in weight loss and weight loss maintenance. However, I still remain convinced that exercise is and should be a cornerstone in obesity treatment.

The trouble with exercise interventions is the same as is the subject of Gary Taubes recent blog post. The trouble is controlling for variables. If overweight people are included in an exercise intervention, it is very likely that they will also be more health conscientious when it comes to other lifestyle factors. When interventions that include both diet and exercise approaches are carried out, the researchers will try to control for the effect of different variables by doing multivariate analyses. But the analyses cannot and do not say anything about causation. Do people exercise because they are losing weight or are they losing weight because they exercise?

The fact that exercise recommendations are based on the correlation between exercise and weight loss and the fact that no study can point to a definitive causal link, does not mean that that causal link is not there. It does not make it less likely that exercise do cause weight loss and prevent weight gain. It just means we have to be careful when interpreting and to be open to new information.

The reporting of mean weight loss may also be deceiving. Boutcher and Dunn writes: “The results of exercise programmes designed to reduce body fat are disappointing. However, the reporting of weight loss as mean values disguises those individuals who do lose significant amounts of fat.”[6] Again, weight loss in those who actually do lose weight when exercising might be caused by many things, but it might also be caused by exercise. In addition, there is the trouble with reporting only weight loss, and not body composition.

Despite the lack of support from many scientific trials there are physiological mechanisms that make it likely that physical activity can prevent or protect against weight gain. There are also many risk factors related to the metabolic syndrome that are improved, seemingly by exercise alone – and if so, why should not fat mass be improved? The above mechanisms are the ones we have to efficiently address if we are to use physical activity as a weight loss tool. In addition many clues may in fact be hidden in articles whose conclusions does not favor exercise.

I will break this subject into several posts. Next posts theme: does the amount of energy expended during exercise affect the amount of fat mass lost?

References

1. Garrow JS, Summerbell CD: Meta-analysis: effect of exercise, with or without dieting, on the body composition of overweight subjects. Eur J Clin Nutr 1995, 49: 1-10.

2. Manthou E, Gill JM, Wright A, Malkova D: Behavioural Compensatory Adjustments to Exercise Training In Overweight Women. Med Sci Sports Exerc 2009.

3. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK: American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2009, 41: 459-471.

4. Fogelholm M, Kukkonen-Harjula K: Does physical activity prevent weight gain–a systematic review. Obes Rev 2000, 1: 95-111.

5. Lee IM, Djousse L, Sesso HD, Wang L, Buring JE: Physical activity and weight gain prevention. JAMA 2010, 303: 1173-1179.

6. Boutcher SH, Dunn SL: Factors that may impede the weight loss response to exercise-based interventions. Obes Rev 2009, 10: 671-680.

Energy in, energy out and the fairies in the back of my garden

Science philosopher Karl Popper proposed that science is easily performed. A theory must be falsifiable and the role of science is to prove a theory wrong. On the other hand if a theory resists constant attempts of falsification the probability of it being true increases. This is a very satisfying, concrete and mechanistic view of science; it is also not how science actually works. As Paul “Anything goes” Feyerabend commented, theories often survive falsification through changing the interpretations of results and sometimes by simply disregarding the results. Science is often performed blindfolded.

Assumptions are a major part of science. Sometimes they are confirmed other times they are disproven, and occasionally they form the foundation of an entire research area despite being completely wrong. The result is a branch of science where all results are interpreted in the light of its major underlying faulty theory. All results and assumptions that spring from such a major underlying theory are thus very likely to be wrong.

As far as I can tell, the whole “calories in, calories out” to lose or maintain body weight, is about as scientific as religion. I would like for nothing more than to be proven wrong on this. It would be great if someone would show up and say, “this is where you are wrong: you have forgotten to consider factor x.” I would like to be proven wrong on this, because I really don’t like the consequence of being right. The consequence is that a whole area of health science rests on a foundation of bollocks.

The correspondence between what is observed and what is stated 
I know of a number of people who are and have always been lean, who have never bothered to keep a constant record of their energy intake and energy expenditure. Some of these people have taken educations in health, nutrition or some related subject and as a consequence they start caring about how much they eat and how much they exercise. After a short while these people are convinced that the reason they are lean is their strong will and ability to always mach their energy intake to their expenditure. It is a strange and a little frightening experience to observe this change in cognition.

I have always been thin. I have never bothered about how much energy I eat or how much I use. Yet somehow my weight stays the same. Some days I hardly eat, some days I feast, some days I spend being horizontal and some days I exercise at high intensities. The fact that my weight doesn’t change does not mean I have some superpower. It is simply the way we are as humans and as animals. Most people are relatively weight stable all the time despite large fluctuations in energy intake and energy expenditure. But how can this be?

Energyman! My superpower. I can eat as much as I want, without gaining weight.
When an overweight person talks to his doctor he is instructed to count calories and make sure to expend a certain amount of energy every day to lose weight – perhaps start using the stairs instead of the elevator. But why does the overweight person need to be this obsessed with thermodynamics when most people do not?

Some clever scientist have tried to answer this question by creating an ad hoc hypothesis that states there must be a “set-point” hidden somewhere in the brain that determines our weight. The overweight have a set-point set to high. That is why they are overweight and why dieting, using a strategy based on energy reductions, don’t work. The set-point theory was invented much because dieting did not produce the results expected. It is an unproven theory and it will probably never be falsified, because it likely describes biological processes in equilibrium that appear to be a set point. The theory also has not gotten us any closer to understanding the problem that is overweight.

The rhetoric
If you are overweight it means you take in, or have at some point taken in, more energy than you expended and the excess energy is stored on your body. This is a statement of the obvious and health personnel and lay people alike often reduce it to: “Overeating causes overweight.” This statement however, makes as much sense as Willy Wonka. It is what is known as a tautology. It is a tautology because overeating means eating so much that you gain weight. The statement falls into the category of statement such as; free gift, added bonus, short summary and lying politician.

Similar to the above, it is stated that overweight is caused by to little physical activity. But the word overweight by definition means or implies that energy intake has exceeded energy expenditure. They are both very silly things to say. They make no sense and do not move the discussion forward.

Building on a tautology
You often hear well educated people say that the only thing that matters to people who wants to lose weight is to use more energy or consume less energy i.e. you must eat less than you expend. The statement rests on this equation:

Change in energy stores = energy intake – energy expenditure 

This equation is a form of the first law of thermodynamics which states that energy can be transformed, but cannot be created or destroyed. The equation is sound. It is true and makes sense. What does not make sense is the way it is commonly used.

One very important thing to note about the equation is that it does not have an arrow of causation. That is, it is just as likely that you expend more energy because your energy stores are changing as it is that your energy stores are changing (losing weight) because you are expending energy. It is also just as likely that you eat more because you are gaining weight as it is that you are gaining weight because you eat more. I’ll give you some concrete examples of this in a bit.

Logic, as the equation is, it still does not tell us why energy expenditure might be less than energy intake, which is the only important question we want to answer.

What comes first
Gary Taubes uses the example of a child hitting puberty. When we reach puberty we start growing due to a change in the hormonal milieu. As a consequence, food intake also increases to support the increased growth. In this example, increased growth cause increased food intake. Is it thus likely that increased growth as seen in obesity may cause increased food intake and not the other way around? Yes it is, and here is why:

Many studies have been performed where scientists mess about with the brain of rodents. One strategy is to do a VentroMedial Hypothalamic lesion, (VMH lesions). These damages to a part of the hypothalamus cause a greatly increased food intake and the concomitant overweight in animals. This part of the brain is thought to control hunger and satiety. The increased food intake from VMH lesions was thus thought to be because of an increased hunger signaling from the brain. But the increase in hunger may not have been caused directly be the lesions. VMH lesions does cause increased food intake, but it also cause disruptions in the fat metabolism. It increases fat storage (for example by increasing insulin levels).

Hyperphagia (abnormal hunger and food intake) associated with the development of obesity is also accompanied by a metabolic state characterized by a large deposition of fat in fat tissues. This shift in fuel partitioning toward storage is independent of food intake and occurs before the change in food intake in most animal models studied.

People with the Prader-Willi syndrome are usually very overweight and are known for having a voracious appetite. The syndrome is due to a chromosomal error that affects the hypothalamus and the hunger is thought to be due to disruptions in the hunger center of the brain. But even the great hunger characteristic of this condition may be caused by excessive deposition of fat. When people with PWS are given a low carbohydrate ketogenic diet that makes the fat tissue release its energy rather than storing it, hunger decreases.

Some rodent models (ob/ob) produce little leptin and become very overweight. Both fa/fa rats and db/db rats have a leptin receptor defect which renders them very overweight. But their genetic defect is a defect that causes increased fat storage which makes them overweight even if calories are reduced. When obese Zucker rats (fa/fa) are put on low calorie diets their bodies respond as if it was starving. They lose muscle mass and their organs decrease in size, but their fat percentage remains the same. The increased fat storage cause increased hunger and reduced energy expenditure. In these rodents (as in many humans) low calorie diets does not make energy stored in the fat tissue available for use and so they simply starve.

If we reduce our carbohydrate intake we can lose weight without the hunger often observed in low calorie trials. Boden et al demonstrated that a 14 day low carbohydrate diet gave similar measurements of hunger compared to a regular diet, despite having 1000kcal less energy/day. In one trial the researchers put mice on a low carb ketogenic diet and observed the energy expenditure of the mice increasing (15% higher total heat output and 34% increased oxygen consumption). It seems that when insulin and glucose levels drop, the fat tissue pour out stored energy resulting in increased physical activity and heat production.

Phelan and coworkers compared people who had lost weight with low carb to people who had lost weight with low calorie. Those using low carb reported consuming more energy, expending fewer calories in weekly physical activity and reported much lower dietary restraint, yet regained the same amount of weight as low calorie. 

This actually makes a lot of sense. Because our feelings of hunger and satiety are not determined by how much energy is available for the body, but how much energy is available to specific cells. It is an important distinction to make.

Why we are hungry 

Recipe for disaster. istockphoto
The cells that make up our body get the energy they need to maintain proper function from two sources; the food we eat and the energy stored in the body. When we eat we consume much more energy than is acutely needed and the extra energy is stored for later use. The cells that monitor the energy availability are situated in the liver. When they sense there is a lack of energy the body does several things. It increases our hunger to make us eat. It also makes us tiered and less energetic in order to conserve energy. If more energy is not supplied the body decides it is starving and starts shutting down energy consuming functions not needed for survival.

In the muscles the myostatin production may be increased by lack of energy. Muscle tissue is energy demanding tissue and not vital in large amounts. It thus breaks down when we starve independent of the size of our fat tissue.

In women, menstrual cycle disturbances can be a sign of insufficient energy availability to cells. Insulin injections can for example halt the reproductive function in animals and most likely in humans as well. This is how G.N. Wade put it 1996; “When food intake is limited or when an inordinate fraction of the available energy is diverted to other uses such as exercise or fattening[my bold], reproductive attempts are suspended in favor of processes necessary for individual survival.

There is no direct correlation between the amount of energy stored in the fat cells and the amount of energy available for use. If the fat cells for some reason are reluctant to give out energy or the oxidation of fatty acids are hindered, the body often does not have enough energy to keep all systems functioning and tells our brain it is starving. That is why an overweight person can be in a catabolic state or simply being hungry despite the large amounts of energy stored.

If there was a direct correlation between the energy stored and how much was available for use we would expect overweight people to be more like a Duracell bunny and not being hungry. This is not the case.

As early as 1953 Albert Pennington wrote that; ”Energy expenditure is an index of calorie nutrition at a cellular level,” and thus hinted that increased energy expenditure may be caused by greater availability of oxidizable fuels, i.e. we run because we are losing weight.

Increased release of energy from fat tissue makes us sated and energetic. Increased fat storage makes us hungry and tiered. Inhibiting fatty acid release increases food intake while inhibiting the building of triglycerides reduce food intake. This holds true in several animal models and in humans. But data also show that a large lipolysis is not always enough to stimulate decreased food intake if the oxidation of fatty acids to ATP in the liver is somehow reduced. The satiety signal is then not created.

We eat because we are getting fat and we run because we are losing weight. Remember the nonexistent arrow of causation.

About counting calories
Here is small calculation stolen from a Gary Taubes lecture:

Let’s say there is a person whose caloric intake is 2700kcal per day, which is quite the likely number.

2700kcal/day makes a total of 1000000kcal per year. That’s 10 million kcal in a decade or roughly 12 tons of food.

For a person to keep his weight within 5kg in the course of a decade he must have an accuracy in controlling energy intake and expenditure of 0,4% or 11kcal/day.

Having this kind of accuracy is impossible. 11kcal is the equivalent of a medium sized fart. What this shows, is that it is highly unlikely that energy balance is matter of cognitive control. We cannot tell people to count calories because it rests on an assumption of an inhuman accuracy equivalent to that of a very, very accurate machine.

Energy intake and energy expenditure are not independent factors 
There is a consequence of the reasoning that claims people must control of their energy intake and energy expenditure to not gain weight. The consequence is that all people who are overweight are so because they lack the willpower to be in energy equilibrium (gluttony and sloth). A second consequence of the theory is that everybody who’s lean is lean because they manage to control their expenditure and intake.

As illustrated, this is highly unlikely. And the fact that most people don’t care about energy inn vs. energy out, but still remain the same weight, should be enough to make the whole energy terror go away.

Also, if an overweight person is told that eating less or exercising more will make them lose weight, then the assumption is that energy expenditure and energy intake are independent factors. That is, that you can change one factor without the change affecting the other factor. The caveat is that this is not how the body actually works.

This is how Mark I. Friedman puts it; “Energy storage, expenditure, and intake can and do change and in doing so influence each other.

In 1998 J.E. Blundell put it bluntly; “…there is a widely held belief that physical activity is a poor strategy for losing weight, since the energy expended drives up hunger and food intake to compensate for the energy deficit incurred.

In 1977, when The National Institutes of Health hosted their second conference on obesity and weight control, they concluded that: “The importance of exercise in weight control is less than might be believed, because increases in energy expenditure due to exercise also tend to increase food consumption, and it is not possible to predict whether the increased caloric output will be outweighed by the greater food intake.

In a 1995 meta-analysis, the effect of exercise on weight loss and conservation of fat free mass was determined. The authors concluded thusly: “Aerobic exercise causes a modest loss in weight without dieting. Exercise provides some conservation of FFM during weight loss by dieting, probably in part by maintaining glycogen and water.

In a 1995 edition of The New England Journal of Medicine Jules Hirsch reported in collaboration with Leibel and Rosenbaum, that calorie restriction in overweight cause decreased energy expenditure and decreased metabolic activity adjusted for fat free mass. What they showed is that overweight people who are starved respond like thin people who are starved, by down regulating metabolism.

Jules Hirsch later said, in an interview with science journalist Gary Taubes:

Of all the damn unsuccessful treatments, the treatment of weight reduction by diet for obese people just doesn´t seem to work.

In the 1998 version of the Handbook of obesity, Bray, Bouchard and James describe countless of interventions based on calorie reduction to lose weight. Most of these failed at producing long term weight loss. The authors write that; “Energy intake is clearly elevated after significant loss of body mass. Furthermore, during weight gain, body weight does not increase monotonically but usually plateaus at higher levels.” The authors still sums it all up by recommending caloric restriction as the only sensible strategy to use.

In 2002, a Cochrane systematic review of low calorie and low fat diets for weight loss was published. The analysis showed that low fat diets were as effective as low calorie diets and that both diet strategies produced a weight loss that in the word of the authors was;”…so small as to be clinically insignificant.” The article is now, for some reason, withdrawn.

In 2000, Fogelholm and Kukkonen-Harjula concluded that everybody who lost weight with low calorie dieting eventually regained the lost weight. They also found that exercise could not prevent this weight regain. Their conclusion; ”…the role of prescribed physical activity in prevention of weight gain remains modest.

There are numerous examples from the scientific literature illustrating clearly how energy intake and expenditure are highly dependent factors. Neither traditional dieting nor exercise actually works. The misinterpretation that led people to believe intake and expenditure are independent factors forms the basis of both dietary recommendations as well as many other aspects of our lives. It is the reason that the cardio machine at your local gym has a silly calorie counter on the panel, and it forms the basis of the long held belief that the more energy you burn during exercise the more weight you’ll lose. 

What is the point of exercising if you can’t count calories?
The worst and most absurd recommendations are those claiming that if you take the stairs instead of the elevator you will expend a little more energy each day, that during the course of the year, results in x amount of kilos lost. It is as rational as the fairies in the back of my garden. 

About exercise 
If energy intake and expenditure are dependent factors, then we would not expect exercise to be a good weight loss method in itself. As illustrated from some of the quotes, exercise very often doesn’t make us thinner. It still can though. But it is important to remember that although exercise may make you lose weight, it is by no means obvious that the weight lost is because of the extra energy spent. It is in fact very unlikely that this is the mechanism.

The likely explanation for weight loss following increased exercise, is increased muscular insulin sensitivity accompanied by other factors that together cause a reduced fat storing, making fat reserves more available for use. And when a larger percentage of your body’s energy demand comes from your fat stores, you lose weight.

Contrary to popular belief, it is in fact likely that people who are lean are physically active because they are lean. Their bodies are often not very effective fat storers. Instead, their bodies supply a constant flow of energy producing a desire for or need to move about. The runner is running because he is lean, not necessarily the other way around.

And speaking of runners – in 1989 a group of Dutch scientists made 9 women and 18 men train for 18 months with the goal of running a marathon. During the 18 months the men lost 2,5kg of fat. The women didn’t lose any weight. The men increased their energy intake, the women didn’t. The women thus increased their energy expenditure without an obvious change in energy intake. However the women cut down on their fat intake and increased their intake of carbohydrates.

In a very recent report by Hopkins, King and Blundell, this is how they consider exercise for weight loss:

Recent evidence indicates that longer term exercise is characterized by a highly variable response in eating behaviour. Individuals display susceptibility or resistance to exercise-induced weight loss, with changes in energy intake playing a key role in determining the degree of weight loss achieved.»

There is no correlation between the energy expended during a bout of exercise and resulting weight loss. If our body was an isolated system, exercise could be considered the equivalent of opening a valve and letting some steam out. If a body was an isolated system such a correlation would be present, but the body is complex and not disconnected from its surroundings. The calorie hypothesis reduces it to the complexity of legos.

What we eat is more important than how much we eat. What we eat determines both what happens to the energy eaten and the energy stored in the body. You are not what you eat; you are what your body does with what you eat.

Speaking of fairies 
The Norwegian dietary guidelines, as many other countries guidelines, are based largely on a document from the World Cancer Research Fund. It is a tome of a document that is held in high regard by many. Despite its size it is a horrible, unscientific document. It is not unlikely that a large enough group of blindfolded chimpanzees could have produced something of higher quality.

One way the WCRF document is flawed is in its use of the calorie hypothesis as a foundation for everything it has to say about overweight.

In chapter 8, p 322, “Determinants of weight gain, overweight, and obesity,” the WCRF has this to say:

… a review of the epidemiological literature should be amplified by consideration of established knowledge on mechanisms, including basic thermodynamics and mechanisms of energy input, output, and balance.

For the most part the report bases its conclusions (also those about causation) on epidemiologic studies. To further show of their incompetence the authors of the WCRF report writes: “As stated, the physiological cause of weight gain, overweight, and obesity is the consumption of more energy from foods and drinks than is used.

As I have already explained, this makes absolutely no sense at all. And yet, this is the basis of my governments’ dietary recommendations.

To top it all of here is another memorable quote:

The Panel has given special emphasis to the substantial body of robust experimental evidence, both in humans and in relevant animal models, underpinned by the principles of thermodynamics. To reach its conclusions, the Panel interpreted the epidemiological findings in the light of this experimental evidence. Thus, the Panel notes the associations between specific foods and food groups with weight gain, overweight, and obesity, and has interpreted them, in the light of the experimental evidence, as indicating a general effect of energy density [my bold] rather than as several different specific effects of particular foods and drinks.

What does all this mean?
A number of studies have demonstrated that hunger occurs when fat storage is too high. Reducing fat storage reduce hunger. The best way to reduce fat storage is to reduce glucose and insulin levels. The best strategy to do this is to mind what you eat not how much. The body takes care of the how much part of its own. This is quite different from the conclusion reached from the calorie hypothesis which simply tells us to eat less.

If you want to lose weight it is implicit that you want to lose fat. To lose fat you need to mobilize the fat tissues e.g. make the fat tissue give out energy. This will make sure that a larger percentage of the energy you use comes from your own body stores. It will reduce the feeling of hunger while reducing your weight.

It is beyond human control to be in energy equilibrium. It is not how a body works.

As I said in the introduction to this piece of rambling, I would like for nothing more than to be shown that the calorie hypothesis is not flawed, as I argue it is. There is a comment section under the post. Consider this a plea rather than a challenge.

PS.

Most of this is based on the writings of Gary Taubes. If you haven’t already read his work, do it!